The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88 (2018)
- Authors:
- USP affiliated authors: ZAMBONI, DARIO SIMÕES - FMRP ; ALVES FILHO, JOSÉ CARLOS FARIAS - FMRP ; CUNHA, FERNANDO DE QUEIROZ - FMRP
- Unidade: FMRP
- DOI: 10.1007/s00011-018-1135-x
- Subjects: PNEUMONIA; NEUTRÓFILOS; QUIMIOCINAS; BACTÉRIAS GRAM-NEGATIVAS
- Keywords: Nod1; MyD88; Pseudomonas aeruginosa; Pneumonia; Neutrophil migration; Chemokine
- Agências de fomento:
- Language: Inglês
- Imprenta:
- Source:
- Título: Inflammation Research
- ISSN: 1023-3830
- Volume/Número/Paginação/Ano: v. 67, n. 5, p. 435-443, 2018
- Este periódico é de acesso aberto
- Este artigo NÃO é de acesso aberto
-
ABNT
SÔNEGO, Fabiane et al. The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88. Inflammation Research, v. 67, n. 5, p. 435-443, 2018Tradução . . Disponível em: https://doi.org/10.1007/s00011-018-1135-x. Acesso em: 29 jan. 2026. -
APA
Sônego, F., Castanheira, F. V. S., Horta, C. V., Kanashiro, A., Czaikoski, P. G., Zamboni, D. S., et al. (2018). The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88. Inflammation Research, 67( 5), 435-443. doi:10.1007/s00011-018-1135-x -
NLM
Sônego F, Castanheira FVS, Horta CV, Kanashiro A, Czaikoski PG, Zamboni DS, Alves Filho JCF, Cunha F de Q. The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88 [Internet]. Inflammation Research. 2018 ; 67( 5): 435-443.[citado 2026 jan. 29 ] Available from: https://doi.org/10.1007/s00011-018-1135-x -
Vancouver
Sônego F, Castanheira FVS, Horta CV, Kanashiro A, Czaikoski PG, Zamboni DS, Alves Filho JCF, Cunha F de Q. The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88 [Internet]. Inflammation Research. 2018 ; 67( 5): 435-443.[citado 2026 jan. 29 ] Available from: https://doi.org/10.1007/s00011-018-1135-x - MyD88-, but not Nod1- and/or Nod2-deficient mice, show increased susceptibility to polymicrobial sepsis due to impaired local inflammatory response
- 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
- Failure of neutrophil migration to infection focus correlates with sepsis outcome: critical role of TLR, nitric-cGMP-PKG pathway and chemokines receptors
- Regulation of type 17 helper T-cell function by nitric oxide during inflammation
- Blockage of eosinopoiesis by IL-17A is prevented by cytokine and lipid mediators of allergic inflammation
- Targeting neutrophils in sepsis
- PPAR-γ/IL-10 axis inhibits MyD88 expression and ameliorates murine polymicrobial sepsis
Informações sobre o DOI: 10.1007/s00011-018-1135-x (Fonte: oaDOI API)
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
