Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages
Autor(a) principal: | |
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Data de Publicação: | 2003 |
Outros Autores: | |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://dx.doi.org/10.1128/IAI.71.3.1225-1233.2003 http://repositorio.unifesp.br/handle/11600/27156 |
Resumo: | In most primary or continuous cell cultures infected with the Q-fever agent Coxiella burnetii, bacteria are typically sheltered in phagolysosome-like, large replicative vacuoles (LRVs). We recently reported that only a small proportion of mouse peritoneal macrophages (PMPhi) infected with a nonvirulent, phase II strain of C. burnetti developed LRVs and that their relative bacterial load increased only slowly. in the majority of infected PM(D, the bacteria were confined to the small vesicles. We show here that nitric oxide (NO) induced by the bacteria partially accounts for the restricted development of LRVs in primary macrophages. Thus, (i) PMPhi and bone marrow-derived macrophages (BMMPhi) challenged with phase II C. burnetii produced significant amounts of NO; (ii) the NO synthase inhibitors aminoguanidine and N-methyl-L-arginine reduced the production of NO and increased the frequency of LRVs (although the relative bacterial loads of individual LRVs did not change, the estimated loads per well increased appreciably); (iii) gamma interferon (IFN-gamma) or the NO donor sodium nitroprusside, added to BMMPhi prior to or after infection, reduced the development and the relative bacterial loads of LRVs and lowered the yield of viable bacteria recovered from the cultures; and (iv) these effects of IFN-gamma may not be entirely dependent on the production of NO since IFN-gamma also controlled the infection in macrophages from inducible NO synthase knockout mice. It remains to be determined whether NO reduced the development of LRVs by acting directly on the bacteria; by acting on the traffic, fusion, or fission of cell vesicles; or by a combination of these mechanisms. |
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Repositório Institucional da UNIFESP |
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Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophagesIn most primary or continuous cell cultures infected with the Q-fever agent Coxiella burnetii, bacteria are typically sheltered in phagolysosome-like, large replicative vacuoles (LRVs). We recently reported that only a small proportion of mouse peritoneal macrophages (PMPhi) infected with a nonvirulent, phase II strain of C. burnetti developed LRVs and that their relative bacterial load increased only slowly. in the majority of infected PM(D, the bacteria were confined to the small vesicles. We show here that nitric oxide (NO) induced by the bacteria partially accounts for the restricted development of LRVs in primary macrophages. Thus, (i) PMPhi and bone marrow-derived macrophages (BMMPhi) challenged with phase II C. burnetii produced significant amounts of NO; (ii) the NO synthase inhibitors aminoguanidine and N-methyl-L-arginine reduced the production of NO and increased the frequency of LRVs (although the relative bacterial loads of individual LRVs did not change, the estimated loads per well increased appreciably); (iii) gamma interferon (IFN-gamma) or the NO donor sodium nitroprusside, added to BMMPhi prior to or after infection, reduced the development and the relative bacterial loads of LRVs and lowered the yield of viable bacteria recovered from the cultures; and (iv) these effects of IFN-gamma may not be entirely dependent on the production of NO since IFN-gamma also controlled the infection in macrophages from inducible NO synthase knockout mice. It remains to be determined whether NO reduced the development of LRVs by acting directly on the bacteria; by acting on the traffic, fusion, or fission of cell vesicles; or by a combination of these mechanisms.UNIFESP, Escola Paulista Med, Disciplina Parasitol, Dept Microbiol Imunol & Parasitol, BR-04023062 São Paulo, BrazilUNIFESP, Escola Paulista Med, Disciplina Parasitol, Dept Microbiol Imunol & Parasitol, BR-04023062 São Paulo, BrazilWeb of ScienceAmer Soc MicrobiologyUniversidade Federal de São Paulo (UNIFESP)Zamboni, Dario S [UNIFESP]Rabinovitch, Michel [UNIFESP]2016-01-24T12:33:44Z2016-01-24T12:33:44Z2003-03-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion1225-1233application/pdfhttp://dx.doi.org/10.1128/IAI.71.3.1225-1233.2003Infection and Immunity. Washington: Amer Soc Microbiology, v. 71, n. 3, p. 1225-1233, 2003.10.1128/IAI.71.3.1225-1233.2003WOS000181270900024.pdf0019-9567http://repositorio.unifesp.br/handle/11600/27156WOS:000181270900024engInfection and Immunityinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP2024-07-31T02:03:31Zoai:repositorio.unifesp.br/:11600/27156Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestbiblioteca.csp@unifesp.bropendoar:34652024-07-31T02:03:31Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.none.fl_str_mv |
Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages |
title |
Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages |
spellingShingle |
Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages Zamboni, Dario S [UNIFESP] |
title_short |
Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages |
title_full |
Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages |
title_fullStr |
Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages |
title_full_unstemmed |
Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages |
title_sort |
Nitric oxide partially controls Coxiella burnetii phase II infection in mouse primary macrophages |
author |
Zamboni, Dario S [UNIFESP] |
author_facet |
Zamboni, Dario S [UNIFESP] Rabinovitch, Michel [UNIFESP] |
author_role |
author |
author2 |
Rabinovitch, Michel [UNIFESP] |
author2_role |
author |
dc.contributor.none.fl_str_mv |
Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Zamboni, Dario S [UNIFESP] Rabinovitch, Michel [UNIFESP] |
description |
In most primary or continuous cell cultures infected with the Q-fever agent Coxiella burnetii, bacteria are typically sheltered in phagolysosome-like, large replicative vacuoles (LRVs). We recently reported that only a small proportion of mouse peritoneal macrophages (PMPhi) infected with a nonvirulent, phase II strain of C. burnetti developed LRVs and that their relative bacterial load increased only slowly. in the majority of infected PM(D, the bacteria were confined to the small vesicles. We show here that nitric oxide (NO) induced by the bacteria partially accounts for the restricted development of LRVs in primary macrophages. Thus, (i) PMPhi and bone marrow-derived macrophages (BMMPhi) challenged with phase II C. burnetii produced significant amounts of NO; (ii) the NO synthase inhibitors aminoguanidine and N-methyl-L-arginine reduced the production of NO and increased the frequency of LRVs (although the relative bacterial loads of individual LRVs did not change, the estimated loads per well increased appreciably); (iii) gamma interferon (IFN-gamma) or the NO donor sodium nitroprusside, added to BMMPhi prior to or after infection, reduced the development and the relative bacterial loads of LRVs and lowered the yield of viable bacteria recovered from the cultures; and (iv) these effects of IFN-gamma may not be entirely dependent on the production of NO since IFN-gamma also controlled the infection in macrophages from inducible NO synthase knockout mice. It remains to be determined whether NO reduced the development of LRVs by acting directly on the bacteria; by acting on the traffic, fusion, or fission of cell vesicles; or by a combination of these mechanisms. |
publishDate |
2003 |
dc.date.none.fl_str_mv |
2003-03-01 2016-01-24T12:33:44Z 2016-01-24T12:33:44Z |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1128/IAI.71.3.1225-1233.2003 Infection and Immunity. Washington: Amer Soc Microbiology, v. 71, n. 3, p. 1225-1233, 2003. 10.1128/IAI.71.3.1225-1233.2003 WOS000181270900024.pdf 0019-9567 http://repositorio.unifesp.br/handle/11600/27156 WOS:000181270900024 |
url |
http://dx.doi.org/10.1128/IAI.71.3.1225-1233.2003 http://repositorio.unifesp.br/handle/11600/27156 |
identifier_str_mv |
Infection and Immunity. Washington: Amer Soc Microbiology, v. 71, n. 3, p. 1225-1233, 2003. 10.1128/IAI.71.3.1225-1233.2003 WOS000181270900024.pdf 0019-9567 WOS:000181270900024 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Infection and Immunity |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
1225-1233 application/pdf |
dc.publisher.none.fl_str_mv |
Amer Soc Microbiology |
publisher.none.fl_str_mv |
Amer Soc Microbiology |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
biblioteca.csp@unifesp.br |
_version_ |
1814268278050127872 |