Role of endogenous cytokines in endotoxin- and interleukin-1-induced pulmonary inflammatory response and oxygen tolerance.

Abstract:

:Endotoxin lipopolysaccharide and the cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), are known to protect adult rats against O2 toxicity. However, whether the effect of endotoxin is mediated by these cytokines is not clear. We have previously demonstrated that depletion of 84% rat alveolar macrophages (AM), which reduced lipopolysaccharide (LPS)-induced release of TNF by 86%, had no effect on LPS-induced O2 tolerance. In this study, we demonstrated that coinsufflation of LPS with anti-TNF antibody and IL-1 receptor antagonist (IL-1ra), which completely inhibited LPS-induced TNF and IL-1 activities, had no effect on LPS-induced alveolar inflammatory response and O2 tolerance. Likewise, coinsufflation of IL-1 and anti-TNF antibody, which completely neutralized IL-1-induced TNF activity, had no effect on IL-1-induced alveolar inflammatory response and O2 tolerance. In contrast, IL-1ra completely abolished IL-1-induced inflammatory response and markedly inhibited IL-1-induced O2 tolerance. These results suggest that LPS-induced alveolar inflammatory response and O2 tolerance are not mediated by endogenous TNF and IL-1. Similarly, endogenous TNF does not mediate IL-1-induced alveolar inflammatory response and O2 tolerance.

authors

Tang G,White JE,Lumb PD,Lawrence DA,Tsan MF

doi

10.1165/ajrcmb.12.3.7873200

subject

Has Abstract

pub_date

1995-03-01 00:00:00

pages

339-44

issue

3

eissn

1044-1549

issn

1535-4989

journal_volume

12

pub_type

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