A mouse colitis model study has demonstrated that live fecal bacteria not only induce a defect in the intestinal barrier (a leaky gut) but also intestinal inflammation and injury. Bacteria cell products or protein components could induce intestinal barrier defects or trigger a leaky gut, but without live bacteria, could not cause intestinal inflammation or colitis. Only live bacteria could cause colitis.
Loss of tolerance to proteins of normal bacteria residents in the gut, or endogenous gut flora, plays an important role in intestinal inflammation. However, it is not known why some bacteria do and others do not cause intestinal inflammation.
Oral tolerance to some bacteria appears to develop just as tolerance to certain foods occurs. Loss of tolerance may be due to a variety factors. Factors specific to an individual may include their immunogenetic make-up, underlying or pre-existing gut injury, an immune affecting event or infection, and certain combinations of bacteria, yeast, and food proteins.
When tolerance is lost, inflammation can result that may perpetuate gut injury. The resulting increasingly leaky gut leads to further intolerance. The cycle becomes self perpetuating, as on auto pilot, resulting in an autoimmune process that is difficult to break.
It may be that until altered gut flora is restored to normal and/or certain food protein exposures limited or eliminated, that this cycle continues. Medications like steroids can reduce the inflammation but not necessarily reverse the self-perpetuating process that occurs in Crohn’s disease, for example.
However, the concept of antibiotic use to kill the "bad" bacteria that have altered the normal gut flora, followed by probiotics is gaining steam. This approach is being advocated to prevent the development of irritable bowel syndrome as well as colitis and Crohn’s disease after infection or gastroenteritis. The concept of elimination of foods that are known for or suspected to be causing injury when interacting with altered bacteria and/or yeast levels bacteria in the gut is also receiving more attention.
This makes sense. The presence of antibodies to bacteria and yeast components in Crohn’s disease are indication of loss of tolerance to endogenous flora. The presence of antibodies to gliadin and the specific proteins endomysial and tissue transglutaminase indicates a loss of tolerance to gluten in celiac disease.
In both instances, the presence of these specific antibodies indicate a loss of intestinal barrier function, or leaky gut, that allows foreign bacteria and food proteins to come in contact with the genetically predisposed gut immune system. Once activated, the immune system has difficulty shutting down. Instead this self-perpetuating cycle of injury, inflammation and leaky gut continues, often fueled by bad gut bacteria levels and ongoing food protein stimulation.
The billion-dollar question may be how do you protect the gut from injury and activation of an altered gut immune response? Is it by taking probiotics regularly? Is it by avoiding certain foods? As the food doc, I offer these ideas as food for thought as we continue to explore together the links between the leaky gut, bacteria, and food.
Reference: Sydora BC et. al. “Bacterial antigens alonecan influence intestinal barrier integrity, but live bacteria are required for initiation of intestinal inflammation and injury. Inflammatory Bowel Disease. 2006;12(6):429-436.
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