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Chapter 18 : Probiotics and Other Organisms in Allergy and Autoimmune Diseases
Category: Clinical Microbiology
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The incidences of several chronic inflammatory disorders have been increasing strikingly in the developed countries. These include allergic disorders (asthma and hay fever) and some autoimmune diseases. The validity of the pathways is supported by clinical trials and experimental models in which microorganisms that are depleted from the environment in rich countries have been shown to treat allergy, autoimmunity, or intestinal inflammation. This chapter discusses current progress in this area. All of the classes of organisms discussed in the chapter have immunoregulatory potential, and workers studying probiotics might benefit from the experience of those working with killed mycobacteria or helminths, and vice versa. There have been extremely few studies of the actual effects on the human immune system of the probiotics and other microbes used in clinical trials. The chapter outlines a few studies that address the issue of immunoregulation. The reports of clinical trials involving helminths do not present any data on changes in parameters of immunoregulation.
Immunoregulatory organisms stimulate Treg responses. These organisms cause a pattern of maturation of DC such that these drive regulatory Treg rather than Th1 or Th2 effector cells. TLR2, TLR9, NOD2, and DC-SIGN expressed by the DC can be involved. Moreover, the regulation-inducing materials tend to contain TLR2 agonists, and there is evidence in studies of mice and humans that TLR2 is expressed by Treg, which can be directly triggered to proliferate via TLR2 ligands. Increased induction of DCreg and Treg leads to two mechanisms that help to control inappropriate inflammation. First, continuous exposure to Old Friends causes continuous background activation of Treg specific for the Old Friends themselves. The result is a constant background of bystander suppression. Secondly, these DCreg cells sample self, gut contents, and allergens and induce Treg specific for target antigens, thereby suppressing inflammation.