Heat-Killed Fusobacterium nucleatum Triggers Varying Heme-Related Inflammatory and Stress Responses Depending on Primary Human Respiratory Epithelial Cell Type

Molecules

Ai Kotani¹  MarniE. Cueno²  Hajime Tanaka²  Kenichi Imai²  Keiko Nodomi²  Muneaki Tamura²  Noriaki Kamio²  Ryo Koike³ 

[1] Department of Hematological Malignancy, Institute of Medical Science, Tokai University, Kanagawa 259-1193, Japan;Department of Microbiology, Nihon University School of Dentistry, Tokyo 101-8310, Japan;Division of Oral Structural and Functional Biology, Nihon University Graduate School of Dentistry, Tokyo 101-8310, Japan;

关键词: Fusobacterium nucleatum;    fusobacterial adhesin;    heat-killed;    heme;    inflammatory response;    virulence potential;   

DOI  :  10.3390/molecules25173839

来源: DOAJ

【 摘 要 】

Fusobacterium nucleatum (Fn) is generally an opportunistic oral pathogen that adheres to mammalian mucosal sites, triggering a host inflammatory response. In general, Fn is normally found within the human oral cavity; however, it was previously reported that Fn is a risk factor for certain respiratory diseases. Surprisingly, this was never fully elucidated. Here, we investigated the virulence potential of heat-killed Fn on primary human tracheal, bronchial, and alveolar epithelial cells. In this study, we measured the secretion of inflammatory- (IL-8 and IL-6), stress- (total heme and hydrogen peroxide), and cell death-related (caspase-1 and caspase-3) signals. We established that the inflammatory response mechanism varies in each epithelial cell type: (1) along tracheal cells, possible Fn adherence would trigger increased heme secretion and regulated inflammatory response; (2) along bronchial cells, potential Fn adherence would simultaneously initiate an increase in secreted H₂O₂ and inflammatory response (ascribable to decreased secreted heme amounts); and (3) along alveolar cells, putative Fn adherence would instigate the increased secretion of inflammatory responses attributable to a decrease in secreted heme levels. Moreover, regardless of the epithelial cell-specific inflammatory mechanism, we believe these are putative, not harmful. Taken together, we propose that any potential Fn-driven inflammation along the respiratory tract would be initiated by differing epithelial cell-specific inflammatory mechanisms that are collectively dependent on secreted heme.

【 授权许可】

Unknown