The Role of Immunological Reaction and Pro Inflammatory Mediators in Acne Vulgaris Etiopathogenesis, Applications in Dermatology Practice

Abstract

Lely Nurjanti

Introduction: Acne vulgaris was not infectious-very common-chronic inflammatory-self limitting disease of pilosebaceous units. Affected approximately 85% of adolescent as physiological acne and 10- 15% was manifest as clinical acne. Four major factors were involved in the etiopathogenesis: follicular hyperkeratinization, increased sebum production, abnormality of microbial flora and inflammation process. Acne vulgaris inflammation process was divided into early stages (adaptive Th1 cell & innate immune complement to non spesific antigen) and late stages (innate & adaptive immune response to spesific antigen). Acne vulgaris dermal inflammation was not directly caused by bacteria in the dermis, but it was resulted from biologically active mediators that diffused from follicle. Pro inflammatory mediators in acne had no protective role but it had harmfull effect caused persistent inflammation, soft tissue destruction and scar formation, cell cycles control disturbances-cell survival&apoptosis, termination of differentiation & proliferation, hyperkeratinization, sebaceous glands hypertrophy and lipogenesis, pruritus, pigmentation. Biological active mediators were produced in innate immune response by the binding of the PAMPs bacterial’s to innate surface PPRs (TLR2 & TLR4) of the keratinocytes, sebocytes & phagocytes, through innate cell cytoplasm PPRs-NLRP3 inflammasome activation, through PAR2 gene activation, through FGFR2 of keratinocytes activation. Biological active mediators were also produced by adaptive immune response by the binding bacteria that had been recognized by APC (through MHC class II) to the CD4+ of naive T cells that activated Th1, Th2, Th17 and Treg.

Case Report: 5 cases of acne vulgaris 3rd to 4th grade in female, 20-30 years old that had been treated by combination of topical tretinoin 0,05% and flucinolone acetonide 0,025% for 4 weeks were reported. The result were good (decreased acne to 1st grade to no acne), no side effects were reported. Tretinoin 0,025% was choosen as maintain treatment.

Discussion: Treatment of choices for chronic inflammation in acne were anti immunological reaction/pro inflammatory antagonists drugs. Steroid (acted in NFÆ?B pathway) and tretinoin (antagonist TLR2 and FGFR2) topical combination had good result. Tretinoin decreased comedo, sebum production & hyperkeratinization, normalized keratinization and differentiation, replaced disorganized collagen fibers & formed thicker-elastic epidermis (skin rejuvenation), decreased PIH and scar/keloid formation. Steroid decreased chronic persistent inflammation & scar formation and decreased erythema & irritancy that were caused by tretinoin.

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