CD33 is downregulated by influenza virus H1N1pdm09 and induces ROS and the TNF-α, IL-1β, and IL-6 cytokines in human mononuclear cells.

ABSTRACT: The influenza A virus (IAV) H1N1pdm09 induces exacerbated inflammation, contributing to disease complications. Inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), favor an inflammatory response that aids viral replication and survival. A pathway by which spontaneous TNF-α production occurs involves either the reduction of Siglec-3 (CD33) levels or the absence of its ligand, sialic acid. Influenza virus uses sialic acid to enter cells by reducing their expression; however, the role of CD33 in IAV H1N1pdm09 stimulation and its relationship with inflammation have not yet been studied. To evaluate the role of CD33 in proinflammatory cytokine production in IAV H1N1pdm09 stimulation, peripheral blood mononuclear cells from healthy subjects were incubated with IAV H1N1pdm09. We o

SUBMITTER: Guzman-Beltran S 

PROVIDER: S-EPMC8882749 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature