| First Author | Chenery AL | Year | 2019 |
| Journal | J Immunol | Volume | 203 |
| Issue | 10 | Pages | 2724-2734 |
| PubMed ID | 31586037 | Mgi Jnum | J:282044 |
| Mgi Id | MGI:6370234 | Doi | 10.4049/jimmunol.1900640 |
| Citation | Chenery AL, et al. (2019) Inflammasome-Independent Role for NLRP3 in Controlling Innate Antihelminth Immunity and Tissue Repair in the Lung. J Immunol 203(10):2724-2734 |
| abstractText | Alternatively activated macrophages are essential effector cells during type 2 immunity and tissue repair following helminth infections. We previously showed that Ym1, an alternative activation marker, can drive innate IL-1R-dependent neutrophil recruitment during infection with the lung-migrating nematode, Nippostrongylus brasiliensis, suggesting a potential role for the inflammasome in the IL-1-mediated innate response to infection. Although inflammasome proteins such as NLRP3 have important proinflammatory functions in macrophages, their role during type 2 responses and repair are less defined. We therefore infected Nlrp3 (-/-) mice with N. brasiliensis Unexpectedly, compared with wild-type (WT) mice, infected Nlrp3 (-/-) mice had increased neutrophilia and eosinophilia, correlating with enhanced worm killing but at the expense of increased tissue damage and delayed lung repair. Transcriptional profiling showed that infected Nlrp3 (-/-) mice exhibited elevated type 2 gene expression compared with WT mice. Notably, inflammasome activation was not evident early postinfection with N. brasiliensis, and in contrast to Nlrp3 (-/-) mice, antihelminth responses were unaffected in caspase-1/11-deficient or WT mice treated with the NLRP3-specific inhibitor MCC950. Together these data suggest that NLRP3 has a role in constraining lung neutrophilia, helminth killing, and type 2 immune responses in an inflammasome-independent manner. |
