Assessment of Interleukin‐18 gene polymorphism and serum levels in oral lichen planus in an Indian population

Abstract

Background Oral lichen planus (OLP) is a chronic, inflammatory disease with uncertain etiology. The aim of this study was to assess Interleukin‐18 (IL‐18) gene polymorphism and serum levels in OLP cases of Indian origin and to compare them with a control population of similar background. Methods The assessment of single‐nucleotide polymorphisms (SNPs) of IL‐18 gene at promoter regions −137(G/C) and −607(C/A) was done in 70 OLP cases and 70 healthy controls using sequence‐specific primer‐polymerase chain reaction (SSP‐PCR). In a subset of this cohort, comprising of 41 OLP cases and 41 controls, serum IL‐18 levels were assessed using enzyme‐linked immunosorbent assay (ELISA). Results Mean serum levels of IL‐18 among OLP cases were significantly higher when compared to controls. Genotypic and allelic frequencies of IL‐18 at position −137(G/C) showed that GG genotype and allele G was significantly higher in OLP cases, whereas, GC genotype and C allele was high in the control group. Polymorphism of IL‐18 at position −607(C/A) showed no significant differences. Conclusions Gene polymorphism at −137GG genotype and allele G seems to be associated with genetic susceptibility to OLP whereas −137GC and allele C may have a protective role against its development. However, our study lacks clear statistical correlation, the differences observed could be caused by sampling problems and the results could not be fully representative of Indian patients with OLP. Further studies are warranted to explore the role of IL‐18 genetic polymorphisms in OLP development.

Immune mechanisms in oral lichen planus

“…IL‐12 and IL‐18 synergistically enhance IFN‐γ mRNA transcription by activating the transcription factors STAT4 and AP‐1, whilst inhibiting the synthesis of IL‐10, a Th2‐associated cytokine (Nakahira et al, 2002). In support of this, IL‐18 serum levels are elevated in OLP patients and an IL‐18 genetic polymorphism has been associated with OLP susceptibility (Negi et al, 2019), although more studies are needed to investigate the role of IL‐18 in regulating Th1 differentiation in OLP.…”

Immunological abnormalities in lichen planus

“…In lichen planus a statistically significant higher mean serum level of IL-18 was found compared to healthy controls [33]. Moreover, it was observed that in a group of erosive lichen planus compared to nonerosive lichen planus an elevated level of IL-18 is present, but it is unclear whether these findings are statistically significant and could help to base the diagnosis the erosive subtype of lichen planus [33,34].…”

“…U chorych z liszajem płaskim odnotowano statystycznie znamienny wzrost średniego stężenia IL-18 w porównaniu z osobami zdrowymi z grupy kontrolnej [33]. Zaobserwowano ponadto, że w grupie pacjentów z postacią nadżerkową liszaja płaskiego (w porównaniu z postacią nienadżerkową) występuje podwyższone stężenie IL-18.…”

“…Zaobserwowano ponadto, że w grupie pacjentów z postacią nadżerkową liszaja płaskiego (w porównaniu z postacią nienadżerkową) występuje podwyższone stężenie IL-18. Nie ma jednak pewności, czy różnica ta jest znamienna statystycznie i może być podstawą do rozpoznania podtypu nadżerkowego liszaja płaskiego [33,34].…”

Rise and exacerbation of oral lichen planus in the background of SARS-CoV-2 infection

“…Raised cytokines: Several interleukins (IL) such as IL1, 2, 4, 5, 6, 8, 10, 12, 17, and 18 have been implicated in the causation and progression of oral lichen planus. [7] Genetic polymorphisms of IL-18 [31] , TNFα [32] , [33] , [34] , [35] , IFNγ [36] , [37] , [38] , IL-10 [33] , [35] , IL-17 [39] , IL-1ß [34] , IL-12 [40] , IL-8 [41] , IL-4 [37] have also been associated with OLP. Histopathologically, they damage the basement membrane and cause widespread tissue destruction leading to the formation of clinically observable lesions.…”