Kansenshogaku Zasshi
Online ISSN : 1884-569X
Print ISSN : 0387-5911
ISSN-L : 0387-5911
The Role of IL-10 in Patients with SIRS (Systemic Inflammatory Response Syndrome)
In Relation to TNF Activity
Shin KAWAISusumu SAKAYORIHiroyuki KOBAYASHI
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Keywords: SIRS, organ failure, IL-10, TNF
JOURNAL FREE ACCESS

1995 Volume 69 Issue 7 Pages 765-771

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Abstract

The role of IL-10 (Interleukin 10) in the patients with SIRS was demonstrated in relation to the TNF (Tumor Necrosis Factor).
1. Clinical observations Thirty three materials of IL-10 and 43 materials of TNF were taken from a total of 46 patients with SIRS. And their concentration of serum were compared with those of healthy volunteers (TNF: n=12, IL-10: n=9). The value of IL-10 and TNF in SIRS patients was significantly higher than those of healthy volunteers (p>0.05 in IL-10, p<0.01 in TNF). Also, the values of both IL-10 and TNF in the patients with MOF (n=22) were higher than those of the patients without MOF (n=24) (p< 0.05 in IL-10, p<0.01 in TNF).
Both the serum values of IL-10 and TNF in 7 patients with SIRS, whose materials were obtained at two points of their clinical course, were decreased in accordance with the favorable prognosis. In these patients, the changes in IL-10 and TNF were observed in parallel.
2. Experimental observations Five 4 week ICR mice were used in an experimental study. The serum concentration of TNF and IL-10 increased to the maximum at 2 hours after 4 mg/kg of LPS injection. TNF level disappeared at 6 hours, but IL-10 level still remained at this point.
Both the serum and BALF levels of TNF increased by LPS injection which was inhibited by the intraabdominal pretreatment of 200μg of IL-10 (in serum: p<0.1, in BALF: p<0.05). By preincubation of mice alveolar macrophages with IL-10, TNF production from the macrophage resulting from LPS loading also was significantly inhibited (p<0.01).
3. From the above, it may be concluded that IL-10 inhibits TNF secretion from monocyte and protects against the pathogenic activity of TNF in the SIRS patient.

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© The Japansese Association for Infectious Diseases
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