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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.)

Impaired expression of CXCL5 and matrix metalloproteinases in the lungs of mice with high susceptibility to Streptococcus pneumoniae infection

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Mancuso, Rubia I. [1] ; Miyaji, Eliane N. [1] ; Silva, Cristiane C. F. [2] ; Portaro, Fernanda V. [2] ; Soares-Schanoski, Alessandra [1] ; Ribeiro, Orlando G. [3] ; Oliveira, Maria Leonor S. [1]
Total Authors: 7
[1] Inst Butantan, Lab Bacteriol, Ave Vital Brasil 1500, BR-05503900 Sao Paulo, SP - Brazil
[2] Inst Butantan, Lab Imunoquim, Sao Paulo, SP - Brazil
[3] Inst Butantan, Lab Imunogenet, Sao Paulo, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: IMMUNITY INFLAMMATION AND DISEASE; v. 6, n. 1, p. 128-142, MAR 2018.
Web of Science Citations: 1

Introduction: Streptococcus pneumoniae colonizes the nasopharynx of healthy individuals establishing a commensal relationship with the host. In some conditions, bacteria invade the lower respiratory tract and innate immune responses are crucial to avoid diseases such as pneumonia, sepsis, or meningitis. Methods: Here, we compared the susceptibility to pneumococcal respiratory infection of two outbred mouse lines, AIRmin and AIRmax, selected for low or high acute inflammatory responses, respectively. Results: AIRmin mice showed increased susceptibility to infection with different pneumococcal serotypes, when compared to AIRmax. Significant higher numbers of alveolar macrophages expressing the CD206 mannose receptor were observed in AIRmin mice when compared to AIRmax mice. Despite this difference, secretion of several cytokines and chemokines in the respiratory tract of AIRmin and AIRmax mice, after infection, was similar. The only exception was CXCL5, which was highly induced after pneumococcal infection in AIRmax mice but not in AIRmin mice. Reduced expression of the matrix metalloproteinases (MMP) 2, 3, 8, and 9, as well as reduced activities of MMPs were also observed in the lungs of AIRmin mice, after infection. Such impaired responses may have contributed to the low influx of neutrophils observed in the airways of these mice. Finally, high percentages of macrophages and neutrophils in apoptosis or necrosis, at the site of infection, were also observed in AIRmin mice, suggesting that leukocyte functionality is also compromised. Conclusions: Our results indicate that CXCL5 and MMPs contribute to the resistance to pneumococcal infection in mice. (AU)

FAPESP's process: 13/26052-7 - Evaluation of the effects of inflammation on the respiratory infection caused by Streptococcus pneumoniae in mice
Grantee:Rubia Isler Mancuso
Support type: Scholarships in Brazil - Master
FAPESP's process: 14/11087-2 - Effect of acute inflammatory responses on respiratory infections due to Streptococcus pneumoniae in animal models
Grantee:Maria Leonor Sarno de Oliveira
Support type: Regular Research Grants
FAPESP's process: 15/15364-3 - Toxic potential analysis of proteases and peptides present in scorpion Tityus serrulatus venom and the blockage capacity of commercial antivenoms: enhancing the knowledge of venom and its mechanism of action
Grantee:Fernanda Calheta Vieira Portaro
Support type: Regular Research Grants