Reactive oxidants mediate TNF-α-induced leukocyte adhesion to rat mesenteric venular endothelium

Y. Morita, M. G. Clemens, Lloyd S Miller, U. Rangan, S. Kondo, M. Miyasaka, T. Yoshikawa, G. B. Bulkley

Research output: Contribution to journalArticle

Abstract

We investigated the role of reactive oxygen metabolites (ROMs) as potential mediators of tumor necrosis factor-α (TNF-α)-stimulated neutrophil adhesion to rat mesenteric venules in vivo, using intravital microscopy and fixed whole mount preparations of mesentery. Intraperitoneal injection of TNF-α significantly increased leukocyte rolling, adhesion, and emigration in a dose- and time-dependent manner. Leukocyte adhesion and emigration, but not rolling, were significantly attenuated by prior intravenous administration of monoclonal anti-intercellular adhesion molecule-1 (ICAM-1). Rolling leukocyte flux was significantly attenuated by intravenous preadministration of superoxide dismutase (SOD), catalase, or both. Only catalase or SOD plus catalase significantly inhibited leukocyte adhesion. Catalase alone inhibited emigration. Moreover, postadhesive treatment with catalase but not SOD, 4 h after TNF-α administration reduced the flux of rolling (but not adherent) leukocytes that had previously increased in response to TNF-α. Intragastric allopurinol (50 mg/kg at 3 and 18 h before TNF-α administration) or 3 wk of a tungsten-enriched diet substantially inhibited xanthine oxidase activity but had no significant effects on the above parameters of neutrophil dynamics. In parallel experiments using fixed whole mount preparations of the mesoappendix stained specifically for neutrophil esterase, neutrophil adhesion 2 h after TNF-α administration was also inhibited by continuous intravenous administration of catalase but not by SOD, intragastric allopurinol, or tungsten diet. These findings suggest that ROMs, apparently not from xanthine oxidase, are important mediators of TNF-α-induced upregulation of neutrophil adhesion in rat mesenteric venules.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume269
Issue number6 38-6
StatePublished - 1995

Fingerprint

tumor necrosis factors
endothelium
Oxidants
oxidants
Endothelium
adhesion
leukocytes
Catalase
Leukocytes
Tumor Necrosis Factor-alpha
catalase
neutrophils
Neutrophils
rats
Superoxide Dismutase
Emigration and Immigration
superoxide dismutase
Leukocyte Rolling
allopurinol
tungsten

Keywords

  • catalase
  • intercellular adhesion molecule- 1
  • intravital microscopy
  • superoxide dismutase
  • xanthine oxidase

ASJC Scopus subject areas

  • Physiology
  • Agricultural and Biological Sciences(all)

Cite this

Reactive oxidants mediate TNF-α-induced leukocyte adhesion to rat mesenteric venular endothelium. / Morita, Y.; Clemens, M. G.; Miller, Lloyd S; Rangan, U.; Kondo, S.; Miyasaka, M.; Yoshikawa, T.; Bulkley, G. B.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 269, No. 6 38-6, 1995.

Research output: Contribution to journalArticle

Morita, Y, Clemens, MG, Miller, LS, Rangan, U, Kondo, S, Miyasaka, M, Yoshikawa, T & Bulkley, GB 1995, 'Reactive oxidants mediate TNF-α-induced leukocyte adhesion to rat mesenteric venular endothelium', American Journal of Physiology - Heart and Circulatory Physiology, vol. 269, no. 6 38-6.
Morita, Y. ; Clemens, M. G. ; Miller, Lloyd S ; Rangan, U. ; Kondo, S. ; Miyasaka, M. ; Yoshikawa, T. ; Bulkley, G. B. / Reactive oxidants mediate TNF-α-induced leukocyte adhesion to rat mesenteric venular endothelium. In: American Journal of Physiology - Heart and Circulatory Physiology. 1995 ; Vol. 269, No. 6 38-6.
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AU - Kondo, S.

AU - Miyasaka, M.

AU - Yoshikawa, T.

AU - Bulkley, G. B.

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AB - We investigated the role of reactive oxygen metabolites (ROMs) as potential mediators of tumor necrosis factor-α (TNF-α)-stimulated neutrophil adhesion to rat mesenteric venules in vivo, using intravital microscopy and fixed whole mount preparations of mesentery. Intraperitoneal injection of TNF-α significantly increased leukocyte rolling, adhesion, and emigration in a dose- and time-dependent manner. Leukocyte adhesion and emigration, but not rolling, were significantly attenuated by prior intravenous administration of monoclonal anti-intercellular adhesion molecule-1 (ICAM-1). Rolling leukocyte flux was significantly attenuated by intravenous preadministration of superoxide dismutase (SOD), catalase, or both. Only catalase or SOD plus catalase significantly inhibited leukocyte adhesion. Catalase alone inhibited emigration. Moreover, postadhesive treatment with catalase but not SOD, 4 h after TNF-α administration reduced the flux of rolling (but not adherent) leukocytes that had previously increased in response to TNF-α. Intragastric allopurinol (50 mg/kg at 3 and 18 h before TNF-α administration) or 3 wk of a tungsten-enriched diet substantially inhibited xanthine oxidase activity but had no significant effects on the above parameters of neutrophil dynamics. In parallel experiments using fixed whole mount preparations of the mesoappendix stained specifically for neutrophil esterase, neutrophil adhesion 2 h after TNF-α administration was also inhibited by continuous intravenous administration of catalase but not by SOD, intragastric allopurinol, or tungsten diet. These findings suggest that ROMs, apparently not from xanthine oxidase, are important mediators of TNF-α-induced upregulation of neutrophil adhesion in rat mesenteric venules.

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