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How harmless bacteria on skin defence against harmful bacteria?

How harmless bacteria on skin defence against harmful bacteria?


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I have read that there are some harmless bacteria live on skin and they also have role in protecting body against some harmful bacteria but how do they do so? I mean how these bacteria are able to resist other bacteria which are harmful?


Relations between organisms in complex ecosystems are various, so I won't give an exhaustive answer, only keys to understanding.

First, you need to consider that a bacterium harmful to humans is not necessary harmul to other bacteria. So there is no reason why our skin microbiota will only target/resist to human pathogens.

What's more, microbes are not inherently harmful to us. Their dangerosity also depends on the capacity of the skin to block them 1.

Then, microbial defence mechanisms depend on the kind of relation they have to the potential pathogen: competition, parasitism, predation, etc.

The article cited below will give you a nice overview on the topic.


1 Cogen, A. L.; Nizet, V.; Gallo, R. L. (2008) Skin microbiota: a source of disease or defence? British journal of dermatology, 158, 3, 442-455; doi: 10.1111/j.1365-2133.2008.08437.x


The Wonderfully Made Design of the Skin and Its Microbiome

Many microbes live in a mutualistic relationship with the human body, make up the human microbiome, and play a role in our health by modulating the immune system. Man is “covered” inside and outside his body with millions of microbes to maintain normal bodily functions and sustain life in our changing world. The skin is the largest organ in the human body and is colonized by millions of microbes. This external colonization of the integumentary system is termed our skin microbiome. Man cannot see it (except with a microscope), but we need it for normal functioning, certainly in a pathogenic world. This article focuses on the skin microbiome, its benefits, and role in creation.

Resident skin bacteria are highly diverse, and an understanding of the skin microbiome is necessary to gain insight into microbial involvement in human skin diseases and disorders. The normal skin microbiota provides clues to the pre-Fall function of bacteria. It is “normal” and critical for our body’s health to be symbiotically inhabited by microbes such as beneficial bacteria. God’s very good creation likely included microbes on the skin, and these can provide clues for human health in the future. The skin microbiome may enable novel probiotic and antibiotic approaches.

Keywords: skin, microbiota, skin microbiome, integumentary system, pre-Fall, post-Fall, immune system, biomatrix, organosubstrate, interwoven complexity, fearfully and wonderfully made, body by design, genesis of germs


Where on the skin are microflora found?

Microorganisms are found all over the skin surface but the species vary with anatomical site.

Skin sites can be grouped into three types:

Dry body sites

Dry sites include the forearms, hands, legs and feet. They have the most diverse microbiota, due to high exposure to the external environment. Coagulase-negative staphylococci predominate (eg, S. epidermedis and S. hominis).

Moist body sites

Corynebacteriam flourish in the moist skin of the skin folds: elbow creases, beneath the breasts, in-between the toes and the groins.

Sebaceous sites

Sebaceous body sites include the head, neck and trunk, where sebaceous glands secrete an oily substance, sebum , allowing cutibacteria to thrive. Demodex mites (Demodex folliculorum and Demodex brevis) and the fungus Malasezzia also congregate in the oily areas of the face.


Bacterial Infection: Be Careful—It Can Become Deadly!

A bacterial infection is nothing to take lightly it can lead to a number of serious afflictions, some of them potentially fatal.

Bacteria are one-cell organisms that are everywhere. Literally. Most bacteria are harmless, and many are beneficial. We need “good” bacteria to digest our food and help arm our immune system. And “good” bacteria destroy “bad” bacteria that may ultimately cause a bacterial infection.

A bacterial infection can be serious, especially if it enters the bloodstream, due to the high potential for drug resistance (see sidebar). Sepsis is a real concern with any bacterial infection. If you suspect a bacterial infection, you need to make a doctor’s appointment. Without proper treatment, a bacterial infection could cause your illness to worsen. For example, strep throat, without treatment, may lead to tonsillitis, ear infection, sinus infection, scarlet fever, rheumatic fever, heart damage, and kidney inflammation, according to ShareCare.com.

Harmful bacteria find their way into your body in different ways, making good hygiene your best defense. (By the way, the Food & Drug Administration says hand sanitizers are not a defense against bacteria). Bacteria can be ingested or spread sexually or through other skin-to-skin contact—and can be found on towels, clothing, and sporting equipment or in your food. Wounds, scratches, and even pimples can open the door for bacteria to grab hold.

Bacteria take advantage of any opportunity presented. Damaged teeth—even when not painful—may have a chip or crack that can allow bacteria to enter the bloodstream. That may result in a bacterial infection, but it could also lead to cancer (lung, kidney, pancreatic), hepatitis, and cardiovascular disease. Signs of leaking bacteria include: periodontitis, bad breath, sore or bleeding gums, or gum or cheek inflammation. And, of course, food poisoning is a well-known bacterial infection. The usual culprits are Escherichia coli (E. coli), Salmonella Eneteritidis (salmonella), and Listeria monocytogenes or Listeria Monocytogenes (listeria).

The Battle Between Good and Evil Bacteria

In a study published in Current Biology, researchers at the University of Oxford showed that bacteria approach conflict in much the same way as an army, responding to a threat with a coordinated, collective retaliation.

The research team studied pairs of E. coli strains as they fought against each other. Each strain uses a specific toxin to try to overcome its competitor. A strain is immune to its own toxins, but it can kill other strains. This type of competitive interaction plays a key role in how individual bacteria establish themselves in a community, such as the human gut. By engineering the strains to have a fluorescent-green color, the authors were able to clearly follow their combat in real time.

Not all strains of bacteria fight the same way. Each approaches conflict with a different level of attack, some being hyper-aggressive and others more passive. The researchers noted that strains can detect an attack from an incoming toxin and respond quickly to warn the rest of the colony and mount a counter attack together.

“Our research shows that what appear to be simple organisms can function in a very sophisticated manner,” says senior author Kevin Foster. “Their behavior is more complex than we have previously given them credit for. Much like social insects, such as honeybees and wasps, and social animals like birds and mammals who use alarm calls when under predation, they are capable of generating a coordinated attack.”

Since the human body plays host to vast numbers of bacteria, particularly our gut microbiome, this effectively means that there is a bacterial war going on inside us. Understanding bacterial competition can help us to understand how bacteria spread, where, and why.

“We know from other studies that toxins are important for whether or not a particular strain will establish in a community. But understanding how bacteria release toxins and out-compete others is very important for understanding the spread of infection,” says Foster.

Bacterial Infection Symptoms

ILLNESSES ASSOCIATED WITH BACTERIAL INFECTION

  • Bacterial meningitis
  • Bacterial vaginosis
  • Boils
  • Cellulitis
  • Chlamydia
  • Folliculitis
  • Gonorrhea
  • Impetigo
  • Otitis media
  • Sepsis
  • Sore/strep throat
  • Syphilis

Symptoms of a bacterial infection vary with the actual illness the bacteria causes, but can include:

  • An area painful to the touch
  • Chills
  • Cough, with phlegm
  • Fatigue
  • Fever
  • Headache (warm and red)
  • Muscular pain
  • Pain
  • Respiratory distress or pain
  • Sweating
  • Swelling in the area
  • Vomiting

What types of illnesses can arise from a bacterial infection? There are numerous, from boils to pneumonia, from septic arthritis to urinary tract infections (see list in sidebar).

Bacterial Infection and the Flu

An infection with both the flu (which is caused by a virus) and bacteria can be a fatal combination, say scientists from the University of Vienna. The influenza virus attacks the upper-respiratory tract—the nose, throat and bronchi—and, rarely, also the lungs. Although people die from the flu every year, a main cause of death in people having the flu is a secondary bacterial infection.

When someone has the flu, susceptibility to bacterial infection increases. One type of bacteria that the immune system usually prevents from spreading and harming us is Legionella pneumophila. (Infection with Legionella pneumophila is called Legionnaires’ disease.) However, in some circumstances, such as when we’re infected with influenza virus, Legionella can cause pneumonia, which if left untreated can leave the lung permanently damaged and even cause death.

“In our model system, an infection with influenza and Legionella was fatal,” says lead author Amanda Jamieson. “We expected that this would be caused by the bacteria growing and spreading like crazy, but what we actually found was that the number of bacteria didn’t change, which was a big surprise.”

The researchers showed that the damage to the lung tissue caused by a co-infection with flu and Legionella is not properly repaired, as the influenza virus suppresses the body’s ability to repair tissue damage. In case of an additional Legionella infection, this may lead to fatal pneumonia. However, treatment with drugs that activate tissue-repair pathways significantly improved the outcome. This suggests that new treatment options to deal with co-infections of flu and bacteria should be explored.

For related reading, please visit these posts:

BACTERIAL INFECTION AND DRUG RESISTANCE

More than 2 million people each year get a bacterial infection that is resistant to antibiotics, according to the Centers for Disease Control and Prevention (CDC). Some 23,000 of them die from a drug-resistant bacterial infection.

The CDC has a list of 18 organisms (17 bacteria and 1 fungus) that have shown signs of being drug-resistant threats. Antimicrobial agents like antibiotics have been used against these organisms since the 1940s. Now, more than 70 years later, we’re seeing the drugs become less effective. That’s because it’s unlikely any of the drugs always killed every organism it was targeting, which means it left behind organisms that were able to adapt to the drug and become resistant to its effects.

Three of those 18 organisms are listed by the CDC as an “Urgent Hazard Level.” All three are bacteria. The CDC says these threats may not be widespread, but they have the potential to become so, which is why bacterial infections like these are monitored closely. These bacteria are:


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Immune System and Response: Natural Defence, Cell Mediated Immuniuty, Antibodies and Lymphocytes. (2017). In ScienceAid. Retrieved Jun 24, 2021, from https://scienceaid.net/biology/micro/immune.html

MLA (Modern Language Association) "Immune System and Response: Natural Defence, Cell Mediated Immuniuty, Antibodies and Lymphocytes." ScienceAid, scienceaid.net/biology/micro/immune.html Accessed 24 Jun 2021.

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Bacteria living on skin may affect how wounds heal

The thin layer of microorganisms covering our skin may play an important role in wound healing, according to a new UK study discussed at a scientific meeting in the US. The researchers hope the findings will help improve how we treat chronic wounds, a common ailment among the elderly.

Dr. Matthew Hardman, a senior research fellow at the University of Manchester Healing Foundation Centre, presented the study at the Experimental Biology 2014 meeting in San Diego, CA, on April 28th.

Having just got used to the fact that our gut is home to trillions of bacteria, we now learn that we spend our whole lives clothed in a thin veneer of microorganisms.

However, compared with what we know about gut bacteria, we are only just beginning to find out about those that colonize our skin, says Dr. Hardman, who explains the value of the new findings:

“This study gives us a much better understanding of the types of bacterial species that are found in skin wounds, how our cells might respond to the bacteria and how that interaction can affect healing.”

“It’s our hope that these insights could help lead to better treatments to promote wound healing that are based on sound biology,” he adds.

Around 1 in 20 elderly people live with wounds that never seem to heal. These chronic wounds are a significant health problem and often result from diabetes or poor blood circulation, such as that which develops when a person is confined to a wheelchair or bed.

Share on Pinterest The findings suggest there may be a particular bacterial pattern or “signature” for wounds that do not heal.

Such wounds can persist unhealed for years, says Dr. Hardman, and there are no good treatments to help them heal. Plus, there are no reliable ways to tell if they ever will.

“There’s a definite need for better ways to both predict how a wound is going to heal and develop new treatments to promote healing,” he adds.

For their study, he and his colleagues compared skin bacteria from people with chronic wounds with those of people whose wounds did heal.

They found marked differences in the bacterial colonies of the two groups, suggesting there may be a particular bacterial pattern or “signature” for wounds that do not heal.

Dr. Hardman says their findings support the idea that you could profile the bacteria from a wound swab to see if the wound is likely to heal quickly or persist, and then use that to make treatment decisions.

The team carried out tests on mice to see if they could discover why some wounds heal while others do not. They found mice with a particular mutation in a gene had more harmful bacteria and healed more slowly than mice with the normal variant of the gene.

The gene has been linked to Crohn’s disease and is known to help cells identify and react to bacteria.

“Presumably, the mice’s defect in the ability to identify bacteria means that they aren’t able to mount the right type of response,” suggests Dr. Hardman, who says their findings are consistent with the idea that our genes determine the mix of bacteria on our skin, and this in turn affects how it heals when wounded.

“Taken together,” he concludes, “our studies in humans and mice offer good evidence that the skin microbiome has a direct effect on how we heal.”

He says by learning more about skin bacteria perhaps we can help doctors decide treatments that address the harmful bacteria without affecting any potential beneficial ones.

The Medical Research Council and the Healing Foundation funded the study.

In 2012, Medical News Today learned how a common, apparently harmless, skin-dwelling bacterium may be responsible for chronic sinusitis, a painful recurring condition that strikes more than 1 in 10 Americans every year.

In that study, researchers at the University of California-San Francisco suggested that sinusitis may be connected to the loss of normal microbial diversity that occurs in the sinuses as a result of infection when they are subsequently colonized by the culprit bacterium Corynebacterium tuberculostearicum.


Distinguishing deadly Staph bacteria from harmless strains

The Staphylococcus aureus pan-genome -- a survey of 64 strains -- is made up of a "core" genome and a "dispensable" genome. Credit: NIAID

Staphylococcus aureus bacteria are the leading cause of skin, soft tissue and several other types of infections. Staph is also a global public threat due to the rapid rise of antibiotic-resistant strains, including methicillin-resistant Staphylococcus aureus or MRSA. Yet Staph also commonly colonize our nasal passages and other body sites without harm. To better understand these bacteria and develop more effective treatments, University of California San Diego researchers examined not just a single representative Staph genome, but the "pan-genome"—the genomes of 64 different strains that differ in where they live, the types of hosts they infect and their antibiotic resistance profiles.

This effort, published June 6 by the Proceedings of the National Academy of Sciences, places all Staph genes into one of two categories: the core genome or the dispensable genome.

The study resulted from a collaboration between Bernhard Palsson, PhD, Distinguished Professor of Bioengineering and Pediatrics, and Victor Nizet, MD, professor of pediatrics and pharmacy. Experiments were mostly performed by Jonathan Monk, then a graduate student in Palsson's lab.

"The most exciting thing about this study is the computational ability to analyze so many strains simultaneously—an unlimited number, really—to better understand the interrelationships between fundamental metabolism of the organisms and its virulence, or ability to cause human disease," said Nizet, a pediatrician and infectious disease researcher.

Palsson is a pioneer in systems biology, a scientific field that combines experimental and computational methods to capture a multi-layered view of complex living systems and how they work. In this study, Monk and Palsson used genome-scale models—computer simulations—of Staph metabolism to systematically analyze the ability of 64 Staph strains to thrive in more than 300 different environments.

On average, a single Staph genome encodes 2,800 genes. But here the researchers found a total of 7,457 genes across 64 strains of the bacterium—the Staph pan-genome. Nineteen percent of the pan-genome (1,441 genes) made up what the team calls the "core genome," referring to the genes essential for life and encoded by all strains. In contrast, the vast majority of the Staph pan-genome was dispensable, and more variable across strains—39 percent (2,871 genes) were deemed "accessory," meaning they were present in some but not all strains, and the remaining 42 percent (2,871 genes) "unique," meaning they were found in only one strain.

Dispensable genes give the strains that possess them advantages under particular environmental conditions, such as adaption to distinct living spaces, the ability to colonize new human or animal hosts and antibiotic resistance.

"Knowledge from a single strain is never sufficient to represent an entire species," Palsson said. "Now, the Staph pan-genome could help us be smarter about our analyses of bacterial virulence and how bacteria respond to or resist antibiotics."

"This study provides an essential roadmap—one that describes what it means to be Staphylococcus aureus ," Nizet said. "We can now use this information to test any number of hypotheses. For example, we might identify a system that's essential for the bacterium's life and now we can take that information back to the lab, study those genes and the proteins they encode in depth, and screen for new therapeutics that specifically target that pathway."

Palsson and Nizet recently received a five-year, $9.5-million award from the National Institute of Allergy and Infectious Diseases at the National Institutes of Health to establish an interdisciplinary center to define the systems biology of antibiotic resistance.


How harmless bacteria on skin defence against harmful bacteria? - Biology

Show all 20 random questions

  1. ? produces an antiseptic liquid when irritated
  2. ? acts as a barrier to germs and produces an antiseptic oil
  3. ? sticky mucous traps microbes which is removed by cilia cells
  4. ? platelets produce clots which dry to form a barrier to germs
  5. ? white cells surround and destroy microbes
  1. ? produces an antiseptic liquid when irritated
  2. ? acts as a barrier to germs and produces an antiseptic oil
  3. ? sticky mucous traps microbes which is removed by cilia cells
  4. ? platelets produce clots which dry to form a barrier to germs
  5. ? contains acid that kills most harmful bacteria
  1. ? white cells surround and destroy microbes
  2. ? acts as a barrier to germs and produces an antiseptic oil
  3. ? sticky mucous traps microbes which is removed by cilia cells
  4. ? platelets produce clots which dry to form a barrier to germs
  5. ? contains acid that kills most harmful bacteria
  1. ? produces an antiseptic liquid when irritated
  2. ? acts as a barrier to germs and produces an antiseptic oil
  3. ? sticky mucous traps microbes which is removed by cilia cells
  4. ? platelets produce clots which dry to form a barrier to germs
  5. ? contains acid that kills most harmful bacteria
  1. ? produces an antiseptic liquid when irritated
  2. ? acts as a barrier to germs and produces an antiseptic oil
  3. ? sticky mucous traps microbes which is removed by cilia cells
  4. ? contains acid that kills most harmful bacteria
  5. ? white cells surround and destroy microbes
  1. ? contains acid that kills most harmful bacteria
  2. ? acts as a barrier to germs and produces an antiseptic oil
  3. ? sticky mucous traps microbes which is removed by cilia cellsbes which is moved by cilia cells
  4. ? platelets produce clots which dry to form a barrier to germs
  5. ? white cells surround and destroy microbes
  1. ? it has a protein coat, has genes, no cytoplasm, can only reproduce in living 'host' cells and damages them, not destroyed by antibiotics, extremely small (many cannot be seen even with a powerful optical microscope)
  2. ? it has a cell wall (not cellulose) and cell membrane, has genes and cytoplasm, no nucleus, produces toxins, can reproduce outside living cells and is destroyed by antibiotics
  3. ? it is a single cell or cellular filaments with nucleus containing genes surrounded by cytoplasm but does not contain chlorophyl
  1. ? it has a protein coat, has genes, no cytoplasm, can only reproduce in living 'host' cells and damages them, not destroyed by antibiotics, extremely small (many cannot be seen even with a powerful optical microscope)
  2. ? it has a cell wall (not cellulose) and cell membrane, has genes and cytoplasm, no nucleus, produces toxins, can reproduce outside living cells and is destroyed by antibiotics
  3. ? it is a single cell or cellular filaments with nucleus containing genes surrounded by cytoplasm but does not contain chlorophyl
  1. ? it has a protein coat, has genes, no cytoplasm, can only reproduce in living 'host' cells and damages them, not destroyed by antibiotics, extremely small (many cannot be seen even with a powerful optical microscope)
  2. ? it has a cell wall (not cellulose) and cell membrane, has genes and cytoplasm, no nucleus, produces toxins, can reproduce outside living cells and is destroyed by antibiotics
  3. ? it is a single cell or cellular filaments with nucleus containing genes surrounded by cytoplasm but does not contain chlorophyl
  1. ? injection of dead or weakened micro-organism to stimulate production of antibodies
  2. ? the result of a micro-organism entering the body and causing disease
  3. ? kills, or prevents the growth of bacteria on external parts of the body
  4. ? kills, or prevents the growth of bacteria in the body
  5. ? a micro-organism that can cause a disease
  1. ? injection of dead or weakened micro-organism to stimulate production of antibodies
  2. ? the result of a micro-organism entering the body and causing disease
  3. ? kills, or prevents the growth of bacteria on external parts of the body
  4. ? kills, or prevents the growth of bacteria in the body
  5. ? a protein made by white blood cells that can help destroy microbes
  1. ? injection of dead or weakened micro-organism to stimulate production of antibodies
  2. ? the result of a micro-organism entering the body and causing disease
  3. ? kills, or prevents the growth of bacteria on external parts of the body
  4. ? kills, or prevents the growth of bacteria in the body
  5. ? a protein made by white blood cells that can help destroy microbes
  1. ? a protein made by white blood cells that can help destroy microbes
  2. ? the result of a micro-organism entering the body and causing disease
  3. ? a protein made by white blood cells that can help destroy microbes
  4. ? kills, or prevents the growth of bacteria in the body
  5. ? a micro-organism that can cause a disease
  1. ? injection of dead or weakened micro-organism to stimulate production of antibodies
  2. ? a protein made by white blood cells that can help destroy microbes
  3. ? kills, or prevents the growth of bacteria on external parts of the body
  4. ? kills, or prevents the growth of bacteria in the body
  5. ? a micro-organism that can cause a disease
  1. ? injection of dead or weakened micro-organism to stimulate production of antibodies
  2. ? the result of a micro-organism entering the body and causing disease
  3. ? kills, or prevents the growth of bacteria on external parts of the body
  4. ? kills, or prevents the growth of bacteria in the body
  5. ? a protein made by white blood cells that can help destroy microbes
  1. ? 2.0g sugar, 20 o C
  2. ? 3.5g sugar, 35 o C
  3. ? 2.0g sugar, 35 o C
  4. ? 3.5g sugar, 20 o C
  1. ? 2.0g sugar, 20 o C
  2. ? 3.5g sugar, 35 o C
  3. ? 2.0g sugar, 35 o C
  4. ? 3.5g sugar, 20 o C

You can grow micro-organisms in a __(1)__ containing a gelatinous layer of __(2)__ mixed with __(3)__ to feed on. The __(4)__ are spread across the gel using a __(5)__ wire loop.

Which word(s) is/are missing from __(1)__? [8c-20]

You can grow micro-organisms in a __(1)__ containing a gelatinous layer of __(2)__ mixed with __(3)__ to feed on. The __(4)__ are spread across the gel using a __(5)__ wire loop.

Which word(s) is/are missing from __(2)__? [8c-21]

You can grow micro-organisms in a __(1)__ containing a gelatinous layer of __(2)__ mixed with __(3)__ to feed on. The __(4)__ are spread across the gel using a __(5)__ wire loop.

Which word(s)) is/are missing from __(3)__? [8c-22]

You can grow micro-organisms in a __(1)__ containing a gelatinous layer of __(2)__ mixed with __(3)__ to feed on. The __(4)__ are spread across the gel using a __(5)__ wire loop.

Which word(s) is/are missing from __(4)__? [8c-23]

You can grow micro-organisms in a __(1)__ containing a gelatinous layer of __(2)__ mixed with __(3)__ to feed on. The __(4)__ are spread across the gel using a __(5)__ wire loop.

Which word(s) is/are missing from __(5)__? [8c-24]

  1. ? antibiotics like penicillin, stop bacteria reproducing
  2. ? viruses can't cause diseases
  3. ? white blood cells can't kill harmful micro-organisms
  4. ? antibodies in your blood help form a protective scab over a cut
  5. ? while still in the womb, a baby cannot get antibodies from its mother
  1. ? antibiotics like penicillin, stop viruses reproducing
  2. ? viruses can cause diseases
  3. ? white blood cells can't kill harmful micro-organisms
  4. ? antibodies in your blood help form a protective scab over a cut
  5. ? while still in the womb, a baby cannot get antibodies from its mother
  1. ? antibiotics like penicillin, stop viruses reproducing
  2. ? viruses can't cause diseases
  3. ? white blood cells can kill harmful micro-organisms
  4. ? antibodies in your blood help form a protective scab over a cut
  5. ? while still in the womb, a baby cannot get antibodies from its mother
  1. ? antibiotics like penicillin, stop viruses reproducing
  2. ? viruses can't cause diseases
  3. ? white blood cells can't kill harmful micro-organisms
  4. ? platelets in your blood help form a protective scab over a cut
  5. ? while still in the womb, a baby cannot get antibodies from its mother
  1. ? antibiotics like penicillin, stop viruses reproducing
  2. ? viruses can't cause diseases
  3. ? white blood cells can't kill harmful micro-organisms
  4. ? antibodies in your blood help form a protective scab over a cut
  5. ? while still in the womb, a baby can get antibodies from its mother
  1. ? drinking water is treated with chlorine before domestic use
  2. ? the result of being injected with a dead or weakened form of a micro-organism to stimulate antibody production
  3. ? using yeast and sugar solution to make alcohol
  4. ? milk is treated to remove some fat to make it semi-skimmed
  1. ? drinking water is treated with chlorine before domestic use
  2. ? the result of being injected with a dead or weakened form of a micro-organism to stimulate antibody production
  3. ? using yeast and sugar solution to make alcohol
  4. ? milk is heated to a high temperature for a short time before selling to customer
  1. ? drinking water is treated with chlorine before domestic use
  2. ? the result of being injected with a dead or weakened form of a micro-organism to stimulate antibody production
  3. ? using yeast and sugar solution to make alcohol
  4. ? milk is heated to a high temperature for a short time before selling to customer
  1. ? drinking water is treated with chlorine before domestic use
  2. ? the result of being injected with a dead or weakened form of a micro-organism to stimulate antibody production
  3. ? using yeast and sugar solution to make alcohol
  4. ? milk is heated to a high temperature for a short time before selling to customer

Very small living things that can only be seen with a __(1)__ and are called __(2)__. Some are __(3)__ like __(4)__ used in breadmaking. However, others are __(5)__ causing diseases like __(6)__.

Which missing word is __(1)__? [8c-34]

  1. ? microscope
  2. ? microbes
  3. ? useful
  4. ? yeast
  5. ? harmful
  6. ? cholera

Very small living things that can only be seen with a __(1)__ and are called __(2)__. Some are __(3)__ like __(4)__ used in breadmaking. However, others are __(5)__ causing diseases like __(6)__.

Which missing word is __(2)__? [8c-35]

  1. ? microscope
  2. ? microbes
  3. ? useful
  4. ? yeast
  5. ? harmful
  6. ? cholera

Very small living things that can only be seen with a __(1)__ and are called __(2)__. Some are __(3)__ like __(4)__ used in breadmaking. However, others are __(5)__ causing diseases like __(6)__.

Which missing word is __(3)__? [8c-36]

  1. ? microscope
  2. ? microbes
  3. ? useful
  4. ? yeast
  5. ? harmful
  6. ? cholera

Very small living things that can only be seen with a __(1)__ and are called __(2)__. Some are __(3)__ like __(4)__ used in breadmaking. However, others are __(5)__ causing diseases like __(6)__.

Which missing word is __(4)__? [8c-37]

  1. ? microscope
  2. ? microbes
  3. ? useful
  4. ? yeast
  5. ? harmful
  6. ? cholera

Very small living things that can only be seen with a __(1)__ and are called __(2)__. Some are __(3)__ like __(4)__ used in breadmaking. However, others are __(5)__ causing diseases like __(6)__.

Which missing word is __(5)__? [8c-38]

  1. ? microscope
  2. ? microbes
  3. ? useful
  4. ? yeast
  5. ? harmful
  6. ? cholera

Very small living things that can only be seen with a __(1)__ and are called __(2)__. Some are __(3)__ like __(4)__ used in breadmaking. However, others are __(5)__ causing diseases like __(6)__.


Nonspecific Immune Responses (Innate Immune Responses)

Cytokines (including interleukins 1 and 6, tumor necrosis factor-alpha, and interferon-gamma) are produced principally by macrophages and activated lymphocytes and mediate an acute-phase response that develops regardless of the inciting microorganism. The response involves fever and increased production of neutrophils by the bone marrow. Endothelial cells also produce large amounts of interleukin-8, which attracts neutrophils.

The inflammatory response directs immune system components to injury or infection sites and is manifested by increased blood supply and vascular permeability, which allows chemotactic peptides, neutrophils, and mononuclear cells to leave the intravascular compartment.

Microbial spread is limited by engulfment of microorganisms by phagocytes (eg, neutrophils, macrophages). Phagocytes are drawn to microbes via chemotaxis and engulf them, releasing phagocytic lysosomal contents that help destroy microbes. Oxidative products such as hydrogen peroxide are generated by the phagocytes and kill ingested microbes. When quantitative or qualitative defects in neutrophils result in infection (eg, chronic granulomatous disease), the infection is usually prolonged and recurrent and responds slowly to antimicrobial drugs. Staphylococci, gram-negative organisms, and fungi are the pathogens usually responsible.


Welcome to The Academic Times

R esearchers studying thale cress plants have discovered that the microbiome, a collection of benign bacteria that live in and on the plant, stimulates a common immune response that helps train the immune system to combat harmful pathogens.

The findings, published Monday in Nature Plants, could have implications for protecting crops against pathogens, which, together with pests, cost the global agricultural industry $540 billion per year.

"Although these microbes are harmless and not pathogenic, the plant mounts a common response, [which] is important for later encounters [with] pathogens," said senior author Julia Vorholt, a professor of microbiology at ETH Zurich.

In addition to its implications for plant health, the study also identified an interesting parallel between plant and human immunity. Just after birth, humans start to play host to millions of harmless bacteria that impact the number of white blood cells in the body and also help train the immune system to combat malicious infections throughout life.

Plants also host a microbiome, which "may have beneficial functions for the plant that are currently not well understood," according to Vorholt. Despite a growing understanding of the human microbiome, only recently have researchers turned to the microbes on plants to gain insights into their biology.

"Plant biology needs to embrace the microbiome," she said.

The researchers conducted an exploratory study with a set of 39 endogenous bacterial strains found on the leaves of Arabidopsis thaliana, the thale cress. This species has proved to be an ideal model organism in plant biology because, while it is small and easy to grow, it is closely related to economically important plants, such as turnip, cabbage, broccoli and canola.

"I am convinced that our findings can translate to other plant species, including crops," Vorholt said. "The plant immune system is conserved across plants, and also, the microbiota of different plants resemble each other."

The team wanted to know how the plant would respond to each of the individual bacteria in the lab, which required growing nearly 4,000 plants to get a dataset comprehensive enough to draw conclusions. The researchers compared the gene expression and presence of certain metabolic compounds in the experimental plants to those that had never encountered any bacteria.

The researchers found that across all 39 strains, there was a common group of genes that were activated in the plant by the presence of the bacteria, forming a response that the team called the "general non-self response," or GNSR.

"The name reflects that the plants respond to 'non-self,' as the GNSR is only induced when they are colonized by a microbe," Vorholt said.

The team was also able to compare this general response to previous data about the response of plants to pathogens to determine whether the GNSR also occurred when plants got sick, an important step in applying the findings to solving practical problems.

"The analysis clearly indicated overlap in the response," Vorholt confirmed.

The last piece of the puzzle was determining whether the GNSR was in any way involved in the plant defending itself against pathogens. The team used Pseudomonas syringae, a model bacterial strain that has been used in thale cress studies for decades. Originally associated with tomato plants, this species is now known to infect a wide variety of plants, causing fruit damage, leaf destruction and bud death.

The researchers found that plants that lacked even part of the GNSR genes were significantly more vulnerable to the Pseudomonas.

"This suggests that the GNSR constitutes an adaptive defense strategy triggered by the plant microbiota," Vorholt said.

That means the harmless bacteria living in and on the plant indirectly protect the plant from pathogens by stimulating a protective response, suggesting that, as in humans, these bacteria are training the immune system for later battles with harmful microbes.

Now that the team has discovered the GNSR, the next step will be evaluating how the response affects the bacteria themselves. The researchers are also hopeful that insights like theirs will encourage others to consider the microbiome when studying plants.

"Plants are always colonized by [microbes], which means there are no "germ-free" plants. … We need to keep in mind that they are not organisms by themselves, but come with a microbiota that originated from the soil or other sources," Vorholt said. "We are only at the beginning of understanding the molecular basis of how plants integrate all the inputs from the environment."

The study, "A general non-self response as part of plant immunity," published May 17 in Nature Plants, was authored by Benjamin A. Maier, Patrick Kiefer, Christopher M. Field, Lucas Hemmerle, Miriam Bortfeld-Miller, Barbara Emmenegger, Martin Schäfer, Sebastian Pfeilmeier, Shinichi Sunagawa, Christine M. Vogel and Julia A. Vorholt, ETH Zürich.


Watch the video: Types Of Bacteria That Live On Your Skin (July 2022).


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