International Journal of Frontiers in Medicine, 2025, 7(4); doi: 10.25236/IJFM.2025.070406.
Yaoyu Qi1, Shufan Qin1, Ke Liu1, Huiling Jing2
1Shaanxi University of Chinese Medicine, Xianyang, 712046, China
2Xi 'an Affiliated Hospital of Shaanxi University of Chinese Medicine, Xi 'an, 710021, China
This study was designed to elucidate the pivotal role and potential mechanisms of chronic low-grade inflammation in acne pathogenesis, thereby offering new perspectives for clinical management.A comprehensive review of recent literature on acne and inflammation was conducted, with emphasis on the involvement and interplay of inflammatory cytokines, immune signaling pathways, sebaceous gland function, and cutaneous microecological imbalance.Patients with acne frequently exhibit elevated circulating and local levels of key pro-inflammatory mediators, including interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and high-sensitivity C-reactive protein (hs-CRP). These alterations form a pathological network in which localized skin lesions and systemic inflammatory responses mutually reinforce one another, thereby promoting disease persistence and progression. Chronic low-grade inflammation is a central driver throughout the entire course of acne, contributing to its chronicity and therapeutic resistance. Related inflammatory and metabolic biomarkers hold promise as auxiliary indicators for clinical diagnosis, disease stratification, and therapeutic efficacy evaluation.
Acne; Low-Grade Inflammation; Inflammatory Cytokines; Inflammasomes; Sebaceous Glands
Yaoyu Qi, Shufan Qin, Ke Liu, Huiling Jing. Research Progress on Chronic Low-Grade Inflammation and Acne. International Journal of Frontiers in Medicine (2025), Vol. 7, Issue 4: 39-44. https://doi.org/10.25236/IJFM.2025.070406.
[1] Zouboulis C C, Jourdan E, Picardo M. Acne is an inflammatory disease and alterations of sebum composition initiate acne lesions [J]. J Eur Acad Dermatol Venereol, 2014, 28(5): 527-532.
[2] Lkjt, KB. A global perspective on the epidemiology of acne. [J].The British journal of dermatology, 2015,172 Suppl 1(s1):3-12.
[3] Pan Qingli, Shao Lei, Chen Lijie, et al. Research progress on the pathogenesis of acne [J]. Journal of Diagnosis and Therapy on Dermato-venereology, 2018, 25(06): 377-380.
[4] Pietras E M. Inflammation: a key regulator of hematopoietic stem cell fate in health and disease [J]. Blood, the Journal of the American Society of Hematology, 2017, 130(15): 1693-1698.
[5] Zhang Li, Hu Zhibang. Research progress on the pathogenesis of acne inflammation [J]. Shandong Medical Journal, 2018, 58(34): 110-112.
[6] Contassot E, French LE. New insights into acne pathogenesis: Propionibacterium acnes activate the inflammasome. J Invest Dermatol. 2014; 134(2):310 313.
[7] Qin M, Pirouz A, Kim MH, et al. Propionibacterium acnes induce IL 1β secretion via the NLRP3 inflammasome in human monocytes. J Invest Dermatol. 2014; 134(2):381 388.
[8] Żmuda B, Żuberek M, Ślusarczyk D, et al. Acne vulgaris-review on pathogenesis and treatment [J]. Journal of Education, Health and Sport, 2024, 51: 50-63.
[9] Dreno B. What is new in the pathophysiology of acne, an overview. J Eur Acad Dermatol Venereol. 2017; 31(Suppl 5):8-12.
[10] Zhao Min, Wang Xing. Research progress on the role of inflammation in the pathogenesis of acne. Journal of Clinical Dermatology, 2021, 50(1): 20-24.
[11] Kim J. Review of the innate immune response in acne vulgaris: activation of Toll-like receptor 2 in acne triggers inflammatory cytokine responses. Dermatology. 2005;211(3):193-198.
[12] Fang F, Xie Z, Quan J, et al. Baicalin suppresses Propionibacterium acnes-induced skin inflammation by downregulating the NF-κB/MAPK signaling pathway and inhibiting activation of NLRP3 inflammasome [J]. Brazilian Journal of Medical and Biological Research, 2020, 53(12): e9949.
[13] Askari N, Ghazanfari T, Yaraee R, et al. Association between Acne and Serum Pro-inflammatory Cytokines (IL-1α, IL-1β, IL-1Ra, IL-6, IL-8, IL-12 and RANTES) in Mustard Gas-Exposed Patients: Sardasht-Iran Cohort Study. Arch Iran Med. 2017;20(2):86-91.
[14] Mias C, Mengeaud V, Bessou‐Touya S, et al. Recent advances in understanding inflammatory acne: Deciphering the relationship between Cutibacterium acnes and Th17 inflammatory pathway [J]. Journal of the European Academy of Dermatology and Venereology, 2023, 37: 3-11.
[15] Agak GW, Qin M, Nobe J, et al. Propionibacterium acnes Induces an IL-17 Response in Acne Vulgaris that Is Regulated by Vitamin A and Vitamin D. J Invest Dermatol. 2014;134(2):366-373.
[16] Kistowska M,Meier B, Proust T, et al. Propionibacterium acnes promote Th17 and Th17/Th1 responses in acne patients. J Invest Dermatol. 2015; 135(1):110-118.
[17] Ewelina F ,Wioleta K ,Karolina S , et al.The Role of Skin Immune System in Acne[J].Journal of Clinical Medicine,2022,11(6):1579-1579.
[18] Li WH, Zhang Q, Flach CR, Mendelsohn R, Southall MD, Parsa R. In vitro modeling of unsaturated free fatty acid-mediated tissue impairments seen in acne lesions. Arch Dermatol Res. 2017;309(7):529-540.
[19] Camera E, Ludovici M, Galante M, et al. Comprehensive analysis of lipid composition of human skin surface lipids. J Lipid Res. 2010; 51(11):3377-3388.
[20] Ottaviani M, Camera E, Picardo M. Lipid mediators in acne [J]. Mediators of inflammation, 2010, 2010(1): 858176.
[21] Gunter NV, Teh SS, Lim YM, Mah SH. Natural Xanthones and Skin Inflammatory Diseases: Multitargeting Mechanisms of Action and Potential Application. Front Pharmacol. 2020;11:594202. Published 2020 Dec 3.
[22] Kardeh, S., Moein, S. A., Namazi, M. R., & Kardeh, B. (2019). Evidence for the important role of oxidative stress in the pathogenesis of acne. Galen medical journal, 8, e1291
[23] G K T ,M B R ,Corina A , et al.Comparison of the skin microbiota in acne and rosacea.[J]. Experimental dermatology,2020,30(10):1375-1380.
[24] Lomholt HB, Kilian M. Population genetic analysis of Propionibacterium acnes identifies a subpopulation and epidemic clones associated with acne. PLoS One. 2010; 5(8):e12277.
[25] Nagy I, Pivarcsi A, Koreck A, Széll M, et al. Distinct strains of Propionibacterium acnes induce selective human β-defensin-2 and interleukin-8 expression in human keratinocytes through toll-like receptors. J Invest Dermatol. 2005; 124(5):931-938.
[26] Vasarinsh P. Keratinization of pilar structures in acne vulgaris and normal skin[J]. British Journal of Dermatology, 1969, 81(7): 517-524.
[27] Bettoli V, Toni G, Zauli S, Virgili A. Acne mechanica: probable role of IL-1α. G Ital Dermatol Venereol. 2016;151(6):720-721.
[28] Li Shanshan, Zhao Xu, Liu Jipeng, et al. Study on the correlation between the inflammatory degree of acne vulgaris lesions and the levels of IL-8 and TNF-α in peripheral blood [J]. Chinese Journal of Modern Medicine, 2025, 27(01): 47-50.
[29] Rahaman SMA, De D, Handa S, et al. Association of insulin-like growth factor (IGF)-1 gene polymorphisms with plasma levels of IGF-1 and acne severity. J Am Acad Dermatol. 2016;75(4):768-773.