Innate immunity in inflammatory bowel disease

Abstract

The human intestinal tract is home to an enormous bacterial flora. The host defense against microorganisms can be divided into innate and adaptive immunity. The former is the most immediate line of response to immunologic challenges presented by bacteria, viruses, and fungi. The mucosal immune system has evolved to balance the need to respond to pathogens while co-existing with commensal bacteria and food antigens. In inflammatory bowel disease (IBD), this hyporesponsiveness or tolerance breaks down and inflammation supervenes driven by the intestinal microbial flora. Bacteria contain compounds and are recognized by a variety of receptors, including Toll-like receptors (TLRs) and NODs (a family of intracellular bacterial sensors) and are potent stimuli of innate immune responses. Several mutations in these receptors have been associated with development of IBD.

Lactobacillus reuteriprevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions

“…Among PRRs are TLRs, which signal infection, neutralize microbes, and activate proinflammatory pathways (56). Studies in mice deficient in different TLRs have shown that DNA from a commercially available probiotic cocktail (VSL#3) or Escherischia coli strain Nissle 1917 mediated anti-inflammatory effects via TLRs (41).…”

Milk Fat Globule-Epidermal Growth Factor 8 Is Decreased in Intestinal Epithelium of Ulcerative Colitis Patients and Thereby Causes Increased Apoptosis and Impaired Wound Healing

“…Studies suggest that abnormal innate and adaptive immunities, genetic susceptibility and environmental factors collaboratively lead to the disease (1)(2)(3)(4). UC is characterized by elevated production of proinflammatory mediators, repeated intestinal injury and cell restitution and increased apoptosis of intestinal epithelial cells (IECs), which leads to impaired mucosal barrier function (5)(6)(7)(8).…”

MyD88 signaling in nonhematopoietic cells protects mice against induced colitis by regulating specific EGF receptor ligands

“…The onset of inflammatory bowel disease (IBD) typically occurs in the second and third decades of life, and a majority of affected individuals progress to relapsing and chronic disease (2). IBD depends upon host immunity, and both innate and adaptive immune systems have been implicated (3,4). Evidence from animal models indicates that failure to suppress immunity to the abundant intestinal foreign antigen load can cause inflammation.…”