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PubMed · 10897669

[Modulation of SIRS].

S Kawai
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Abstract

SIRS is a systemic inflammatory reaction occurring in the course of several diseases and it is considered that SIRS is hyper-cytokinemia. Recently, the control mechanism of IL-10 anti-inflammatory cytokine for the superfluous inflammatory reaction by inflammatory cytokines such as TNF has received considerable attention. IL-10 tends to inhibit monocytes/macrophages and the production of TNF, IL-1 and IL-8 is suppressed. In addition, the production of oxygen radicals and proteases from activated neutrophils is directly suppressed. IL-10 seems to control the generation of tissue injury that accompanies neutrophil activation by also suppressing CD11a, CD11b and TNF receptor expression of neutrophil surface directory. In this study, we observed the effect of a drug that controls cytokine production by lymphocytes after LPS loading, using an antibacterial agent and steroids, to observe the effect of the drug on the control mechanism of SIRS. As the result, TNF production by lymphocytes was suppressed by macrolide, new quinolone and fosphomycin. Steroid also dosage-dependently suppressed TNF production of lymphocytes after 24 hours of incubation while IL-10 production increased. From these results, it was considered that some antibacterial agents and steroids have anti-inflammatory or a modulating effect on inflammation. Clinically, the control of inflammation in patients with SIRS by these drugs is expected.

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4-QuinolonesAnti-Bacterial AgentsAnti-Infective AgentsAnti-Inflammatory AgentsHumansInterleukin-1Interleukin-10Interleukin-8MacrolidesMacrophagesNeutrophil ActivationSteroidsSystemic Inflammatory Response SyndromeT-LymphocytesTumor Necrosis Factor-alphaEnglish AbstractJournal ArticleReview

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S Kawai. 2000. [Modulation of SIRS].. https://pubmed.ncbi.nlm.nih.gov/10897669/

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