Figure 2 (IMAGE)
Caption
ASC and NLRP3 are components of the NLRP3 inflammasome that promotes inflammation by activating caspase-1. However, ASC and NLRP3, but not caspase-1, are required for resistance to pneumococcal pneumonia, suggesting a protective role of ASC and NLRP3 independent of the inflammasome. This study aimed to elucidate the mechanism by which ASC and NLRP3 protect the host from pneumococcal pneumonia in an inflammasome-independent manner. Gene expression profiling revealed that the expression of mucosal defense factors, including TFF2 and intelectin-1, is maintained by ASC and NLRP3, but not caspase-1, in the airway during pneumococcal pneumonia. Mechanistically, ASC and NLRP3 maintain the expression of SPDEF, a transcription factor that positively regulates the expression of the mucosal defense factors, by enhancing STAT6 activation. Hence, ASC and NLRP3 are suggested to promote airway mucosal innate immunity by an inflammasome-independent mechanism involving the STAT6-SPDEF pathway.
Credit
Kanazawa University
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