Differential utilization of nuclear factor‐κB signaling pathways for gingival epithelial cell responses to oral commensal and pathogenic bacteria

Abstract

Introduction-Human β-defensin-2 (hBD-2) is an antimicrobial peptide, induced by bacterial stimuli and inflammation, that plays a role in mucosal and skin innate immune defense. The nuclear factor-κB (NF-κB) transcription factor family is important in innate and adaptive immune responses to bacteria and proinflammatory cytokines. NF-κB operates via the traditional IKKβ signaling, as well as an alternative pathway utilizing IKKα signaling, which is important in keratinocyte differentiation. Our previous studies showed that pathogenic, but not commensal, bacteria used NF-κB signaling in hBD-2 induction. The objective of this study was to understand which arm of the NF-κB pathway is involved in gingival epithelial cell responses to pathogenic bacteria, including hBD-2 induction.

Epithelial Innate Immune Response to Acinetobacter baumannii Challenge

“…3C). These findings are consistent with previous reports that hBD-2 induction is regulated by NF-B and not EGFR (32,33).…”

Periodontal Disease and Gingival Innate Immunity – Who Has the Upper Hand?

“…MALT1 induces IKK catalytic activity, resulting in NFκB activation in immune cells (Schulze-Luehrmann and Ghosh 2006). The methylation of MALT1 is associated with silencing of MALT1 gene, which is consistent with our previous reports that F. nucleatum does not utilize the NFκB signaling pathway in the induction of innate immune responses (Chung and Dale 2004;Chung and Dale 2008). Taken together, these data suggest that epigenetic modification of genes, whose function is associated with growth control and inflammation, is differentially regulated by different oral bacteria (Yin and Chung 2011).…”

“…Studies on the regulation of the induction of beta-defensins reveal different ways gingival epithelia respond to the presence of pathogenic and non-pathogenic bacteria. Our group has reported the induction of hBD-2 by GECs in response to commensal bacteria like F. nucleatum and S. gordonii utilized p38 and JNK MAPK pathways, while in response to periopathogenic bacteria like P. gingivalis and A. actinomycetemcomitans, GECs utilized the NF-κB pathway in addition to the aforementioned MAPK (Krisanaprakornkit, Kimball et al 2002;Chung and Dale 2008). Our group has further reported gingival innate immune response to P. gingivalis involves Protease-activated receptor-2 (PAR-2), a G-protein coupled receptor (Chung, Hansen et al 2004;Dommisch, Chung et al 2007).…”

Oral epithelial barrier function and the role of nuclear factor kappa-? pathway in the pathogenesis of aphthous ulceration

“…Abnormal expression of pattern recognition receptors may also play a role in the pathogenesis of aphthous ulcerations. The mucosal reaction to pathogenic bacteria or permeated antigens also activates the postreceptor NF-κB pathway which is the main pathway of adaptive immunity (13,27). A growing number of studies demonstrate that aberrant NF-κB signaling is critical in the development of various inflammatory diseases (13,14,28,29).…”

“…TLR activation results in proinflammatory cytokine secretions such as interleukin-1, tumor necrosis factor-alpha, interleukin-8, interleukin-10, and interferons (27,28). Different types of TLRs recognize different antigenic substances, and the specific location of TLR specify the form of the ensuing immuno-inflammatory reaction.…”