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Titolo:
Amphotericin B both inhibits and enhances T-cell proliferation: Inhibitoryeffect is mediated through H2O2 production via cyclooxygenase pathway by macrophages
Autore:
Kumar, S; Chakrabarti, R;
Indirizzi:
Banaras Hindu Univ, Inst Med Sci, Mol Biol Unit, Varanasi 221005, Uttar Pradesh, India Banaras Hindu Univ Varanasi Uttar Pradesh India 221005 tar Pradesh, India
Titolo Testata:
JOURNAL OF CELLULAR BIOCHEMISTRY
fascicolo: 3, volume: 77, anno: 2000,
pagine: 361 - 371
SICI:
0730-2312(2000)77:3<361:ABBIAE>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENZYMATIC REDUCTION; BIOLOGICAL-ACTIVITY; MOUSE STRAINS; LYMPHOCYTES; INVITRO; PHOSPHATASE; ACTIVATION; AGENTS; PROSTAGLANDIN-E2; SPLENOCYTES;
Keywords:
amphotericin B; cyclooxygenase; catalase; H2O2; immunomodulation; T cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Chakrabarti, R Banaras Hindu Univ, Inst Med Sci, Mol Biol Unit, Varanasi 221005, Uttar Pradesh, India Banaras Hindu Univ Varanasi Uttar Pradesh India 221005 dia
Citazione:
S. Kumar e R. Chakrabarti, "Amphotericin B both inhibits and enhances T-cell proliferation: Inhibitoryeffect is mediated through H2O2 production via cyclooxygenase pathway by macrophages", J CELL BIOC, 77(3), 2000, pp. 361-371

Abstract

Amphotericin B (AmB) has been shown to have both immunosuppressive and -enhancing effects, making its precise nature of action enigmatic. In the present study, we found that AmB inhibited concanavalin A (Con A)-induced T cell proliferation if added within first 30 min of stimulation, after which inhibition began to diminish rapidly. However, AmB did not inhibit T-cell proliferation induced by a combination of PMA and ionomycin. AmB inhibition ofCon A-induced proliferation was completely overcome by cyclooxygenase inhibitor ibuprofen ([alpha-methyl-4-(isobutyl)phenylacetic acid]) and H2O2 scavenger catalase. In fact, in the presence of ibuprofen and catalase, AmB enhanced, instead of suppressing, Con A-induced proliferation in a dose-dependent way. The effect of catalase was limited to the removal of extracellular H2O2 only, as the enzyme did not enter the cells. AmB stimulated H2O2 production by macrophages, but not by a lymphocyte population, which was inhibited by ibuprofen. Our T-cell preparation contained about 3% macrophages, and AmB inhibition of proliferation was further pronounced by increasing themacrophage number by as little as 1%. Finally, AmB inhibition of Con A-induced T-cell proliferation was completely overcome by 2-mercaptoethanol. On the basis of these results, we suggest that AmB stimulates H2O2 production by macrophages through the activation of the cyclooxygenase pathway of arachidonate metabolism. H2O2 then inhibits Con A-induced T-cell proliferation by interfering with an early step of the T-cell receptor signaling pathway through the oxidative modification of some signaling proteins. Our results also show that AmB enhances T-cell proliferation, which can be seen only after blocking its inhibitory effect. J. Cell. Biochem. 77: 361-371, 2000. (C) 2000 Wiley-Liss. Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 05:32:35