Monochloramine inhibits phorbol ester-inducible neutrophil respiratory burst activation and T cell interleukin-2 receptor expression by inhibiting inducible protein kinase C activity

Tetsuya Ogino, Hirotsugu Kobuchi, Chandan K. Sen, Sashwati Roy, Lester Packer, John J. Maguire

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Monochloramine derivatives are long lived physiological oxidants produced by neutrophils during the respiratory burst. The effects of chemically prepared monochloramine (NH2Cl) on protein kinase C (PKC) and PKC-mediated cellular responses were studied in elicited rat peritoneal neutrophils and human Jurkat T cells. Neutrophils pretreated with NH2Cl (30- 50 μM) showed a marked decrease in the respiratory burst activity induced by phorbol 12-myristate 13-acetate (PMA), winch is a potent PKC activator. These cells, however, were viable and showed a complete respiratory burst upon arachidonic acid stimulation, which induces the respiratory burst by a PKC- independent mechanism. The NH2Cl-treated neutrophils showed a decrease in both PKC activity and PMA-induced phosphorylation of a 47-kDa protein, which corresponds to the cytosolic factor of NADPH oxidase, p47(phox). Jurkat T cells pretreated with NH2Cl (20-70 μg) showed a decrease in the expression of the interleukin-2 receptor α chain following PMA stimulation. This was also accompanied by a decrease in both PKC activity and nuclear transcription factor-κB activation, also without loss of cell viability. These results show that NH2Cl inhibits PKC-mediated cellular responses through inhibition of the inducible PKC activity.

Original languageEnglish
Pages (from-to)26247-26252
Number of pages6
JournalJournal of Biological Chemistry
Volume272
Issue number42
DOIs
Publication statusPublished - Oct 17 1997

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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