[A low level of TNF-mediates hemorrhage-induced acute lung injury via p55 TNF receptor].

Abstract

OBJECTIVE:

To examine the temporal relationship of pulmonary TNF-alpha production to acute lung injury (ALI) during hemorrhagic shock (HS).

METHODS:

HS was induced in mice by removal of 30% of calculated total blood volume. Lung TNF-alpha was measured by ELISA. Lung neutrophil accumulation was detected by immunofluorescent staining, and pulmonary microvascular permeability was assessed using Evans blue dye.

RESULTS:

While HS induced a slight and transient increase in lung TNF-alpha, neutrophil accumulation preceded the change in lung TNF-alpha. However, lung neutrophil accumulation and the increase in microvascular permeability were abrogated in TNF-alpha knockout mice, and both were restored by administration of low dose TNF-alpha to TNF-alpha knockout mice prior to HS. Both neutrophil accumulation and microvascular leak were abrogated in p55 TNF-alpha receptor knockout mice, while p75 TNF-alpha receptor knockout mice behaved similar to wild type.

CONCLUSION:

A low level of pulmonary TNF-alpha is sufficient to mediate HS-induced acute lung injury and that the p55 TNF-alpha receptor plays a dominant role in regulating the pulmonary inflammatory response to HS. The results suggest that anti-TNF-alpha strategies for the control of the pulmonary inflammatory response to HS can be directed toward antagonizing the p55 TNF-alpha receptor.

• Authors: Yong Song, Yi Shi, Alden H Harken, Xianzhong Meng, Christopher D Raeburn
• Journal: Zhonghua yi xue za zhi (Zhonghua Yi Xue Za Zhi) Vol. 83 Issue 8 Pg. 691-4 (Apr 25 2003) ISSN: 0376-2491 [Print] China
• PMID: 12887831 (Publication Type: Journal Article)

Chemical References

• Antigens, CD
• Receptors, Tumor Necrosis Factor
• Receptors, Tumor Necrosis Factor, Type I
• Tumor Necrosis Factor-alpha

Topics

• Animals
• Antigens, CD (physiology)
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Neutrophils (physiology)
• Receptors, Tumor Necrosis Factor (physiology)
• Receptors, Tumor Necrosis Factor, Type I
• Respiratory Distress Syndrome (etiology)
• Shock, Hemorrhagic (complications)
• Tumor Necrosis Factor-alpha (physiology)