Abstract
Helicobacter pylori colonizes the gastric mucosa of at least half of the human population, causing a worldwide infection that appears in early childhood and if not treated, it can persist for life. The presence of symptoms and their severity depend on bacterial components, host susceptibility, and environmental factors, which allow H. pylori to switch between commensalism and pathogenicity. H. pylori-driven interactions with the host immune system underlie the persistence of the infection in humans, since the bacterium is able to interfere with the activity of innate and adaptive immune cells, reducing the inflammatory response in its favour. Gastritis due to H. pylori results from a complex interaction between several T cell subsets. In particular, H. pylori is known to induce a T helper (Th)1/Th17 cell response-driven gastritis, whose impaired modulation caused by the bacterium is thought to sustain the ongoing inflammatory condition and the unsuccessful clearing of the infection. In this review we discuss the current findings underlying the mechanisms implemented by H. pylori to alter the T helper lymphocyte proliferation, thus facilitating the development of chronic infections and allowing the survival of the bacterium in the human host.
Highlights
Helicobacter pylori is a human pathogen responsible for an infection involving nearly half of the world’s population, frequently associated with chronic inflammation of the gastric mucosa that can lead to peptic ulceration and gastric cancer in susceptible individuals [1, 2]
We provided evidence that an enhanced expression of COX-2 occurs during H. pylori colonization of the human stomach and may induce downregulation of T helper 1 (Th1) signaling pathway, representing a mechanism by which H. pylori may interfere with normal T-cell activation in human gastric mucosa [35]
In contrast to the majority of bacterial pathogens, which temporarily cause virulent disease and are cleared by the pathogenspecific adaptive immune response, H. pylori successfully establishes a persistent infection in its host in spite of the presence of vigorous innate and adaptive immune response
Summary
Helicobacter pylori is a human pathogen responsible for an infection involving nearly half of the world’s population, frequently associated with chronic inflammation of the gastric mucosa that can lead to peptic ulceration and gastric cancer in susceptible individuals [1, 2]. The Th1 proliferation in gastric mucosa infected by H. pylori involves signals provided by antigen-presenting cells and cytokines produced in response to the components of the pathogen, such as LPS, resulting in enhanced secretion of IFN-γ itself, IL-12, and IL-18 [11].
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