The mechanism on Prevotella melaninogenica promoting the inflammatory progression of oral lichen planus

Abstract

Oral lichen planus (OLP) is a common chronic inflammatory disease occurring in the oral mucosa. Bacteria is a key driver of mucosal immune response and can induce changes in gene expression and function of epithelial keratinocytes. IL-36γ can induce the expression of antimicrobial peptides, cytokines and chemokines, and is widely involved in many chronic inflammatory diseases. Our aim is to explore the role of IL-36γ in pathological process of OLP when Prevotella melaninogenica (P. melaninogenica) invades oral mucosa. The expression of IL-36γ in OLP lesions and mice was detected by immunohistochemistry. Recombinant human IL-36Gamma (rhIL-36γ) was used to treat oral keratinocytes and the expression levels of inflammatory cytokines were detected by qRT-PCR and ELISA. The expression of IL-36γ and TRPV1 was detected by western blotting following co-culturing P. melaninogenica with oral keratinocytes. The mRNA expression of IL-36γ was detected by qRT-PCR. From our results, IL-36γ was upregulated in OLP lesions. Exogenous rhIL-36γ promoted the expression of pro-inflammatory cytokines and antibacterial peptides in oral keratinocytes. The expression of IL-36γ was significantly increased following the stimulation of P. melaninogenica in oral keratinocytes and mice. TRPV1 activation was induced by P. melaninogenica and its activation enhanced the expression of IL-36γ. IL-36Ra could reduce the inflammation in OLP in vitro. In summary, overexpression of IL-36γ in OLP lesions could promote its pathogenesis by inducing inflammation. P. melaninogenica invasion of oral keratinocytes could induce the expression of IL-36γ by the activation of TRPV1, thereby regulating the interaction between bacteria and oral epithelial cells.

Floxed Il1rl2 Locus with mCherry Reporter Element Reveals Distinct Expression Patterns of the IL-36 Receptor in Barrier Tissues

“…cans fungi [48], but may also promote gingivitis, periodontitis, and lichen planus [47,[49][50][51][52]. We found that the mCherry Il1rl2 reporter was highly expressed in epithelial cells on the dorsal surface of the tongue (Figure 7A, black arrow).…”

“…The IL-36 system has been shown to activate expression of proinflammatory cytokines in oral epithelial cells [44,45]. This activity may be beneficial for the control of bacteria, e.g., Porphyromonas gingivalis and Prevotella melaninogenica [46,47], and Candida albicans fungi [48], but may also promote gingivitis, periodontitis, and lichen planus [47,[49][50][51][52]. We found that the mCherry Il1rl2 reporter was highly expressed in epithelial cells on the dorsal surface of the tongue (Figure 7A, black arrow).…”

Identification of proteotoxic and proteoprotective bacteria that non-specifically affect proteins associated with neurodegenerative diseases

“…Such various effects of individual species could be explained by large variability in their genomes. 42 The species, P. intermedia, P. nigrescense, and P. melanigencia have been consistently associated with infection, [43][44][45] inflammation, [46][47][48][49] and have also been linked to AD and associated mortality. 50 Conversely, it has been shown that P. buccae and P. corporis, two strains of Prevotella that exhibited strong suppression of protein aggregation and the associated toxicity, were found not to induce inflammation.…”

Salivary Interleukin-6 Level in Iraqi Patients with Oral Lichen Planus receiving Platelet-Rich Plasma Injections

“…Recent research has shown that PRP, either alone or in conjunction with other treatments, has the power to change the level of IL-6 in the saliva of OLP patients (12). Salivary level of IL-6 maybe used as a reliable marker for evaluating the therapeutic effectiveness of medications in OLP patients (13). Peripheral blood mononuclear cells and tissueinfiltrating mononuclear cells from OLP lesions both have the capacity to make tumour necrosis factor-alpha (TNF-α).…”