Role of IL-17A in acute inhalational pneumonia caused by highly virulent and multidrug-resistant Staphylococcus aureus
10.19405/j.cnki.issn1000–1492.2026.04.002
- VernacularTitle:IL-17A在高耐药且高毒力金黄色葡萄球菌急性吸入性肺炎中的作用
- Author:
Qi KUANG
1
;
Xiaoyu ZHU
2
;
Lu LI
2
;
Xueyan WANG
1
;
Peijie YAN
2
;
Lili ZHANG
2
;
Meng LÜ
2
;
Lingfei HU
2
;
Dongsheng ZHOU
2
;
Wenhui YANG
1
Author Information
1. School of Basic Medical Sciences， Anhui Medical University， Hefei 230032
2. Academy of Military Medical Sciences， Academy of Military Sciences， Beijing 100071
- Publication Type:Journal Article
- Keywords:
IL-17A;
Staphylococcus aureus;
pneumonia;
pro-inflammatory effect;
neutrophil;
gene knockout
- From:
Acta Universitatis Medicinalis Anhui
2026;61(4):599-605
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the role of interleukin （IL）-17A in acute inhalational pneumonia induced by the highly drug-resistant and hypervirulent Staphylococcus aureus strain USA300-R in mice. MethodsAn acute inhalational pneumonia model was established in mice using an aerosolized pulmonary delivery technique. RNA sequencing （RNA-seq） and enzyme-linked immunosorbent assay （ELISA） were employed to examine the expression dynamics of Il17a mRNA and IL-17A protein， respectively， in the lungs of infected mice. Il17a knockout （Il17a-/-） mice were generated using CRISPR/Cas9 gene editing technology. The survival rate， body weight， bacterial load in lung tissue， and histopathological changes were compared between Il17a-/- and wild-type （WT） mice following inhalational infection with USA300-R. Results12 hours after USA300-R infection， compared to pre-infection， the expression level of Il17a mRNA in lung tissue and the level of IL-17A protein in bronchoalveolar lavage fluid （BALF） increased by approximately 50-fold （P<0.01） and 6-fold （P<0.001）， respectively. Compared to WT mice， Il17a-/- mice exhibited approximately 10-fold higher bacterial loads in lung tissue at both 12 and 24 hours post-infection （P<0.001， P<0.05）. However， they showed significantly attenuated lung histopathological injury， reduced alveolar wall thickening， markedly decreased neutrophil infiltration， and an approximately 50% improvement in survival rate （P<0.05）. ConclusionIn acute Staphylococcus aureus USA300-R inhalational pneumonia， IL-17A contributes to bacterial clearance by recruiting neutrophils； however， excessive neutrophil infiltration exacerbates pulmonary inflammation and injury， reduces survival rates， and represents a potential therapeutic target.
