tetano
Editor, Senior Moderator
Gene
. 2024 May 11:148559.
doi: 10.1016/j.gene.2024.148559. Online ahead of print. Investigate the potential impact of Hemagglutinin from the H1N1 strain on severe pneumonia
Yu-Bi Zheng[SUP] 1 [/SUP], Song Lu[SUP] 2 [/SUP], Tian-Bao Chu[SUP] 2 [/SUP], Gui-Feng Pang[SUP] 2 [/SUP], Lin-Ying Yang[SUP] 2 [/SUP], Qing Zhang[SUP] 3 [/SUP]
Affiliations
The most prevalent glycoprotein on the influenza virus envelope is called hemagglutinin (HA), yet little is known about its involvement in the pathophysiology and etiology of severe influenza pneumonia. Here, after stimulating human bronchial epithelial cells (16-HBE) and mice with HA of H1N1 for 12 h, we investigated the proliferation, migration, inflammatory cytokines expression, and apoptosis in 16-HBE and the pathological damage in mouse lung tissue. The expression of inflammatory cytokines plasminogen activator inhibitor 1(PAI-1), urokinase-type (uPA) and tissue-type (tPA) plasminogen activators, and apoptosis were all enhanced by HA, which also prevented the proliferation and migration of bronchial epithelial cells. HA enhanced up-regulated PAI-1, uPA, and tPA protein expression within mouse lung tissue and caused lung injury. In conclusion, HA alone, but not the whole H1N1 virus, induces lung tissue injury by inhibiting cell proliferation and migration, while promoting the expression of inflammatory cytokines and apoptosis.
Keywords: Apoptosis; Hemagglutinin; Human bronchial epithelial cells; Influenza virus; Migration; Plasminogen activator inhibitor 1; Tissue plasminogen activators; U rokinase-plasminogen activators.
. 2024 May 11:148559.
doi: 10.1016/j.gene.2024.148559. Online ahead of print. Investigate the potential impact of Hemagglutinin from the H1N1 strain on severe pneumonia
Yu-Bi Zheng[SUP] 1 [/SUP], Song Lu[SUP] 2 [/SUP], Tian-Bao Chu[SUP] 2 [/SUP], Gui-Feng Pang[SUP] 2 [/SUP], Lin-Ying Yang[SUP] 2 [/SUP], Qing Zhang[SUP] 3 [/SUP]
Affiliations
- PMID: 38740352
- DOI: 10.1016/j.gene.2024.148559
The most prevalent glycoprotein on the influenza virus envelope is called hemagglutinin (HA), yet little is known about its involvement in the pathophysiology and etiology of severe influenza pneumonia. Here, after stimulating human bronchial epithelial cells (16-HBE) and mice with HA of H1N1 for 12 h, we investigated the proliferation, migration, inflammatory cytokines expression, and apoptosis in 16-HBE and the pathological damage in mouse lung tissue. The expression of inflammatory cytokines plasminogen activator inhibitor 1(PAI-1), urokinase-type (uPA) and tissue-type (tPA) plasminogen activators, and apoptosis were all enhanced by HA, which also prevented the proliferation and migration of bronchial epithelial cells. HA enhanced up-regulated PAI-1, uPA, and tPA protein expression within mouse lung tissue and caused lung injury. In conclusion, HA alone, but not the whole H1N1 virus, induces lung tissue injury by inhibiting cell proliferation and migration, while promoting the expression of inflammatory cytokines and apoptosis.
Keywords: Apoptosis; Hemagglutinin; Human bronchial epithelial cells; Influenza virus; Migration; Plasminogen activator inhibitor 1; Tissue plasminogen activators; U rokinase-plasminogen activators.