| First Author | Kumar A | Year | 2022 |
| Journal | Infect Immun | Volume | 90 |
| Issue | 5 | Pages | e0010322 |
| PubMed ID | 35404106 | Mgi Jnum | J:325511 |
| Mgi Id | MGI:7286392 | Doi | 10.1128/iai.00103-22 |
| Citation | Kumar A, et al. (2022) Essential Role of NLRP3 Inflammasome in Mediating IL-1beta Production and the Pathobiology of Staphylococcus aureus Endophthalmitis. Infect Immun 90(5):e0010322 |
| abstractText | Staphylococcal endophthalmitis is one of the leading causes of blindness following ocular surgery and trauma. Dysregulated inflammation during bacterial endophthalmitis causes host-induced inflammatory damage and vision loss if it remains unchecked. Emerging evidence indicates that inflammasome plays a critical role in regulating innate immunity in various infectious and inflammatory diseases. However, the role of the inflammasome in endophthalmitis remains elusive. Here, using a mouse model of Staphylococcus (S) aureus endophthalmitis, we show that NLRP3/ASC/Caspase-1 signaling regulates IL-1beta production in endophthalmitis. We also show that S. aureus and its cell wall components and toxins induce the activation of the NLRP3 inflammasome complex in mouse eyes. Moreover, we found that both infiltrating neutrophils and retinal microglia contribute toward NLRP3 activation and IL-1beta production in S. aureus-infected eyes. Furthermore, our data using NLRP3(-/-) and IL-1beta(-/-) mice revealed that NLRP3 and IL-1beta deficiency leads to increased intraocular bacterial burden and retinal tissue damage. Altogether, our study demonstrated an essential role of NLRP3 inflammasome activation in regulating innate immune responses in bacterial endophthalmitis. |
