Cytokines

Kidney International (1992) 41, 600–603; doi:10.1038/ki.1992.90

Tumor necrosis factor alpha and mesangial cells

Laurent Baud1, Bruno Fouqueray1, Carole Philippe1 and Abdelaziz Amrani1

1INSERM U. 64, Hôpital Tenon, Paris, France

Correspondence: Laurent Baud MD, INSERM U64, Hôpital Tenon, 4 rue de la Chine, 75020 Paris, France.

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Abstract

Bacterial infections promote important alterations in immune, hemodynamic, and metabolic function which can result in irreversible shock. These changes are mediated by host-secreted cytokines rather than by direct action of the endotoxin lipopolysaccharide (LPS) derived from the cell wall of bacteria. One cytokine that has been extensively studied for its role in infection is macrophage-derived tumor necrosis factor alpha (TNFalpha) [1]. Three observations suggest that TNFalpha has a central involvement in endotoxic shock: (i) High levels of TNFalpha can be found in blood of animals and humans with endotoxic shock; (ii) When injected to animals, TNFalpha causes a syndrome similar to endotoxic shock, with hypotension, decreased tissue perfusion, organ failure, and lactic acidosis; (iii) The effects of LPS can be prevented by prior passive immunization of animals with polyclonal or monoclonal antibody directed against TNFalpha.

During severe bacterial infections, acute renal insufficiency occurs frequently and contributes significantly to the morbidity and mortality of the shock. In vivo studies indicate that LPS induces an increase in renal vascular resistance and a decrease in glomerular filtration rate [2]. A variety of mediators could contribute to these hemodynamic changes. They include: arachidonic acid metabolites (thromboxane A2, TXA2; leukotrienes, LT), platelet activating factor (PAF), adenosine, catecholamines, angiotensin II and cytokines. Their synthesis is probably initiated by the release of TNFalpha [3]. The present paper discusses the cellular origin of TNFalpha within the kidney, and reviews the mechanisms whereby factors released in response to TNFalpha participate in controlling the secretion of this cytokine.

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