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-Helicobacter pylori persistently colonizes the gastric mucosa of humans, infecting roughly every other individual worldwide. The prevalence of H. pylori is decreasing in most parts of the developed world due to improved sanitation, reduced transmission and more frequent use of antibiotics in childhood.
-As a consequence of the loss of H. pylori from Western societies, the incidence of peptic ulcer disease and of gastric cancer has decreased continuously in populations affected by this trend. At the same time, allergies and chronic inflammatory disorders have become more common; epidemiological and experimental evidence suggests an inverse causal association between the loss of H. pylori and the rise in these immunological disorders.
-The initial colonization of the hostile environment of the gastric mucosa requires specific adaptations: these include flagella-based motility, production of urease enzyme, chemotaxis and helical cell shape.
-To establish persistent infection, H. pylori has evolved to avoid recognition by pattern recognition receptors of the innate immune system, and to preferentially activate receptors coupling to anti-inflammatory signaling pathways. Its pathogen-associated molecular patterns are substantially less bioactive than those of related gram-negative enteropathogens.
-Another H. pylori persistence strategy involves the prevention and manipulation of T-cell-mediated adaptive immunity. Specific virulence factors are produced by all strains of H. pylori to block T-cell activation, proliferation and effector functions, and to preferentially induce T-regulatory over T-effector responses. Asymptomatic carriers are more likely to preferentially generate Treg responses and to harbor dense H. pylori populations than patients with peptic ulcer disease.
-H. pylori causes gastric disease due to its production of vacuolating cytotoxin and a pathogenicity island-encoded type IV secretion system; both virulence determinants act in concert to promote the production of pro-inflammatory cytokines, to disrupt cell polarity and to cause tissue damage. The advantage for the bacteria of the production of these virulence determinants remains poorly understood, and may involve improved iron acquisition or enhanced transmission.
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原文地址：http://www.cnblogs.com/biopy/p/4295889.html
