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Tumor necrosis factor-α in macrophages of heart, liver, kidney, and in the pituitary gland

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Abstract.

Tumor necrosis factor-α (TNFα) is an important mediator in bacterial lipopolysaccharide (LPS)-induced fever and shock. New data on TNFα-producing macrophages in heart, pituitary gland, kidneys and liver in correlation with TNFα plasma levels are reported here. In adult rabbits, core temperature and TNFα plasma levels are significantly increased at 3 and 24 h after treatment with LPS. After a delay of 6–12 h, the number of TNFα-containing macrophages, determined by immunohistochemistry, increases more than fivefold in all organs investigated. With the exception of the pituitary gland, the increase in cell number is correlated with the degree of cellular injury, indicating the involvement of TNFα in LPS-induced organ damage that is accompanied by the synthesis of the cytokine. Cortisol levels also increase for at least 24 h after LPS treatment, show peak values 6 h after interleukin-1 treatment, and are unchanged after TNFα treatment, indicating the different effects of these factors on the hypothalamo-hypophyseal-adrenocortical axis. This study provides evidence that macrophageal TNFα of multi-organ origin is involved in LPS-induced tissue injury and supports the concept of a systemic inflammatory response syndrome. We also show for the first time that in the anterior lobe of the pituitary gland TNFα is a normal constituent in cells producing growth hormone but not ACTH. Moreover, most cells of the intermediate lobe are positive for TNFα.

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Received: 31 July 1995 / Accepted: 27 January 1996

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Arras, M., Höche, A., Bohle, R. et al. Tumor necrosis factor-α in macrophages of heart, liver, kidney, and in the pituitary gland. Cell Tissue Res 285, 39–49 (1996). https://doi.org/10.1007/s004410050618

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  • Key words: Tumor necrosis factor-α
  • Pituitary gland
  • Heart
  • Cortisol
  • Macrophages
  • Lipopolysaccharide
  • Systemic inflammatory response syndrome
  • Rabbit