[The role of TNF in septic ARDS].
This study was performed to demonstrate the role of TNF in septic ARDS. The interaction with neutrophil and TNF was examined in both in vitro and in rat experimental observation. The results obtained are as follows: Serum level of natural TNF was significantly increased immediately after the endotoxin injection into the rat vein. In in vitro observation, TNF activated neutrophil and enhanced super oxide production and elastase was released from neutrophil. On the other hand, TNF was inactivated by contact with elastase released from activated PMNs both in dose and in time dependently. Also, in the in vivo study, the serum level of natural TNF that was enhanced by endotoxin injection was continued for a longer period in neutropenic rats than in the normal rat. The lung tissue injury such as cell infiltration, capillary congestion and increased intrapulmonary fluid in morphometric determination were observed only when the extremely high dose of TNF was injected. These findings were more significantly observed in the neutropenic rats than in the normal neutrophil rat. The weaker interaction of PMNs elastase to TNF is suspected in such neutropenic animals. From the above, the role of TNF in septic ARDS may be explained as follows: By endotoxin injection, TNF is released from stimulated macrophages. The released TNF activates neutrophil which plays the main role of septic ARDS. In the usual system, lung tissue damage induced by TNF is inhibited, because TNF is inactivated by elastase released from activated PMNs. However, in neutropenic state, PMNs elastase is not enough to inhibit the TNF action, then the tissue damage is directly induced by TNF. As my conclusion, the role of TNF in septic ARDS is to provide two different ways by the host is condition. One is to activate neutrophils in the usual condition and the another is to introduce direct damage of lung tissue in the neutropenic state.
Sakayori
S
S
First Department of Medicine, Kyourin University.
D000818:Animals; D009504:Neutrophils / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000378:metabolism*; D018805:Sepsis / Q000150:complications*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D014409:Tumor Necrosis Factor-alpha