Bibliometric analysis of recent research on the association between TRPV1 and inflammation.

TRPV1 channel is a sensitive ion channel activated by some noxious stimuli and has been reported to change many physiological functions after its activation. In this paper, we present a scientometric approach to explore the trends of the association between TRPV1 channel and inflammation and our goal is to provide creative directions for future research. The related literature was retrieved from Web of Science Core Collection and then analyzed by CiteSpace and VOSviewer. A total of 1533 documents were screened. The most productive country, institution, journal, author, cited journal, cited author, and references were the United States, University of California, San Francisco, Pain, Lu-yuan Lee, Nature, Michael J. Caterina, and Caterina MJ (Science, 2000), respectively. The most influential country and institution were Switzerland and University of California, San Francisco, respectively. The cooperation among countries or institutions was extensive. Amounts of documents were distributed in molecular, biology, genetics. TRPV1-associated neurons, neuropeptides, neuropathic pain, neuroinflammation, and neurogenic inflammation were mainly hotspots in this field. The research has presented valuable data about previous studies in the link of TRPV1 channel and inflammation.

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

Oral lichen planus (OLP) is a common chronic inflammatory disease occurring in the oral mucosa. Bacteria are a key driver of mucosal immune responses 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 the pathological process of OLP when Prevotella melaninogenica (P. melaninogenica) invades the 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.