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Ciclosporin‐Dependent, nu ‐Independent, Mucosal Interleukin 6 Response to Gram‐Negative Bacteria
Author(s) -
HEDGES S.,
LINDER H.,
MAN P.,
EDÉN C. SVANBORG
Publication year - 1990
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1990.tb02776.x
Subject(s) - secretion , microbiology and biotechnology , bacteria , gram negative bacteria , interleukin , immunology , biology , ciclosporin , cytokine , endocrinology , kidney , escherichia coli , biochemistry , genetics , gene
Regulation of the mucosal inflammatory response to Gram‐negative bacteria was analysed. The interleukin 6 (IL‐6) secretion, influx of polymorphonuclear leucocytes into urine, and bacterial clearance from the kidneys were compared between Balb/c ( nu / nu ) and nu /± mice, with and without ciclosporin (CsA) treatment. There was no significant influence of the nu genotype on any of the host responses measured. CsA pretreatment significantly decreased II‐6 secretion in both nu / nu and nu /± mice, but did not affect bacterial clearance or the leucocyte response in any mouse strain tested. Tissue damage, in addition to bacterial infection, resulted in significantly higher levels of IL‐6 than bacterial infection alone. Tissue‐damaged mice were significantly less likely to clear the bacterial infection than their non‐damaged counterparts, but there was no significant difference in the leucocyte response. CsA pretreatment did not significantly reduce the levels of IL‐6 in the tissue‐damaged mice. These results demonstrate that the mucosal inflammatory response to Gram‐negative infection, including IL‐6 secretion, is nu ‐independent, and that bacterial infection alone or in combination with tissue damage induce IL‐6 secretion by two different pathways.