Host‐bacteria interactions in the intestine: homeostasis to chronic inflammation

Abstract

In the past decade it has become clear that the gut constitutes an important frontier of the body, which not only regulates the selective entry of nutrients while keeping vigilant against pathogens but also is largely responsible for shaping the immune response to educate the organism to recognize self from non-self. The very notion of self has undergone a dramatic change, with the acknowledgment that our 'selves' include a plethora of microbial species that actively participate in our body's homeostasis. The immune system continuously adapts to the microbiota in a cyclic, dynamic cross talk where intestinal epithelial cells play an important role in instructing noninflammatory responses for a steady-state control of bacterial growth, or triggering inflammatory mechanisms that can clear the gut from harmful invaders. The system is complex and robust in the sense that many players with partially overlapping roles act to keep the integrity of the intestinal mucosal barrier. Failure of these mechanisms involves genetic and environmental triggers and leads to inflammatory bowel disease. In this review, we seek to collect the state-of-the-art knowledge about how host and microbiota interact to promote gut homeostasis and provide evidences of malfunctioning of the described mechanisms in human inflammatory bowel disease.

Murine Gut Microbiota Is Defined by Host Genetics and Modulates Variation of Metabolic Traits

“…The gastrointestinal tract contains a vast community of organisms that collectively comprise the microbiota, which is critical for the development of the intestinal epithelium and mucosal immunity as well as contributing digestive metabolic functionalities [1], [2]. The composition of this complex community is established early in life and influenced soon after birth by maternal environment and stochastic exposure to different microbes.…”

Structural, functional and molecular analysis of the effects of aging in the small intestine and colon of C57BL/6J mice

“…Protection against invading microorganisms is provided by several defense mechanisms. Besides a mucous layer present on top of a continues layer of epithelial cells covering the surface of the intestine, a wide variety of immunological cells and tissue structures are present in the mucosa and submucosa of the intestinal wall [1,4,5]. …”

Human prophylactic vaccine adjuvants and their determinant role in new vaccine formulations

“…The microbiota has an essential role in promoting the development of IgA-producing plasma cells and there is evidence that this enhancing effect is driven by specific bacterial species (44). TLR5 has been demonstrated to promote IgA + B-cell differentiation.…”

“…Mice deficient in activation-induced cytidine deaminase, which leads to a loss of IgA-producing plasma cells, exhibit expansion of anaerobic, particularly segmented filamentous bacteria in the small intestine (53). TLR agonists can act directly on B cells in the presence of transforming growth factor-beta (TGF-β) to promote IgA class switching in B cells (44). A population of tumor necrosis factor (TNF)/inducible nitric oxide synthase (iNOS)-producing DCs in the intestinal lamina propria produces nitric oxide and this leads to the induction of B cell-activating factor of the TNF family (BAFF) and a proliferation-inducing ligand (APRIL), which promote activation-induced cytidine deaminase expression and IgA class switching (54).…”