Skip to main content
Top
Published in: Inflammation Research 5/2018

01-05-2018 | Original Research Paper

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

Authors: Fabiane Sônego, Fernanda V. S. Castanheira, Catarina V. Horta, Alexandre Kanashiro, Paula G. Czaikoski, Dario S. Zamboni, José Carlos Alves-Filho, Fernando Q. Cunha

Published in: Inflammation Research | Issue 5/2018

Login to get access

Abstract

Objective and design

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.

Subjects

Wild-type, Nod1−/− and MyD88−/− mice, all with a C57Bl/6 background.

Methods

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.

Results

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.

Conclusion

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.
Appendix
Available only for authorised users
Literature
17.
go back to reference Sabharwal N, Dhall S, Chhibber S, Harjai K. Molecular detection of virulence genes as markers in Pseudomonas aeruginosa isolated from urinary tract infections. Int J Mol Epidemiol Genet. 2014;5(3):125–134.PubMedPubMedCentral Sabharwal N, Dhall S, Chhibber S, Harjai K. Molecular detection of virulence genes as markers in Pseudomonas aeruginosa isolated from urinary tract infections. Int J Mol Epidemiol Genet. 2014;5(3):125–134.PubMedPubMedCentral
24.
go back to reference Skerrett SJ, Liggitt HD, Hajjar AM, Wilson CB. Cutting edge: myeloid differentiation factor 88 is essential for pulmonary host defense against Pseudomonas aeruginosa but not Staphylococcus aureus. J Immunol. 2004;172(6):3377–3381.CrossRefPubMed Skerrett SJ, Liggitt HD, Hajjar AM, Wilson CB. Cutting edge: myeloid differentiation factor 88 is essential for pulmonary host defense against Pseudomonas aeruginosa but not Staphylococcus aureus. J Immunol. 2004;172(6):3377–3381.CrossRefPubMed
29.
go back to reference Power MR, Li B, Yamamoto M, Akira S, Lin TJ. A role of Toll-IL-1 receptor domain-containing adaptor-inducing IFN-beta in the host response to Pseudomonas aeruginosa lung infection in mice. J Immunol. 2007;178(5):3170–3176.CrossRefPubMed Power MR, Li B, Yamamoto M, Akira S, Lin TJ. A role of Toll-IL-1 receptor domain-containing adaptor-inducing IFN-beta in the host response to Pseudomonas aeruginosa lung infection in mice. J Immunol. 2007;178(5):3170–3176.CrossRefPubMed
Metadata
Title
The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88
Authors
Fabiane Sônego
Fernanda V. S. Castanheira
Catarina V. Horta
Alexandre Kanashiro
Paula G. Czaikoski
Dario S. Zamboni
José Carlos Alves-Filho
Fernando Q. Cunha
Publication date
01-05-2018
Publisher
Springer International Publishing
Published in
Inflammation Research / Issue 5/2018
Print ISSN: 1023-3830
Electronic ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-018-1135-x

Other articles of this Issue 5/2018

Inflammation Research 5/2018 Go to the issue