Figure 1 (IMAGE)

Kanazawa University

Figure 1

Caption

(a) Mice of the indicated genotypes were infected with Streptococcus pneumonia intranasally, and CFU counts in the lung were determined 48 h after infection. Casp1/11-/-, Nlrp3-/-, and Pycard-/- mice are deficient in caspase-1, NLRP3, and ASC, respectively. The result suggests that NLRP3 and ASC, but not caspase-1, are required for host resistance to pneumococcal pneumonia. (b) NLRP3 and ASC form the NLRP3 inflammasome in response to distinct stimuli, including S. pneumoniae. The inflammasome recruits and activates caspase-1, thereby promoting inflammation. However, NLRP3 and ASC seem to protect against pneumococcal pneumonia in a caspase-1-independent manner, suggesting an alternative mechanism for host defense that involves NLRP3 and ASC.

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Kanazawa University

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