A narrative review of research progress on the role of NLRP3 inflammasome in acne vulgaris

Zhu, Wei; Wang, Hailin; Bu, Xian‐Le; Zhang, Junbo; Lu, Yuangang

doi:10.21037/atm-21-5924

Cited by 10 publications

(5 citation statements)

References 58 publications

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“…Inflammasomes are large intracellular signaling complexes which initiate the inflammatory response. Some studies have shown that the nucleotide oligomerization domain (NOD)‐like receptor family pyrin containing 3 (NLRP3) inflammasome is linked to acne pathofisiology 26 . Some strains of P. acnes can activate the NLRP3 inflammasome and promote IL‐1β secretion 27 …”

Section: Resultsmentioning

confidence: 99%

Sun exposure, a relevant exposome factor in acne patients and how photoprotection can improve outcomes

Piquero-Casals¹,

Morgado‐Carrasco

Rozas‐Muñoz

et al. 2023

J of Cosmetic Dermatology

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Background Acne pathophysiology includes a complex interaction among inflammatory mediators, hyperseborrhea, alteration of keratinization and follicular colonization by Propionibacterium acnes. Aims To describe the impact of the exposome on acne and how photoprotection can improve outcomes. Methods A narrative review of the literature was carried out; searches with Google Scholar and Pubmed from January 1992 to November 2022 were performed. The keywords used were “acne,” “sunscreens,” “photoprotection,” “cosmetics,” “cosmeceuticals,” “pathogenesis,” “etiology,” “exposome,” “sunlight,” “stress,” “lack of sleep,” “diet,” “postinflammatory hyperpigmentation,” “pollution,” “exposome,” “ultraviolet radiation,” and “visible light.” Results Environmental factors such as solar radiation, air pollution, tobacco consumption, psychological stress, diverse microorganisms, nutrition, among others, can trigger or worsen acne. Solar radiation can temporarily improve lesions. However, it can induce proinflammatory and profibrotic responses, and produce post‐inflammatory hyperpigmentation and/or post‐inflammatory erythema. While photoprotection is widely recommended to acne patients, only four relevant studies were found. Sunscreens can significantly improve symptomatology or enhance treatment and can prevent post‐inflammatory hyperpigmentation. Furthermore, they can provide camouflage and improve quality of life. Based on acne pathogenesis, optimal sunscreens should have emollient, antioxidant and sebum controlling properties. Conclusions The exposome and solar radiation can trigger or worsen acne. UV light can induce post‐inflammatory hyperpigmentation/erythema, and can initiate flares. The use of specifically formulated sunscreens could enhance adherence to topical or systemic therapy, camouflage lesions (tinted sunscreens), decrease inflammation, and reduce the incidence of post‐inflammatory hyperpigmentation/erythema.

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Section: Resultsmentioning

confidence: 99%

Sun exposure, a relevant exposome factor in acne patients and how photoprotection can improve outcomes

Piquero-Casals¹,

Morgado‐Carrasco

Rozas‐Muñoz

et al. 2023

J of Cosmetic Dermatology

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“…These studies suggest that IL1R1 is a key factor in the development of skin inflammation, and acne belongs to chronic inflammatory diseases of the skin. It has been shown that porphyrins produced by Cutibacterium acnes activate NLRP3 inflammatory vesicles and promote IL-1β secretion ( 34 – 36 ). Therefore, we consider that the IL-1β-IL-1R signaling pathway may emerge as a key player in the developmental mechanism of severe acne.…”

Section: Discussionmentioning

confidence: 99%

DNA methylation mediated genetic risk in severe acne in a young men population

Wu¹,

Chen²,

Bo³

et al. 2023

Front. Med.

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BackgroundAcne is a chronic inflammatory skin disease that affects the pilosebaceous follicle and is influenced by heredity, hormones, inflammation, and the environment. At present, the recognized pathogenesis mainly includes four categories: excessive sebum secretion, excessive Cutibacterium acnes proliferation, excessive keratinization of sebaceous glands in hair follicles, and inflammatory mechanisms. Previous studies have found that DNA methylation is closely related to some chronic inflammatory skin diseases, and there is evidence that DNA methylation is controlled by genetic factors, making us want to know the relationship between DNA methylation, genetic variation and acne.Materials and methodsIn our previous study, we performed genome-wide DNA methylation analysis in peripheral blood samples from 44 patients with severe acne and 44 unaffected normal subjects, and identified 23 differentially methylated probes (DMPs). In this study, we identified single nucleotide polymorphisms (SNPs) associated with severe acne by genome-wide association analysis in these 88 samples. To test the association between SNPs and DMPs, we conducted DNA methylation quantitative trait loci (methQTL) analysis. Next, causal inference testing (CIT) was used to determine whether genetic variation influences DNA methylation, which impacts disease phenotypes.ResultWe found 38,269 SNPs associated with severe acne. By methQTL analysis, we obtained 24 SNP-CpG pairs that reached the threshold (FDR < 0.05), which included 7 unique CpGs and 22 unique methQTL SNPs. After CIT analysis, we found that 11 out of 24 pairs of SNP-CpG showed a weakened SNP effect after adjustment for methylation, indicating a methylation-mediated relationship between SNPs and severe acne. These 11 SNP-CpG pairs consist of four unique CpG sites and 11 SNPs, of which three CpG sites, cg03020863, cg20652636, and cg19964325, are located on the gene body of PDGFD, the intron of SH2D6, and the 5’UTR of the IL1R1 gene, respectively.ConclusionDuring this study, the DNA methylation of certain genes was found to be influenced by genetic factors and mediated the risk of severe acne in a young Chinese male population, providing a new perspective on the pathogenesis of severe acne.

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“…Another recent review [120] explores the complex molecular pathways triggered in acne by pathogenic C. acnes strains via TLR and the activation by PAMPs and DAMPs (pattern/damage-associated molecular patterns) of PRRs (pattern recognition receptors) such as NOD (nucleotide-binding oligomerization domain) receptors and NLR (NOD-like receptors), with the subsequent assembly of the NLRP3 inflammasome, the activation of caspase-1 and the subsequent cascade of proinflammatory cytokines like IL-1β and IL-8. Some potentially useful inhibitors of this pathway, including NLRP3 inhibitors baicalein, eucalyptol extracted from Laurus nobilis, superoxide dismutases, auranofin (an antirheumatic colloidal gold compound), or ROS production inhibitor polyphyllin I may be successfully used in future therapeutic protocols for acne.…”

Section: Novel Therapeutic Approachesmentioning

confidence: 99%

Adult Female Acne: Recent Advances in Pathophysiology and Therapeutic Approaches

Amuzescu,

Tampa,

Matei

et al. 2024

Cosmetics

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Adult acne is a chronic inflammatory disease of the pilosebaceous unit characterized by the excessive production of abnormal sebum favoring an imbalance of the skin microbiota and the hyperproliferation of Cutibacterium acnes and other virulent microbial strains, leading to an inflammatory environment, innate immunity overactivation, and keratinocyte hyperproliferation in hair follicles pores. Degraded keratinocytes plug the pores, consequently forming microcomedons, which can later evolve to papules, nodules, pustules and scars. Distinct from juvenile acne, in adult female acne (AFA) the symptomatology occurs or persists in postadolescence (after age 25). Although hyperandrogenism or the excessive sensitivity of androgen receptors are the main causes, AFA can be triggered by multiple factors, either including or not including androgen disturbances. The prevalence in adult women is 15–20%. Hyperandrogenism is present in 50% of cases; 70% of hyperandrogenism cases feature polycystic ovary syndrome (PCOS), a complex endocrine and metabolic condition. Genetic susceptibility occurs in 80% of acne cases, often with familial inheritance. Beyond classical stepwise therapeutic protocols (topical agents, isotretinoin, antibiotics, hormonal therapy with estrogens, progestins, spironolactone), novel approaches include the highly effective topical antiandrogen clascoterone, the management of insulin resistance by diet, exercise, stress avoidance, and adjuvant therapies such as berberine. Vaccines against the pathogenic proinflammatory C. acnes hyaluronidase A are in development.

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A narrative review of research progress on the role of NLRP3 inflammasome in acne vulgaris

Cited by 10 publications

References 58 publications

Sun exposure, a relevant exposome factor in acne patients and how photoprotection can improve outcomes

Sun exposure, a relevant exposome factor in acne patients and how photoprotection can improve outcomes

DNA methylation mediated genetic risk in severe acne in a young men population

Adult Female Acne: Recent Advances in Pathophysiology and Therapeutic Approaches

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