tetano
Editor, Senior Moderator
Immunohorizons
. 2025 Nov 24;9(12):vlaf055.
doi: 10.1093/immhor/vlaf055. Preceding influenza infection impacts neutrophil response to Aspergillus fumigatus and Staphylococcus aureus
Nima Naghshtabrizi[SUP] 1 [/SUP], Kara L Nickolich[SUP] 1 [/SUP], Ravineel B Singh[SUP] 1 [/SUP], Ellyse M Cipolla[SUP] 2 [/SUP], Mark E Snyder[SUP] 1 [/SUP], Dhivyaa Rajasundaram[SUP] 2 [/SUP], Radha Gopal[SUP] 2 [/SUP], John F Alcorn[SUP] 2 [/SUP], Keven M Robinson[SUP] 1 [/SUP]
Affiliations
Influenza infection predisposes individuals to secondary pneumonia caused by a range of pathogens, including both bacterial and fungal organisms. Neutrophils are critical effector cells during infection. In this study, we analyzed the transcriptional pathways of lung neutrophils isolated from mouse models of influenza-associated pulmonary aspergillosis (IAPA) and post-influenza methicillin-resistant Staphylococcus aureus (MRSA) pneumonia to examine the immunopathological mechanisms underlying post-influenza super-infection. Pathways associated with neutrophil chemotaxis and degranulation were inhibited in IAPA compared to singular A. fumigatus infection and pathways associated with neutrophil recruitment and phagocytosis were inhibited in IAPA compared to singular influenza infection. Pathways associated with neutrophil recruitment and degranulation were inhibited in post-influenza MRSA pneumonia compared to singular MRSA infection and pathways associated with cytokine signaling were inhibited in post-influenza MRSA pneumonia compared to singular influenza infection. When the 2 types of super-infection were directly compared, pathways related to cytokine induction and neutrophil function were inhibited in IAPA neutrophils compared to post-influenza MRSA pneumonia. These data demonstrate that influenza causes neutrophil dysfunction, predisposing to secondary fungal and bacterial infections.
Keywords: influenza A virus; invasive pulmonary aspergillosis; methicillin-resistant Staphylococcus aureus; neutrophils.
. 2025 Nov 24;9(12):vlaf055.
doi: 10.1093/immhor/vlaf055. Preceding influenza infection impacts neutrophil response to Aspergillus fumigatus and Staphylococcus aureus
Nima Naghshtabrizi[SUP] 1 [/SUP], Kara L Nickolich[SUP] 1 [/SUP], Ravineel B Singh[SUP] 1 [/SUP], Ellyse M Cipolla[SUP] 2 [/SUP], Mark E Snyder[SUP] 1 [/SUP], Dhivyaa Rajasundaram[SUP] 2 [/SUP], Radha Gopal[SUP] 2 [/SUP], John F Alcorn[SUP] 2 [/SUP], Keven M Robinson[SUP] 1 [/SUP]
Affiliations
- PMID: 41285034
- PMCID: PMC12643476
- DOI: 10.1093/immhor/vlaf055
Influenza infection predisposes individuals to secondary pneumonia caused by a range of pathogens, including both bacterial and fungal organisms. Neutrophils are critical effector cells during infection. In this study, we analyzed the transcriptional pathways of lung neutrophils isolated from mouse models of influenza-associated pulmonary aspergillosis (IAPA) and post-influenza methicillin-resistant Staphylococcus aureus (MRSA) pneumonia to examine the immunopathological mechanisms underlying post-influenza super-infection. Pathways associated with neutrophil chemotaxis and degranulation were inhibited in IAPA compared to singular A. fumigatus infection and pathways associated with neutrophil recruitment and phagocytosis were inhibited in IAPA compared to singular influenza infection. Pathways associated with neutrophil recruitment and degranulation were inhibited in post-influenza MRSA pneumonia compared to singular MRSA infection and pathways associated with cytokine signaling were inhibited in post-influenza MRSA pneumonia compared to singular influenza infection. When the 2 types of super-infection were directly compared, pathways related to cytokine induction and neutrophil function were inhibited in IAPA neutrophils compared to post-influenza MRSA pneumonia. These data demonstrate that influenza causes neutrophil dysfunction, predisposing to secondary fungal and bacterial infections.
Keywords: influenza A virus; invasive pulmonary aspergillosis; methicillin-resistant Staphylococcus aureus; neutrophils.