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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
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]
Total Authors: 8
Affiliation:
[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
Total Affiliations: 2
Document type: Journal article
Source: Inflammation Research; v. 67, n. 5, p. 435-443, MAY 2018.
Web of Science Citations: 1
Abstract

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)

FAPESP's process: 08/11593-4 - PARTICIPATION OF NOD-LIKE RECEPTORS ON INFLAMMATORY RESPONSE IN POLYMICROBIAL SEPSIS
Grantee:Fabiane Sônego
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 11/19670-0 - Mechanisms involved in the pathophysiology of rheumatoid arthritis, pain and sepsis
Grantee:Fernando de Queiroz Cunha
Support Opportunities: Research Projects - Thematic Grants