In:
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 278, No. 4 ( 2000-04-01), p. R824-R830
Abstract:
A complete understanding of the role for endogenously produced interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), and IL-1 receptor antagonist (IL-1ra) in the acute phase response to inflammation remains unknown. In the present studies, knockout mice lacking either a functional IL-1 type I receptor (IL-1RI − / − ), a TNF type I receptor (TNFR-I − / − ), or both IL-1 type I and TNF type I receptors (IL-1RI − / − /TNFR-I − / − ) received a turpentine abscess. Additional mice deficient in IL-1ra protein (IL-1ra − / − ) or overexpressing IL-1ra protein (IL-1ra tg ) were similarly treated. After a turpentine abscess, IL-1 receptor knockout mice exhibited an attenuated inflammatory response compared with wild-type or animals lacking a functional TNFR-I. Mice overexpressing IL-1ra also had an attenuated hepatic acute phase protein response, whereas IL-1ra knockout mice had a significantly greater hepatic acute phase response. We conclude that the inflammatory response to a turpentine abscess is the result of a balance between IL-1ra expression and IL-1 binding to its type I receptor. Endogenously produced IL-1ra plays a central role in mitigating the magnitude of the IL-1-mediated inflammatory response and, ultimately, the outcome to a turpentine abscess.
Type of Medium:
Online Resource
ISSN:
0363-6119
,
1522-1490
DOI:
10.1152/ajpregu.2000.278.4.R824
Language:
English
Publisher:
American Physiological Society
Publication Date:
2000
detail.hit.zdb_id:
1477297-8
SSG:
12
Bookmarklink