Regulation of human beta-defensin-2 in gingival epithelial cells: the involvement of mitogen-activated protein kinase pathways, but not the NF-kappaB transcription factor family.

摘要: Stratified epithelia of the oral cavity are continually exposed to bacterial challenge that is initially resisted by neutrophils and epithelial factors, including antimicrobial peptides beta-defensin family. Previous work has shown multiple signaling pathways involved in human (hBD)-2 mRNA regulation gingival cells stimulated with a periodontal bacterium, Fusobacterium nucleatum, other stimulants. The goal this study was further characterize these pathways. role NF-kappaB hBD-2 investigated due its importance inflammation infection. Nuclear translocation p65 activation seen F. nucleatum cell wall extract, indicating possible involvement regulation. However, induction not blocked pretreatment two inhibitors, pyrrolidine dithiocarbamate proteasome inhibitor, MG132. To investigate alternative modes regulation, we explored mitogen-activated protein kinase activated p38 c-Jun NH(2)-terminal (JNK) pathways, whereas it had little effect on p44/42. Furthermore, inhibition JNK partially combination inhibitors completely expression. Our results suggest neither essential nor sufficient for induction, via JNK, while phorbol ester induces p44/42 extracellular signal-regulated pathway. Studies provide insight into how expression may be enhanced control infection locally within mucosa thereby reduce microbial invasion underlying tissue.