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Review
. 2010 Apr;59(4):421-6.
doi: 10.1136/gut.2009.179614.

Disruption of NF-kappaB signalling by ancient microbial molecules: novel therapies of the future?

Fang Yan  1 , D Brent Polk
Affiliations
Review

Disruption of NF-kappaB signalling by ancient microbial molecules: novel therapies of the future?

Fang Yan et al. Gut. 2010 Apr.
No abstract available

PubMed Disclaimer

Conflict of interest statement

Competing interests None.

Figures

Figure 1
Figure 1
Impact of NF-κB regulatory microbial products in the intestine. Intestinal epithelial cells and their physical and biochemical adaptations, including tight junctions and the mucus layer, form an integral barrier separating host tissues from the external environment. (A) Protective roles of optimal NF-κB activation in intestinal epithelial cells. (B) Infection and damage to the intestinal epithelium disrupt the integrity leading to microbial translocation, which stimulates pro-inflammatory cytokine production by lamina propria mononuclear cells, such as dendritric cells and macrophages. In addition, infection and damage induce intestinal epithelial cells to produce inflammatory cytokine. (C) NF-κB activation is one of the mechanisms of increased pro-inflammatory cytokine production by lamina propria mononuclear cells and intestinal epithelial cells. Microbe-derived factors suppress pro-inflammatory cytokine production by inhibiting NF-κB activation to attenuate intestinal inflammation. DC, dendritic cell; Mϕ, macrophage; NF-κB, nuclear factor kappa B.
See this image and copyright information in PMC

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