Effects of therapy with interleukin-1 receptor antagonist on pulmonary cytokine expression following hemorrhage and resuscitation

Acute lung injury frequently develops following hemorrhage and is characterized by increased proinflammatory cytokine levels and massive neutrophil accumulation in the lung. Blood loss produces rapid increases in IL-1 alpha and IL-1 beta mRNA expression among pulmonary cell populations. To examine t...

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Bibliographic Details
Published inLymphokine and cytokine research Vol. 13; no. 6; p. 343
Main Authors Abraham, E, Allbee, J
Format Journal Article
LanguageEnglish
Published United States 01.12.1994
Subjects
Animals
Bronchoalveolar Lavage Fluid - immunology
Cytokines - genetics
Gene Expression - drug effects
Hemorrhage - genetics
Hemorrhage - immunology
Interferon-gamma - blood
Interferon-gamma - metabolism
Interleukin 1 Receptor Antagonist Protein
Lung - immunology
Lung Injury
Male
Mice
Mice, Inbred BALB C
Receptors, Interleukin-1 - antagonists & inhibitors
Resuscitation
RNA, Messenger - genetics
RNA, Messenger - metabolism
Sialoglycoproteins - therapeutic use
Tumor Necrosis Factor-alpha - metabolism
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Summary:Acute lung injury frequently develops following hemorrhage and is characterized by increased proinflammatory cytokine levels and massive neutrophil accumulation in the lung. Blood loss produces rapid increases in IL-1 alpha and IL-1 beta mRNA expression among pulmonary cell populations. To examine the role of IL-1 in producing acute inflammatory lung injury after hemorrhage, we treated mice following hemorrhage and resuscitation with recombinant interleukin-1 receptor antagonist (IL-1Ra), a competitive inhibitor of the actions of IL-1. Therapy with IL-1Ra prevented the posthemorrhage increases in pulmonary TNF-alpha levels normally found after blood loss. Administration of IL-1Ra also diminished the increases in IL-1 beta and IL-6 mRNA levels that occur in the lungs following hemorrhage. However, the amounts of TNF-alpha and IFN-gamma mRNA among intraparenchymal pulmonary mononuclear cells remained elevated after hemorrhage despite therapy with IL-1Ra. These results indicate that therapy with IL-1Ra in the posthemorrhage period is capable of normalizing the expression of some, but not all, of the proinflammatory cytokines whose production among pulmonary cellular populations is increased by blood loss.
ISSN:1056-5477