<scp>IL</scp>‐17<scp>C</scp> and its receptor <scp>IL</scp>‐17<scp>RA</scp>/<scp>IL</scp>‐17<scp>RE</scp> identify human oral epithelial cell as an inflammatory cell in recurrent aphthous ulcer

“…Serum levels of IFN-g and IL-17 were significantly increased in RAS patients [48]. Human oral keratinocytes can produce IL-17 and stimulate the production of IL-8 and TNF-a in RAS patients compared with healthy controls [49].…”

Section: Role Of Cytokines In Rasmentioning

confidence: 98%

Recurrent Aphthous Stomatitis: Towards Evidence-Based Treatment?

Challacombe

Alsahaf

Tappuni

2015

Curr Oral Health Rep

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Recurrent aphthous stomatitis is one of the most common oral mucosal diseases seen by dental professionals, and yet its aetiology remains unclear, and its management based on less than robust evidence. The literature remains confused because of the lack of clarity in diagnosis and the lack of a standardised ulcer severity scoring system and agreed outcome measures. However, recent literature is encouraging in meeting these aims. There is agreement that recurrent aphthous stomatitis (RAS) is a localized mucosal disease not secondary to systemic disease and therefore distinguishable from over 40 other types of oral ulcers. Disease severity scores have been introduced and outcome measures have become more standardised. RAS appears to be an autoimmune disease directed at epitopes of heat shock proteins whilst most recent work on aetiology has focused on cytokines and genetics. Pro-inflammatory cytokines including TNF-a and IL-6 and IL-17 are raised in RAS and TNF inhibitors can inhibit episodes of ulceration. Many local antiinflammatory agents will help ulcers heal, and local steroids remain the treatment of choice. Some systemic drugs have evidence-based data indicating efficacy at preventing new ulcers including colchicine, prednisolone, thalidomide, pentoxyfilline and dapsone. The field would benefit from further trials combining local and systemic therapy using defined outcome measures.

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“…Several immunohistochemical studies using clinical samples have indicated that IL-17C is expressed mainly in the epithelial cells, including for inflammatory bowel disease (IBD) (33,34), chronic obstructive pulmonary disease (20), chronic rhinosinusitis with nasal polyposis (35), and recurrent aphthous ulcer (36). Similar to other tissues, our results revealed that IL-17C was present predominantly in the epithelial cells of H. pylori-infected gastric biopsy specimens as well as in chromogranin A-positive endocrine cells (mainly G cells).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-17C in Human Helicobacter pylori Gastritis

et al. 2017

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The interleukin-17 (IL-17) family of cytokines (IL-17A to IL-17F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P ϭ 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected with either cagA-negative or cag pathogenicity island (PAI) mutant. Chemical inhibition of IB kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pyloriinduced diseases remains to be determined.

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IL‐17C and its receptor IL‐17RA/IL‐17RE identify human oral epithelial cell as an inflammatory cell in recurrent aphthous ulcer

Abstract: IL-17C is highly expressed in epithelial cells in RAU lesions, where it seems to stimulate oral keratinocytes via IL-17RA/IL-17RE to produce pro-inflammatory cytokines. Human oral epithelial cells are probably important inflammatory cells in RAU.

Cited by 29 publications

References 24 publications

Serum Th1, Th2 and Th17 cytokine profiles and alpha‐enolase levels in recurrent aphthous stomatitis

Serum Th1, Th2 and Th17 cytokine profiles and alpha‐enolase levels in recurrent aphthous stomatitis

Recurrent Aphthous Stomatitis: Towards Evidence-Based Treatment?

Interleukin-17C in Human Helicobacter pylori Gastritis

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