We humans exist in sea of microorganisms. According to the American Society for Microbiology, there are 10 fold the number of bacteria living in and on our bodies as cells that make up our bodies. Wherever our bodies are exposed to the outside world, for example our digestive tracts, skin, mouth, vagina, etc. we find specific varieties of bacteria and other organisms.
The totality of all the bacteria and other microorganisms that populate our bodies is called the microbiome. The microbiome is highly individualized, with the spectrum of bacteria differing from one person to another; much like an individual’s fingerprints. All people display wide variations in the kinds of bacteria that inhabit them. The types and numbers of bacteria in and on our bodies differ depending on our genetic makeup, our diet, and environmental factors.
Immune cells are found throughout the body where they are always on alert defending the body against infection. Inflammation is the primary way that the immune system controls infections and healing, but overactive immune responses can lead to debilitating inflammatory diseases such as atherosclerosis, diabetes, and bowel disorders.
There is considerable “cross-talk” between the microbiome and the immune cells. Microorganisms influence the responses of the immune system, and the immune system in turn affects the populations of the organisms that inhabit us. For example, evidence suggests that certain bacteria in the gut can decrease inflammation in the gut and decrease chronic disease. [Whether the organisms themselves are producing these molecules, or whether they are triggering immune cells to release anti-inflammatory compounds is not clear.]
Celiac Disease and Diabetes:
Individuals with celiac disease are highly sensitive to foods containing gluten, a protein found in barley, rye, and wheat. People with celiac disease have significant quality of life issues such as bloating, diarrhea, and/or constipation.
When the immune cells of celiacs see gluten, they mount an inflammatory response to try to eliminate the gluten from the intestines. The immune cells produce antibodies that attach to the inner surface of the gut and through inflammatory responses cause direct damage of the gut lining. Inflammatory responses against the body’s own tissues lead to autoimmune (against oneself) disease.
Diabetes is also the result of an autoimmune condition. Inflammatory immune cells destroy specialized cells in the pancreas that produce insulin, a hormone needed to control blood sugar.
Individuals with celiac disease have more than digestive issues, since they have almost 2.5 times a greater chance of developing diabetes than those without intestinal problems. Such conditions are associated with antibodies directed against the insulin-producing cells. When Individuals with celiac disease go on a strict gluten-free diet, they produce fewer anti-insulin-antibodies, suggesting that they are producing less of an inflammatory response.
Gluten intake changes the kinds of bacteria found in the gut. Diabetic-prone mice that eat regular mouse chow containing gluten are more likely to get diabetes than diabetic-prone mice on gluten-free chow. In addition, when the gut bacteria are analyzed, the diabetic-prone mice on gluten have the type of bacteria more often associated with inflammation, than the mice not on gluten. Thus, diet affects the responses of the immune cells and the microbiome.
As followers of this blog are aware, in the face of constantly changing external and internal challenges, the immune system of a healthy person makes adjustments to maintain immune balance, immune homeostasis.
One would expect that if inflammatory and autoimmune responses were better controlled by the body, that individuals with celiac disease and diabetes would experience a far better quality of life.
www.ncbi.nlm.nih.gov/pubmed/22699609
www.ncbi.nlm.nih.gov/books/NBK27169
www.ncbi.nlm.nih.gov/pmc/articles/PMC3256734
www.ncbi.nlm.nih.gov/pmc/articles/PMC2575488
www.ncbi.nlm.nih.gov/pubmed/22913724
www.ncbi.nlm.nih.gov/pubmed/24164337
www.ncbi.nlm.nih.gov/pubmed/24041379 www.sciencedaily.com/releases/2013/11/131113182423.htm
www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078687
