Endogenous Interleukin‐10 is Required for the Defervescence of Fever Evoked by Local Lipopolysaccharide‐Induced and Staphylococcus Aureus‐Induced Inflammation in Rats

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Abstract
We tested the hypothesis that endogenous interleukin (IL)‐10 limits the fever induced by a Gram‐negative bacterial toxin (Escherichia coli lipopolysaccharide, LPS) and a Gram‐positive bacterial toxin (Staphylococcus aureus), when these toxins are injected into a subcutaneous air pouch (i.po.) in rats. Injection of LPS or S. aureus caused fevers that were reduced in amplitude and duration by simultaneous administration of rat recombinant IL‐10. The inhibition of fever by IL‐10 was accompanied by a significant reduction in the toxin‐evoked increases in concentrations of immunoreactive IL‐6 at the site of inflammation and of IL‐6 and IL‐1 receptor antagonist in the circulation. Conversely, neutralisation of endogenous IL‐10 in the pouch increased the amplitude and dramatically increased the duration of toxin‐evoked fever, and augmented toxin‐induced increases in pouch tumour necrosis factor‐α, IL‐1β, and especially IL‐6. Our data support a crucial regulatory role for endogenous IL‐10 in limiting the fever responses during both Gram‐negative and Gram‐positive infections.

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