The host control of a clinical isolate strain of P-aeruginosa infection is independent of Nod-1 but depends on MyD88

Autor(es)

Sonego, Fabiane ^[1] ; Castanheira, Fernanda V. S. ^[1] ; Horta, Catarina V. ^[2] ; Kanashiro, Alexandre ^[1] ; Czaikoski, Paula G. ^[1] ; Zamboni, Dario S. ^[2] ; Alves-Filho, Jose Carlos ^[1] ; Cunha, Fernando Q. ^[1]

Afiliação do(s) autor(es)

^[1] Fac Med Ribeirao Preto, Dept Farmacol, Ave Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Biol Celular & Mol & Bioagentes Patogen, Ave Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Inflammation Research; v. 67, n. 5, p. 435-443, MAY 2018.
• Citações Web of Science: 1

Resumo

The objective of this study was to investigate the role of Nod1 in the recruitment of neutrophils into the infection site and in the establishment of the inflammatory response elicited by a clinical isolate strain of P. aeruginosa in vivo, while comparing it to the well-established role of MyD88 in this process. Wild-type, Nod1 (-/-) and MyD88 (-/-) mice, all with a C57Bl/6 background. Mice were intranasally infected with Pseudomonas aeruginosa DZ605. Bronchoalveolar lavage and blood were harvested 6 or 20 h post-infection for evaluating bacterial load, chemokine levels and neutrophil migration. Survival post-infection was also observed. We show here that wild-type and Nod1 (-/-) mice induce similar lung chemokine levels, neutrophil recruitment, and bacterial load, thus leading to equal survival rates upon P. aeruginosa pulmonary infection. Furthermore, we confirmed the essential role of MyD88-dependent signalling in recruiting neutrophils and controlling P. aeruginosa-induced pulmonary infection. The results suggest that in contrast to MyD88, under our experimental conditions, the absence of Nod1 does not impair the recruitment of neutrophils in response to P. aeruginosa DZ605. (AU)

• Processo FAPESP: 08/11593-4 - Participaçao dos receptores tipo nod na gênese da resposta inflamatória durante a sepse polimicrobiana
• Beneficiário: Fabiane Sônego
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 11/19670-0 - Mecanismos envolvidos na fisiopatologia da artrite reumatóide, dor e sepse
• Beneficiário: Fernando de Queiroz Cunha
• Modalidade de apoio: Auxílio à Pesquisa - Temático