Fas-FasL interaction modulates nitric oxide production in Trypanosoma cruzi-infected mice

Gislâine A. Martins, Stefka B. Petkova, Fabiana S. Machado, Richard N. Kitsis, Louis M. Weiss, Murray Wittner, Herbert B. Tanowitz, João S. Silva

Research output: Contribution to journalArticle

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Abstract

During acute Trypanosoma cruzi infection in mice, many leucocytes undergo apoptosis. Although apoptosis has been ascribed to increased levels of nitric oxide (NO) and Fas-FasL interaction, the importance of this phenomenon in modulating the host response against T. cruzi is unknown. Herein, the role of NO- and Fas-FasL-induced apoptosis in modulating the immune response to T. cruzi was evaluated using mice deficient in Fas expression (MRL/MpJ-Fas lpr) and inducible nitric oxide synthase (iNOS) knockout mice (iNOS-/-). The results showed that besides decreasing apoptosis induction after infection, impairment of the Fas-FasL interaction resulted in decreased NO production, as a consequence of enhanced T helper 2 (Th2) cytokine production. Differently, blockage of NO-induced apoptosis resulted in uncontrolled cytokine production, rather than a biased Th2 cytokine pattern. Together, these results suggested that Fas and FasL-induced apoptosis could be implied in modulation of the immune response against T. cruzi by interfering with cytokine and NO production during the acute phase of the infection.

Original languageEnglish (US)
Pages (from-to)122-129
Number of pages8
JournalImmunology
Volume103
Issue number1
DOIs
StatePublished - 2001

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Trypanosoma cruzi
Nitric Oxide
Apoptosis
Cytokines
Nitric Oxide Synthase Type II
Infection
Knockout Mice
Leukocytes

ASJC Scopus subject areas

  • Immunology

Cite this

Fas-FasL interaction modulates nitric oxide production in Trypanosoma cruzi-infected mice. / Martins, Gislâine A.; Petkova, Stefka B.; Machado, Fabiana S.; Kitsis, Richard N.; Weiss, Louis M.; Wittner, Murray; Tanowitz, Herbert B.; Silva, João S.

In: Immunology, Vol. 103, No. 1, 2001, p. 122-129.

Research output: Contribution to journalArticle

Martins, GA, Petkova, SB, Machado, FS, Kitsis, RN, Weiss, LM, Wittner, M, Tanowitz, HB & Silva, JS 2001, 'Fas-FasL interaction modulates nitric oxide production in Trypanosoma cruzi-infected mice', Immunology, vol. 103, no. 1, pp. 122-129. https://doi.org/10.1046/j.1365-2567.2001.01216.x
Martins, Gislâine A. ; Petkova, Stefka B. ; Machado, Fabiana S. ; Kitsis, Richard N. ; Weiss, Louis M. ; Wittner, Murray ; Tanowitz, Herbert B. ; Silva, João S. / Fas-FasL interaction modulates nitric oxide production in Trypanosoma cruzi-infected mice. In: Immunology. 2001 ; Vol. 103, No. 1. pp. 122-129.
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AU - Kitsis, Richard N.

AU - Weiss, Louis M.

AU - Wittner, Murray

AU - Tanowitz, Herbert B.

AU - Silva, João S.

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AB - During acute Trypanosoma cruzi infection in mice, many leucocytes undergo apoptosis. Although apoptosis has been ascribed to increased levels of nitric oxide (NO) and Fas-FasL interaction, the importance of this phenomenon in modulating the host response against T. cruzi is unknown. Herein, the role of NO- and Fas-FasL-induced apoptosis in modulating the immune response to T. cruzi was evaluated using mice deficient in Fas expression (MRL/MpJ-Fas lpr) and inducible nitric oxide synthase (iNOS) knockout mice (iNOS-/-). The results showed that besides decreasing apoptosis induction after infection, impairment of the Fas-FasL interaction resulted in decreased NO production, as a consequence of enhanced T helper 2 (Th2) cytokine production. Differently, blockage of NO-induced apoptosis resulted in uncontrolled cytokine production, rather than a biased Th2 cytokine pattern. Together, these results suggested that Fas and FasL-induced apoptosis could be implied in modulation of the immune response against T. cruzi by interfering with cytokine and NO production during the acute phase of the infection.

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