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Recombinant human growth hormone improves survival and protects against acute lung injury in murine Staphylococcus aureus sepsis

Objective To investigate whether recombinant human growth hormone (rhGH) reduces mortality and protects against Staphylococcus aureus sepsis-induced acute lung injury. Methods The bacteria-positive rate of blood smears and bacteria colony counts in bacteria plate culture, TNFα and IL-10 plasma level...

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Published in:Inflammation research 2009-12, Vol.58 (12), p.855-862
Main Authors: Yi, C, Cao, Y, Mao, S. H, Liu, H, Ji, L. L, Xu, S. Y, Zhang, M, Huang, Y
Format: Article
Language:English
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Summary:Objective To investigate whether recombinant human growth hormone (rhGH) reduces mortality and protects against Staphylococcus aureus sepsis-induced acute lung injury. Methods The bacteria-positive rate of blood smears and bacteria colony counts in bacteria plate culture, TNFα and IL-10 plasma levels, lung injury score, expression of intercellular adhesion molecule-1 (ICAM-1) as well as activation of nuclear factor-kappa B (NF-κB) in the lungs were determined 6, 12 and 24 h after 140 KM mice were injected with physiologic saline (i.p. group C, n = 20); S. aureus E311122 (1.75 × 10¹² cfu/L, 40 ml/kg, i.p. group S, n = 60); or S. aureus (as group S) with a subsequent treatment of rhGH (1.0 U kg⁻¹ day⁻¹), i.m. group T, n = 60). The cumulative survival rate of an additional 15 mice from each group was followed for 7 days post S. aureus injection. Results rhGH treatment significantly increased IL-10 plasma levels and the 7-day cumulative survival rate, whereas the bacteria-positive rate of blood smears, bacteria colony counts in bacteria plate cultures, lung injury score, ICAM-1 and NF-κB expression in the lungs were significantly reduced. In addition, rhGH treatment significantly suppressed the S. aureus sepsis-induced elevation of TNFα plasma levels. Conclusions These results indicate an ability of rhGH to prevent S. aureus sepsis-induced acute lung injury in mice, which may be attributed to attenuation of increased plasma TNFα levels, and elevated IL-10 plasma levels as well as reduced ICAM-1 expression and inhibited NF-κB activity in the lungs.
ISSN:1023-3830
1420-908X
DOI:10.1007/s00011-009-0056-0