| First Author | Fantuzzi G | Year | 1997 |
| Journal | J Immunol | Volume | 158 |
| Issue | 4 | Pages | 1818-24 |
| PubMed ID | 9029121 | Mgi Jnum | J:110863 |
| Mgi Id | MGI:3641405 | Doi | 10.4049/jimmunol.158.4.1818 |
| Citation | Fantuzzi G, et al. (1997) Response to local inflammation of IL-1 beta-converting enzyme- deficient mice. J Immunol 158(4):1818-24 |
| abstractText | IL-1 beta-converting enzyme (ICE) cleaves pro-IL-1 beta to the mature, released form. Although other proteases can process pro-IL-1 beta, ICE-deficient (ICE -/-) mice do not release mature IL-1 beta in response to endotoxin. The purpose of our study was to investigate the response of ICE -/- mice in two models of local inflammation, turpentine-induced tissue damage and zymosan-induced peritonitis. No differences were observed in the development of the systemic acute phase response after turpentine administration between wild-type and ICE -/- mice, but this response was completely impaired in IL-1 beta -/- mice. Accordingly, the levels of mature IL-1 beta produced in response to turpentine did not differ between wild-type and ICE -/- mice. In contrast, following zymosan-induced peritonitis, the levels of mature IL-1 beta were significantly lower in ICE -/- mice. This was associated with a 50% decrease in cellular infiltrate in ICE -/- mice compared with that in wild-type controls. The reduced production of zymosan-induced mature IL-1 beta in ICE -/- mice was also observed from cultured peritoneal or spleen cells. Our results demonstrate that in turpentine-induced tissue necrosis, precursor IL-1 beta is processed by non-ICE proteases, but in complement-mediated inflammation, ICE participates in the processing of the IL-1 beta precursor. |
