MyD88-, but not Nod1- and/or Nod2-deficient mice, show increased susceptibility to polymicrobial sepsis due to impaired local inflammatory response (2014)
- Authors:
- USP affiliated authors: ZAMBONI, DARIO SIMÕES - FMRP ; ALVES FILHO, JOSÉ CARLOS FARIAS - FMRP ; CUNHA, FERNANDO DE QUEIROZ - FMRP
- Unidade: FMRP
- DOI: 10.1371/journal.pone.0103734
- Subjects: SEPSE; INFLAMAÇÃO
- Language: Inglês
- Imprenta:
- Publisher place: San Francisco
- Date published: 2014
- Source:
- Status:
- Artigo publicado em periódico de acesso aberto (Gold Open Access)
- Versão do Documento:
- Versão publicada (Published version)
- Acessar versão aberta:
-
ABNT
SÔNEGO, Fabiane et al. MyD88-, but not Nod1- and/or Nod2-deficient mice, show increased susceptibility to polymicrobial sepsis due to impaired local inflammatory response. PLOS ONE, v. 9, n. 8, p. e103734-1-e103734-13, 2014Tradução . . Disponível em: https://doi.org/10.1371/journal.pone.0103734. Acesso em: 29 mar. 2026. -
APA
Sônego, F., Castanheira, F. V. S., Czaikoski, P. G., Kanashiro, A., Souto, F. O., França, R. O., et al. (2014). MyD88-, but not Nod1- and/or Nod2-deficient mice, show increased susceptibility to polymicrobial sepsis due to impaired local inflammatory response. PLOS ONE, 9( 8), e103734-1-e103734-13. doi:10.1371/journal.pone.0103734 -
NLM
Sônego F, Castanheira FVS, Czaikoski PG, Kanashiro A, Souto FO, França RO, Nascimento DC, Freitas A, Spiller F, Cunha LD, Zamboni DS, Alves Filho JCF, Cunha F de Q. MyD88-, but not Nod1- and/or Nod2-deficient mice, show increased susceptibility to polymicrobial sepsis due to impaired local inflammatory response [Internet]. PLOS ONE. 2014 ; 9( 8): e103734-1-e103734-13.[citado 2026 mar. 29 ] Available from: https://doi.org/10.1371/journal.pone.0103734 -
Vancouver
Sônego F, Castanheira FVS, Czaikoski PG, Kanashiro A, Souto FO, França RO, Nascimento DC, Freitas A, Spiller F, Cunha LD, Zamboni DS, Alves Filho JCF, Cunha F de Q. MyD88-, but not Nod1- and/or Nod2-deficient mice, show increased susceptibility to polymicrobial sepsis due to impaired local inflammatory response [Internet]. PLOS ONE. 2014 ; 9( 8): e103734-1-e103734-13.[citado 2026 mar. 29 ] Available from: https://doi.org/10.1371/journal.pone.0103734 - The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88
- IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population
- The pattern recognition receptors Nod1 and Nod2 account for neutrophil recruitment to the lungs of mice infected with Legionella pneumophila
- Mechanism of virulence in the murine moldel of legionella longbeachae infection
- Unraveling the pathogenesis of Legionella longbeachae infection: a role of type IV secretion system to induce mice lethality via pulmonary inflammation
- Therapeutic potential and limitations of cholinergic anti-inflammatory pathway in sepsis
- Paradoxical roles of the neutrophil in sepsis: protective and deleterious
- Failure of neutrophil migration to infection focus correlates with sepsis outcome: critical role of TLR, nitric-cGMP-PKG pathway and chemokines receptors
- IL-33 signaling is essential to attenuate viral-induced encephalitis development by downregulating iNOS expression in the central nervous system
- Interleukin-10 rs2227307 and CXCR2 rs1126579 polymorphisms modulate the predisposition to septic shock
Informações sobre a disponibilidade de versões do artigo em acesso aberto coletadas automaticamente via oaDOI API (Unpaywall).
Por se tratar de integração com serviço externo, podem existir diferentes versões do trabalho (como preprints ou postprints), que podem diferir da versão publicada.
Download do texto completo
| Tipo | Nome | Link | |
|---|---|---|---|
| 002679816.pdf | Direct link |
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas