tetano
Editor, Senior Moderator
Am J Physiol Heart Circ Physiol
. 2024 Sep 6.
doi: 10.1152/ajpheart.00646.2023. Online ahead of print. Gestational influenza A virus infection elicits non-resolving vascular dysfunction and T cell accumulation in the aorta of mice
Osezua Oseghale[SUP] 1 [/SUP], Kylie M Quinn[SUP] 2 [/SUP], Madison Coward-Smith[SUP] 3 [/SUP], Felicia Liong[SUP] 4 [/SUP], Mark Miles[SUP] 4 [/SUP], Robert D Brooks[SUP] 5 [/SUP], Ross Vlahos[SUP] 6 [/SUP], John J O'Leary[SUP] 7 [/SUP], Doug A Brooks[SUP] 8 [/SUP], Stella Liong[SUP] 4 [/SUP], Stavros Selemidis[SUP] 9 [/SUP]
Affiliations
T cell accumulation within the aorta promotes endothelial dysfunction and the genesis of cardiovascular disease, including hypertension and atherosclerosis. Viral infection during pregnancy is also known to mediate marked acute endothelial dysfunction, but it is not clear whether T cells are recruited to the aorta and whether the dysfunction persists post-partum. Here, we demonstrate that influenza A virus (IAV) infection during pregnancy in a murine model resulted in endothelial dysfunction of the aorta, which persisted for up to 60 days post-infection and was associated with higher levels of IFN-g mRNA expression within the tissue. In the absence of infection, low numbers of naïve CD4[SUP]+[/SUP] and CD8[SUP]+[/SUP] T cells, central memory T cells and effector memory T cells were observed in the aorta. However, with IAV infection these T cell subsets were significantly increased with a notable accumulation of IAV-specific CD8[SUP]+[/SUP] effector memory T cells. Critically, this increase was maintained out to at least 60 days. In contrast, IAV infection in non-pregnant female mice resulted in modest endothelial dysfunction with no accumulation of T cells within the aorta. These data therefore demonstrate that the aorta is a site of T cell recruitment and retention after IAV infection during pregnancy. Whilst IAV-specific memory T cells could theoretically confer protection against future influenza infection, non-specific memory T cell activation and IFN-g production in the aorta could also contribute to future endothelial dysfunction and cardiovascular disease.
Keywords: T cells; aorta; endothelial dysfunction; influenza; pregnancy.
. 2024 Sep 6.
doi: 10.1152/ajpheart.00646.2023. Online ahead of print. Gestational influenza A virus infection elicits non-resolving vascular dysfunction and T cell accumulation in the aorta of mice
Osezua Oseghale[SUP] 1 [/SUP], Kylie M Quinn[SUP] 2 [/SUP], Madison Coward-Smith[SUP] 3 [/SUP], Felicia Liong[SUP] 4 [/SUP], Mark Miles[SUP] 4 [/SUP], Robert D Brooks[SUP] 5 [/SUP], Ross Vlahos[SUP] 6 [/SUP], John J O'Leary[SUP] 7 [/SUP], Doug A Brooks[SUP] 8 [/SUP], Stella Liong[SUP] 4 [/SUP], Stavros Selemidis[SUP] 9 [/SUP]
Affiliations
- PMID: 39240256
- DOI: 10.1152/ajpheart.00646.2023
T cell accumulation within the aorta promotes endothelial dysfunction and the genesis of cardiovascular disease, including hypertension and atherosclerosis. Viral infection during pregnancy is also known to mediate marked acute endothelial dysfunction, but it is not clear whether T cells are recruited to the aorta and whether the dysfunction persists post-partum. Here, we demonstrate that influenza A virus (IAV) infection during pregnancy in a murine model resulted in endothelial dysfunction of the aorta, which persisted for up to 60 days post-infection and was associated with higher levels of IFN-g mRNA expression within the tissue. In the absence of infection, low numbers of naïve CD4[SUP]+[/SUP] and CD8[SUP]+[/SUP] T cells, central memory T cells and effector memory T cells were observed in the aorta. However, with IAV infection these T cell subsets were significantly increased with a notable accumulation of IAV-specific CD8[SUP]+[/SUP] effector memory T cells. Critically, this increase was maintained out to at least 60 days. In contrast, IAV infection in non-pregnant female mice resulted in modest endothelial dysfunction with no accumulation of T cells within the aorta. These data therefore demonstrate that the aorta is a site of T cell recruitment and retention after IAV infection during pregnancy. Whilst IAV-specific memory T cells could theoretically confer protection against future influenza infection, non-specific memory T cell activation and IFN-g production in the aorta could also contribute to future endothelial dysfunction and cardiovascular disease.
Keywords: T cells; aorta; endothelial dysfunction; influenza; pregnancy.