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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.)

Interleukin 1 Receptor-Driven Neutrophil Recruitment Accounts to MyD88-Dependent Pulmonary Clearance of Legionella pneumophila Infection In Vivo

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Author(s):
Mascarenhas, Danielle P. A. [1] ; Pereira, Marcelo S. F. [1] ; Manin, Graziele Z. [1] ; Hori, Juliana I. [1] ; Zamboni, Dario S. [1]
Total Authors: 5
Affiliation:
[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Cell Biol, BR-05508 Sao Paulo - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Journal of Infectious Diseases; v. 211, n. 2, p. 322-330, JAN 15 2015.
Web of Science Citations: 15
Abstract

Legionella pneumophila, the etiological agent of Legionnaires' disease, triggers activation of multiple innate immune pathways that lead to the restriction of bacterial replication in vivo. Despite the critical role for MyD88 in infection clearance, the receptors and mechanisms responsible for MyD88-mediated pulmonary bacterial clearance are still unclear. Here, we used flagellin mutants of L. pneumophila, which bypass the NAIP5/NLRC4-mediated restriction of bacterial replication, to assess the receptors involved in MyD88-mediated pulmonary bacterial clearance. By systematically comparing pulmonary clearance of L. pneumophila in C57BL/6 MyD88(-/-), TLR2(-/-), TLR3(-/-), TLR4(-/-), TLR9(-/-), IL-1R(-/-), and IL-18(-/-) mice, we found that, while the knockout of a single Toll-like receptor or interleukin 18 resulted only in minor impairment of bacterial clearance, deficiency in the interleukin 1 (IL-1) receptor led to a significant impairment. IL-1/MyD88-mediated pulmonary bacterial clearance occurs via processes involving the recruitment of neutrophils. Collectively, our data contribute to the understanding of the effector mechanisms involved in MyD88-mediated pulmonary bacterial clearance. (AU)

FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
Grantee:Fernando de Queiroz Cunha
Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
FAPESP's process: 14/04684-4 - The inflammasome in the host response against intracellular pathogens and the microbial mechanisms for its evasion
Grantee:Dario Simões Zamboni
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 12/09363-6 - Molecular pathogenesis and subversion of host responses in infections with Legionella spp.
Grantee:Dario Simões Zamboni
Support Opportunities: Regular Research Grants