Open AccessFlare‐up of experimental arthritis in mice with murine recombinant IL‐1
Author(s) -
LOO A. A. J.,
ARNTZ O. J.,
BERG W. B.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb02974.x
Subject(s) - arthritis , immunology , medicine , exacerbation , zymosan , antigen , polyarthritis , inflammation , population , biology , in vitro , biochemistry , environmental health
SUMMARY Intra‐articular injections of murine recombinant IL‐1 (mrIL‐1) during the chronic phase of antigen‐induced arthritis (AIA) induced a flare‐up of the smouldering inflammation. The exacerbation was characterized by acute and transient joint swelling and this coincided with the extravascular accumulation of neutrophils. IL‐1 injected into arthritic joints of neutropenic mice demonstrated that joint swelling was independent of the neutrophil influx into the joint. Both phenomena were absent when IL‐1 was injected into a naive joint. The IL‐1‐induced flare‐up was not T cell mediated as in the antigen‐induced flare‐up, and suggestive evidence is presented that IL‐1 sensitivity depended on the resident macrophage population. This explained why the hypersensitivity is not restricted to the immunologically mediated arthritis but reflects a more general hypersensitivily of previously injured joints, e.g. zymosan‐induced arthritis and IL‐l‐affected joints. In addition, IL‐1 could also potentiate the antigen‐specific flare‐up of chronic AIA and prolongs the duration of the exacerbation. Our data indicate that joints bearing a chronic infiltrate are at risk from exacerbations in two ways: a T cell mediated rechallenge with antigen, and a non‐specific reactivation by systemic and local IL‐1 generation.