| First Author | Ross BX | Year | 2017 |
| Journal | J Immunol | Volume | 198 |
| Issue | 9 | Pages | 3536-3547 |
| PubMed ID | 28330899 | Mgi Jnum | J:247810 |
| Mgi Id | MGI:5927409 | Doi | 10.4049/jimmunol.1602087 |
| Citation | Ross BX, et al. (2017) IL-24 Promotes Pseudomonas aeruginosa Keratitis in C57BL/6 Mouse Corneas. J Immunol 198(9):3536-3547 |
| abstractText | The aim of this study was to elucidate the expression and functions of IL-24 in C57BL/6 mouse corneas in response to Pseudomonas aeruginosa infection. Among IL-20R cytokines, only IL-24 was induced at both mRNA and protein levels by infection at early time points. The upregulation of IL-24 was dampened by flagellin pretreatment, which protects the corneas from microbial infection. Time course studies revealed bimodal early and later peaks of IL-24 expression, a pattern shared with suppressor of cytokine signaling (SOCS)3 but not IL-1beta or IL-6. Silencing of IL-24 enhanced S100A8/A9 expression and suppressed SOCS3, IL-1beta, IL-1RN, and matrix metalloproteinase 13 expression at 6 h postinfection. Downregulation of the IL-24 signaling pathway significantly reduced the severity of keratitis, whereas rIL-24 exacerbated P. aeruginosa-mediated tissue destruction. In vitro, rIL-1beta induced the expression of SOCS3, IL-24, IL-1beta, and IL-6 in primary cultured human corneal epithelial cells. rIL-24, alternatively, stimulated the expression of SOCS3, but not the others. In conclusion, IL-24 promotes P. aeruginosa keratitis through the suppression of early protective mucosal immunity, culminating in increased severity of P. aeruginosa keratitis. |
