bromochloroacetic-acid and Enterovirus-Infections

A recent histopathologic study implicated human tonsillar crypt epithelium as an important site for EV71 replication in EV71-caused fatal cases. This study aimed to confirm the susceptibility of human tonsillar epithelium to EV71. Two human tonsillar epithelial cell lines (UT-SCC-60A and UT-SCC-60B) were susceptive to EV71, and PI3K/AKT, p38, ERK1/2, and JNK1/2 signal pathways were activated. Interferon-α, IL-8, IL-1β, IL-6 and IL-12p40 were induced and regulated by PI3K/AKT, p38, ERK1/2, and JNK1/2 signal pathways. PI3K/AKT pathway activation appeared to suppress the induction of TNF-α, which induced cell survival by inhibiting GSK-3β. The activation of NF-κB was observed but inhibited by these pathways in EV71 infection. Furthermore, ERK1/2 and JNK1/2 were essential for efficient EV71 replication. Human tonsillar epithelial cells support EV71 replication and display innate antiviral immunity in vitro, indicating that human tonsillar epithelial cells may be novel targets for EV71 infection and replication in vivo.

Topics: Animals; Biomarkers; Cell Line; Cytokines; Cytopathogenic Effect, Viral; Disease Susceptibility; Enterovirus A, Human; Enterovirus Infections; Epithelial Cells; Host-Pathogen Interactions; Humans; Inflammation Mediators; Keratins; Lysosomal Membrane Proteins; Membrane Glycoproteins; Mice; Mitogen-Activated Protein Kinases; Mutation; NF-kappa B; Palatine Tonsil; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Receptors, Scavenger; RNA, Viral; Signal Transduction; Viral Proteins; Virus Replication