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Fig. 8 | Parasites & Vectors

Fig. 8

From: NLRP3 inflammasome activation from Kupffer cells is involved in liver fibrosis of Schistosoma japonicum-infected mice via NF-κB

Fig. 8

Proposed mechanism of S. japonicum SEA-mediated NLRP3 inflammasome activation involved in KCs and HSCs activation. As pathogen-associated molecular patterns (PAMPs), S. japonicum SEA is involved in the inflammatory crosstalk between KCs and HSCs, and TLR4-dependent plays a crucial role in liver inflammation during the progression of liver fibrosis. The present study applied LPS/SEA to show the involvement of the NLRP3 inflammasome pathway in the secretion of IL-1β both from KCs and HSCs. IL-1β generated by inflammasome activation will bind to receptors located on the above two kinds of cells, and upregulate fibrotic markers, resulting in their activation and ECM deposition, and leading to liver fibrosis. MCC950 could directly bind to NLRP3 and block NLRP3, suggesting that MCC950 might represent a potential preventing target for liver fibrosis

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Parasites & Vectors

ISSN: 1756-3305

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