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Chapter 11 : Microbial Interference with Host Inflammatory Responses

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Microbial Interference with Host Inflammatory Responses, Page 1 of 2

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Abstract:

This chapter discusses recent findings that may shed light on how pathogens circumvent the usually effective intestinal inflammatory defenses. Additionally, it discusses how nonpathogens and commensals may also have developed signals that inhibit or dampen host inflammatory pathways. Immune and inflammatory evasion by pathogens is an expected facet of parasitic life cycles, especially those that involve invasion into the corpus of the host. Prokaryotic life has an understandable affinity for intimate relationships with eukaryotic organisms. One, AvrBsT, is found in members of phytopathogenic bacteria ( spp.) that mediate the ‘’avirulence’’ function described. An AvrA homolog is present in most enteropathogenic spp. The blockade of proinflammatory pathways by chronic pathogens such as or may allow for long-term carriage that is characteristic of these infections. The chapter addresses how bacteria in the gut are capable of modifying host epithelia for their own purposes, and describes a biochemical pathway in human cells (NF-ΚB) by which both nonpathogens and pathogens may be able to attenuate host defense systems and noted specific effector proteins (Avr/Yop) that may mediate these effects.

Citation: Neish A. 2003. Microbial Interference with Host Inflammatory Responses, p 175-190. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch11

Key Concept Ranking

Bacterial Proteins
0.50551295
African swine fever virus
0.46605617
Type III Secretion System
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0.50551295
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Figures

Image of FIGURE 1
FIGURE 1

The Rel family and IB family. Each member is a separate gene. The 300-amino-acid Rel homology domain is shown as a black rectangle; the 33-amino-acid ankyrin repeats are shown as gray ovals.

Citation: Neish A. 2003. Microbial Interference with Host Inflammatory Responses, p 175-190. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch11
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Image of FIGURE 2
FIGURE 2

The NF-B activation pathway. See text. In unstimulated cells, NF-B (a heterodimer of p50/p65) is sequestered in the cytoplasm by IB. Activation of proinflammatory signaling receptors, such as the TLR, sets in motion a series of enzymatic modifications of IB: phosphorylation, ubiquitination, and degradation. Loss of IB allows NF-B to translocate to the nucleus, bind to the promoters of numerous proinflammatory effector genes, and activate the epithelial proinflammatory program. Perturbation of any of these enzymatic steps could inhibit the entire pathway.

Citation: Neish A. 2003. Microbial Interference with Host Inflammatory Responses, p 175-190. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch11
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