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Chapter 39 : Host Inflammatory Response to Infection

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Abstract:

This chapter talks about some of the challenges from the various layers of the host response to which must adapt in order to survive in the gastric niche. The outcome of a persistent infection interacting with a chronic inflammatory response is discussed in the context of the survival of the organism and the impact this may have on the host. An infection introduced into the digestive tract must immediately deal with antimicrobial factors that exist in the mucous secretions of the oral cavity and stomach. The mucus overlaying the gastric epithelium provides an "antiseptic paint" containing antibodies and antimicrobial factors such as lactoferrin and lysozyme that protect mucosal tissues. Gastric antibodies may be ineffective at limiting the infection for several reasons that are more obvious when one considers how antibodies usually confer protection. Helper T-cell (Th) responses have been viewed as primarily belonging to one of two major subsets, Th1 or Th2, on the basis of their cytokine profile. The presence of an ineffective T-cell response suggests that the selection of a very limited T-cell subset facilitates persistent infection by . Th1 cells and the associated cell-mediated immunity may be tolerable when kept under control, but an overwhelming Th1 response, in combination with host genetics, specific strains of bacteria, and other environmental factors, could contribute to epithelial cell damage and ulcerogenesis. Since humans are believed to be a major reservoir for , the continued survival of the bacterial species depends largely on human-to-human transmission.

Citation: Wang J, Ernst P, Blanchard T. 2001. Host Inflammatory Response to Infection, p 471-480. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch39
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Figure 1

Helper T cell heterogeneity. One of the major immune regulatory mechanisms is the input of helper T cells. As illustrated here, various subsets of Th cells have been described on the basis of their respective cytokine panel. Thl cells are generally considered to be “proinflammatory” in the context of the digestive tract as the production of IFN-γ and TNF contributes to chronic inflammation, including gastritis associated with In contrast, Th2 cells have been described as being important for normal mucosal IgA regulation and the induction of tolerance. While Th2 cells may contribute to some inflammatory conditions and allergies, they still serve to keep Th1 responses in check. Furthermore, Th3 cells have been described as Th2 cells that produce the additional anti-inflammatory cytokine, TGF-β. Tr1 cells are yet another distinct subset of anti-inflammatory T cells and are characterized by their ability to produce high levels of IL-10 and to suppress colitis in animal models. Although the details controlling the development of these subsets are not well known, what is clear is that none of the antiinflammatory subsets are well represented in the chronically infected stomach. Thus, increasing their presence may provide the means to create protective immunity or an immunotherapy to limit the damage caused by inflammation.

Citation: Wang J, Ernst P, Blanchard T. 2001. Host Inflammatory Response to Infection, p 471-480. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch39
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Figure 2

Immune-mediated epithelial cell damage. This figure shows the various means by which the gastric Th1 cells may mediate epithelial cell damage. First, through the direct effect, Th1 cells can induce epithelial cell death. T-cell-derived cytokines can also increase bacterial binding and the damaging effects of infection. In addition, Th1 cells stimulate epithelial cells to produce cytokines that recruit and activate neutrophils. In turn, activated neutrophils can impart an oxidative stress that causes damage to epithelial cells as well as to cellular DNA. Finally, gastric T cells can modulate B-cell responses, possibly leading to the production of antibodies (IgG) that can activate complement (C) and contribute to immune-complex-mediated inflammation.

Citation: Wang J, Ernst P, Blanchard T. 2001. Host Inflammatory Response to Infection, p 471-480. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch39
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Tables

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Table 1

Evidence favoring a role for the host response in defining microbial pathogenesis

Citation: Wang J, Ernst P, Blanchard T. 2001. Host Inflammatory Response to Infection, p 471-480. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch39

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