Targeting S100A9 to prevent <i>Streptococcus pneumoniae-</i>induced allergic asthma exacerbation
نویسندگان
چکیده
Abstract The alarmin S100 calcium-binding protein A9 (S100A9) plays a role in the immunopathology of lung diseases such as asthma and pneumonia. We hypothesized that acute pneumonia induced by S. pneumoniae exacerbates through S100A9 induction increase neutrophilic inflammation NET production. C57BL/6 Wild Type (WT) animals mice deficient for expression (S100A9 −/−) were sensitized challenged with ovalbumin (OVA) infected or not during challenge. In WT mice, comorbidity resulted significant neutrophil recruitment bronchoalveolar lavage fluid (BALF) accompanied an increased perivascular peribronchial leukocyte infiltration, secretion production lungs compared to exposed only allergen. During comorbidity, −/−mice exhibited reduction levels chemoattractant CXCL1 BALF well infiltration into their counterpart. Moreover, showed death. Pharmacological intervention tasquinimod, inhibitor signaling, BB Cl-amidine, NET, protected from reduced comorbidity.Our results provided evidence might be therapeutic target severe triggered infection. Financial support: Sao Paulo Research Foundation (FAPESP), grants 2017/216295 (VLDB) 2019/09881-6 (TFCF-S), Brazilian National Council Scientific Technological Development (CNPq), grant 142139/2019-0 (MMMB).
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ژورنال
عنوان ژورنال: Journal of Immunology
سال: 2023
ISSN: ['1550-6606', '0022-1767']
DOI: https://doi.org/10.4049/jimmunol.210.supp.162.05