tetano
Editor, Senior Moderator
Microb Pathog
. 2022 Apr 27;166:105558.
doi: 10.1016/j.micpath.2022.105558. Online ahead of print.
Neutrophil extracellular traps mediate severe lung injury induced by influenza A virus H1N1 in mice coinfected with Staphylococcus aureus
Tong Yi[SUP] 1 [/SUP], Wenxin Ding[SUP] 1 [/SUP], Yuanzhen Hao[SUP] 1 [/SUP], Lifeng Cen[SUP] 1 [/SUP], Jiyang Li[SUP] 1 [/SUP], Xunlong Shi[SUP] 1 [/SUP], Ting Wang[SUP] 1 [/SUP], Daofeng Chen[SUP] 2 [/SUP], Haiyan Zhu[SUP] 3 [/SUP]
Affiliations
Abstract
Influenza virus and bacterial infection contributed to massive morbidity and mortality. However, the underlying mechanisms were poorly understood. A coinfected model was generating by using sublethal doses of influenza A virus H1N1 A/FM/1/47(H1N1) and methicillin-resistant Staphylococcus aureus (MRSA). Further, the model was optimized to achieve the highest peak of mortality initiated by intranasal infection with 0.2LD[SUB]50[/SUB] H1N1 and 0.16LD[SUB]50[/SUB] MRSA at 3 days interval. Excessive neutrophil recruitment, accompanied by high levels of inflammatory cytokines and chemokines, and increased bacterial and viral load were observed in coinfected mice. Under the inflammatory environments triggered by H1N1 and MRSA, the excessive neutrophil recruitment led to the formation of neutrophil extracellular traps (NETs), associated with severe inflammation and vascular endothelial injury. Importantly, the severity of lung injury could be alleviated by treatment with DNase I or a selective neutrophil elastase inhibitor (NEi). Therefore, our data suggested that excessive neutrophil recruitment and NETs formation contributed to severe inflammation and acute lung injury in coinfected animals.
Keywords: Coinfection; Influenza; Neutrophil extracellular traps; Pneumonia; Staphylococcus aureus.
. 2022 Apr 27;166:105558.
doi: 10.1016/j.micpath.2022.105558. Online ahead of print.
Neutrophil extracellular traps mediate severe lung injury induced by influenza A virus H1N1 in mice coinfected with Staphylococcus aureus
Tong Yi[SUP] 1 [/SUP], Wenxin Ding[SUP] 1 [/SUP], Yuanzhen Hao[SUP] 1 [/SUP], Lifeng Cen[SUP] 1 [/SUP], Jiyang Li[SUP] 1 [/SUP], Xunlong Shi[SUP] 1 [/SUP], Ting Wang[SUP] 1 [/SUP], Daofeng Chen[SUP] 2 [/SUP], Haiyan Zhu[SUP] 3 [/SUP]
Affiliations
- PMID: 35487479
- DOI: 10.1016/j.micpath.2022.105558
Abstract
Influenza virus and bacterial infection contributed to massive morbidity and mortality. However, the underlying mechanisms were poorly understood. A coinfected model was generating by using sublethal doses of influenza A virus H1N1 A/FM/1/47(H1N1) and methicillin-resistant Staphylococcus aureus (MRSA). Further, the model was optimized to achieve the highest peak of mortality initiated by intranasal infection with 0.2LD[SUB]50[/SUB] H1N1 and 0.16LD[SUB]50[/SUB] MRSA at 3 days interval. Excessive neutrophil recruitment, accompanied by high levels of inflammatory cytokines and chemokines, and increased bacterial and viral load were observed in coinfected mice. Under the inflammatory environments triggered by H1N1 and MRSA, the excessive neutrophil recruitment led to the formation of neutrophil extracellular traps (NETs), associated with severe inflammation and vascular endothelial injury. Importantly, the severity of lung injury could be alleviated by treatment with DNase I or a selective neutrophil elastase inhibitor (NEi). Therefore, our data suggested that excessive neutrophil recruitment and NETs formation contributed to severe inflammation and acute lung injury in coinfected animals.
Keywords: Coinfection; Influenza; Neutrophil extracellular traps; Pneumonia; Staphylococcus aureus.