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Fig. 2 | BMC Genomics

Fig. 2

From: Investigating host-bacterial interactions among enteric pathogens

Fig. 2

Probable role of the human proteins (and their neighbors), involved in the core set of HPIs with enteric pathogens, in the activation of inflamsomes in intestinal epithelium cells. NALP3 is a pathogen recognition receptor of the NOD-like receptor (NLR) subfamily. It functions by recognizing pathogen-associated molecular patterns (PAMPs). NALP3 together with proteins like PYCARD/ ASC forms a caspase-1 activation complex known as the NALP3 inflamasome. Activation of NALP3 inflamasome further requires the assistance of focal adhesion kinase and rac 1 from the focal adhesion complex signaling pathway. Interaction of host integrinβ with pathogenic factors (like invasions) acts as the first signal for the activation of NALP3 inflamasomes. The second set of signals for the activation of inflamosomes is mediated through the Type III secretion system translocon. Expression of NALP3 inflamasome in turn results in the release of interleukins, especially IL-18. NALP3 also interacts with NOD2 leading to activation of interleukins through a pathway independent of the caspase recruitment domain-containing proteins. Inhibition of NF-κB is a common strategy adopted by enteric pathogens to block the integrin signaling pathway, thereby evading host’s immune and inflammatory responses.

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