期刊
JOURNAL OF IMMUNOLOGY
卷 170, 期 1, 页码 503-507出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.170.1.503
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- NHLBI NIH HHS [HL-31963] Funding Source: Medline
- NIGMS NIH HHS [GM-29507, GM-61656] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL031963] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R37GM029507, R01GM061656, R01GM029507] Funding Source: NIH RePORTER
IL-6 is known to be an important pro- and anti-inflammatory cytokine, which is up-regulated during sepsis. Our previous work has suggested a role for IL-6 in the up-regulation of C5aR in sepsis. We reported earlier that interception of C5a or C5aR results in improved outcomes in experimental sepsis. Using the cecal ligation/puncture (CLP) model in mice, we now demonstrate that treatment with anti-IL-6 Ab (anti-IL-6) results in significantly improved survival, dependent on the amount of Ab infused. CLP animals showed significantly increased binding of I-125-labeled anti-C5aR to organs when compared to either control mice at 0 h or CLP animals infused with normal rabbit I-125-labeled IgG. Binding of I-125-labeled anti-C5aR to lung, liver, kidney, and heart was significantly decreased in anti-IL-6-treated animals 6 h after CLP. RT-PCR experiments with mRNA isolated from various organs obtained 3, 6, and 12 h after CLP demonstrated increased C5aR mRNA expression during the onset of sepsis, which was greatly suppressed in CLP mice treated with anti-IL-6. These data suggest that IL-6 plays an important role in the increased expression of C5aR in lung, liver, kidney, and heart during the development of sepsis in mice and that interception of IL-6 leads to reduced expression of C5aR and improved survival.
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