tetano
Editor, Senior Moderator
iScience
. 2023 Dec 26;27(1):108775.
doi: 10.1016/j.isci.2023.108775. eCollection 2024 Jan 19. Influenza A virus selectively elevates prostaglandin E[SUB]2[/SUB] formation in pro-resolving macrophages
Paul M Jordan[SUP] 1 2 [/SUP], Kerstin Günther[SUP] 1 [/SUP], Vivien Nischang[SUP] 1 [/SUP], Yuping Ning[SUP] 1 [/SUP], Stefanie Deinhardt-Emmer[SUP] 3 [/SUP], Christina Ehrhardt[SUP] 4 [/SUP], Oliver Werz[SUP] 1 2 [/SUP]
Affiliations
Respiratory influenza A virus (IAV) infections are major health concerns worldwide, where bacterial superinfections substantially increase morbidity and mortality. The underlying mechanisms of how IAV impairs host defense remain elusive. Macrophages are pivotal for the innate immune response and crucially regulate the entire inflammatory process, occurring as inflammatory M1- or pro-resolving M2-like phenotypes. Lipid mediators (LM), produced from polyunsaturated fatty acids by macrophages, are potent immune regulators and impact all stages of inflammation. Using LM metabololipidomics, we show that human pro-resolving M2-macrophages respond to IAV infections with specific and robust production of prostaglandin (PG)E[SUB]2[/SUB] along with upregulation of cyclooxygenase-2 (COX-2), which persists after co-infection with Staphylococcus aureus. In contrast, cytokine/interferon production in macrophages was essentially unaffected by IAV infection, and the functionality of M1-macrophages was not influenced. Conclusively, IAV infection of M2-macrophages selectively elevates PGE[SUB]2[/SUB] formation, suggesting inhibition of the COX-2/PGE[SUB]2[/SUB] axis as strategy to limit IAV exacerbation.
Keywords: Immunology; Virology.
. 2023 Dec 26;27(1):108775.
doi: 10.1016/j.isci.2023.108775. eCollection 2024 Jan 19. Influenza A virus selectively elevates prostaglandin E[SUB]2[/SUB] formation in pro-resolving macrophages
Paul M Jordan[SUP] 1 2 [/SUP], Kerstin Günther[SUP] 1 [/SUP], Vivien Nischang[SUP] 1 [/SUP], Yuping Ning[SUP] 1 [/SUP], Stefanie Deinhardt-Emmer[SUP] 3 [/SUP], Christina Ehrhardt[SUP] 4 [/SUP], Oliver Werz[SUP] 1 2 [/SUP]
Affiliations
- PMID: 38261967
- PMCID: PMC10797193
- DOI: 10.1016/j.isci.2023.108775
Respiratory influenza A virus (IAV) infections are major health concerns worldwide, where bacterial superinfections substantially increase morbidity and mortality. The underlying mechanisms of how IAV impairs host defense remain elusive. Macrophages are pivotal for the innate immune response and crucially regulate the entire inflammatory process, occurring as inflammatory M1- or pro-resolving M2-like phenotypes. Lipid mediators (LM), produced from polyunsaturated fatty acids by macrophages, are potent immune regulators and impact all stages of inflammation. Using LM metabololipidomics, we show that human pro-resolving M2-macrophages respond to IAV infections with specific and robust production of prostaglandin (PG)E[SUB]2[/SUB] along with upregulation of cyclooxygenase-2 (COX-2), which persists after co-infection with Staphylococcus aureus. In contrast, cytokine/interferon production in macrophages was essentially unaffected by IAV infection, and the functionality of M1-macrophages was not influenced. Conclusively, IAV infection of M2-macrophages selectively elevates PGE[SUB]2[/SUB] formation, suggesting inhibition of the COX-2/PGE[SUB]2[/SUB] axis as strategy to limit IAV exacerbation.
Keywords: Immunology; Virology.