Autoimmunity May be Largely Linked to Gut Bacteria
Written By: Courtney Leighton-Kelso
Written By: Courtney Leighton-Kelso
Last Updated On: 17 Sep, 2011 - 07:20pm
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The findings that a genome of bacterium may possibly be a key player in regulating the immune system of mice has been recently published in the latest issue of the Cell Host and Microbe. This study allows us the very first glimpse of how this particular genome can activate a very powerful immune response that can protect mice from infections and other ailments. This very same positive response, however, also initiates harmful inflammation throughout the body.
A large research team was used to conduct this study, led by Professor Dan Littman from the Molecular Immunology NYU School of Medicine and Ivaylo Ivanov, Ph.D from Columbia University Medical Center. The microorganism that was being examined was the segmented filamentous bacteria, also known as SFB. SFB was first identified over 40 years ago, but it was not until 2009 when Dr Littman began examining this particular genome more closely.
It is known to be genetically distinct from the other 1200 bacterial genomes, which suggests that it does play a rather unique role in the gut. In mice, this genome is able to recruit specialized Th17 cells in the small intestine of mice. It was found that these cells were able to protect mice from disease-causing Citrobacter rodentium bacteria. It was also found that mice were then more prone to inflammation and autoimmune arthritis. Researchers believed than that other intestinal bacteria in the gut are able to regulate the immune function and are responsible for preventing inflammation.
“What has become clear in the last couple of years is that individual bacteria can specifically influence particular branches of the immune system,” says Dr Littman.
The research team found that this particular genome lacks many of the genes that would be required for its own survival. It does not have the ability to make amino acids or other nutrients. Therefore, the team deduced that it must be dependant on other bacteria within the gut in order to sustain itself.
While there is no indication that human beings have the SFB genome living within our own guts, Dr Littman believes that there must be similar microorganisms living within us that perform similar functions. “Maybe in humans, there is another bacterium that is different from SFB but behaves functionally in the same way,” says Dr Ivanov.
Recent studies in Japan reveal that intestinal bacteria in human beings can boost the regulatory immune cells in mice, which controlled the inflammatory behavior of the Th17 cells. Dr Littman and his team of NYU collaborators also believe that they may have discovered a microbe in the intestinal tract of those who suffer from rheumatoid arthritis that changes their immune function. These results are leading researchers to look more deeply at how the microbes that live within our bodies can potentially impact our health.
Dr Steven Abramsom, a professor at the Departments of Medicine and Pathology and director of the Rheumatology division at NYU Langone Medical Center is particularly hopeful with the result of this study. “With more than 50 million Americans suffering from at least one autoimmune disease, this research gives scientists and clinicians a greater ability to apply knowledge gained in the laboratory to actual clinical cases, moving it to ‘bench-to-beside’ to give patients a tremendous advantage and physicians the ability to fine-tune medications and protocols based on patient response.”
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The findings that a genome of bacterium may possibly be a key player in regulating the immune system of mice has been recently published in the latest issue of the Cell Host and Microbe. This study allows us the very first glimpse of how this particular genome can activate a very powerful immune response that can protect mice from infections and other ailments. This very same positive response, however, also initiates harmful inflammation throughout the body.
A large research team was used to conduct this study, led by Professor Dan Littman from the Molecular Immunology NYU School of Medicine and Ivaylo Ivanov, Ph.D from Columbia University Medical Center. The microorganism that was being examined was the segmented filamentous bacteria, also known as SFB. SFB was first identified over 40 years ago, but it was not until 2009 when Dr Littman began examining this particular genome more closely.
It is known to be genetically distinct from the other 1200 bacterial genomes, which suggests that it does play a rather unique role in the gut. In mice, this genome is able to recruit specialized Th17 cells in the small intestine of mice. It was found that these cells were able to protect mice from disease-causing Citrobacter rodentium bacteria. It was also found that mice were then more prone to inflammation and autoimmune arthritis. Researchers believed than that other intestinal bacteria in the gut are able to regulate the immune function and are responsible for preventing inflammation.
“What has become clear in the last couple of years is that individual bacteria can specifically influence particular branches of the immune system,” says Dr Littman.
The research team found that this particular genome lacks many of the genes that would be required for its own survival. It does not have the ability to make amino acids or other nutrients. Therefore, the team deduced that it must be dependant on other bacteria within the gut in order to sustain itself.
While there is no indication that human beings have the SFB genome living within our own guts, Dr Littman believes that there must be similar microorganisms living within us that perform similar functions. “Maybe in humans, there is another bacterium that is different from SFB but behaves functionally in the same way,” says Dr Ivanov.
Recent studies in Japan reveal that intestinal bacteria in human beings can boost the regulatory immune cells in mice, which controlled the inflammatory behavior of the Th17 cells. Dr Littman and his team of NYU collaborators also believe that they may have discovered a microbe in the intestinal tract of those who suffer from rheumatoid arthritis that changes their immune function. These results are leading researchers to look more deeply at how the microbes that live within our bodies can potentially impact our health.
Dr Steven Abramsom, a professor at the Departments of Medicine and Pathology and director of the Rheumatology division at NYU Langone Medical Center is particularly hopeful with the result of this study. “With more than 50 million Americans suffering from at least one autoimmune disease, this research gives scientists and clinicians a greater ability to apply knowledge gained in the laboratory to actual clinical cases, moving it to ‘bench-to-beside’ to give patients a tremendous advantage and physicians the ability to fine-tune medications and protocols based on patient response.”
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