New understanding of the pathogenesis of acne: inflammatory response throughout the pathogenesis of acne Acne lesions, routinely divided into inflammatory lesions and non-inflammatory lesions. The previous view was that non-inflammatory acne was only due to excessive sebum production and hyperkeratosis of the follicle opening, while inflammatory acne was only the result of secondary bacterial infection. In fact, it has been demonstrated that an inflammatory response is involved in the formation of microcomedones at the subclinical lesion stage, and Guy et al. detected the pro-inflammatory cytokine IL1α in isolated follicular sebaceous units, which leads to excessive proliferation and abnormal differentiation of keratin-forming cells, thus promoting the formation of clinical microcomedones. used normal hair follicles from acne patients as subclinical lesions and found that their proliferation and differentiation were consistent with those of normal patients, but there was already a significant inflammatory response involved in these follicular sebaceous units (PSUs), with CD4+ T lymphocytes, macrophages, IL1α, and epidermal αintegrins (integrins) Expression was significantly upregulated in all of these mediators, which are important components of inflammatory activation, thus confirming the role of the inflammatory response in microcomedema and thought to precede the hyperkeratotic process.Del Rosso et al. detected gene expression of IL1 and integrins in subclinical skin lesions. Thus, what we consider as non-inflammatory acne (open or closed acne) is essentially an inflammatory response. The inflammatory response is not only involved in early subclinical non-inflammatory acne, but also throughout the pathogenesis of acne, including the formation of inflammatory lesions and later post-inflammatory erythema and post-inflammatory hyperpigmentation or scar formation. this inflammatory process was confirmed by Kang et al. immunohistochemical studies revealed that within acne lesions the expression of pro-inflammatory factors TNFα and IL1β through activation of the NFγB pathway upregulated, followed by upregulation of adhesion molecules such as ICAM1, Eselectin, and VCAM1, and increased the expression of chemokine IL8 as well. Meanwhile, by stimulating mitogenactivated protein kinases (MAP kinases), activator protein1 (AP1) regulates a series of matrix metalloproteinases (matrixmetalloproteinases , MMP) 1, 3, 8, 9, and 13, the latter of which is importantly related to the formation of acne scarring. Pathophysiological effects of P. acnes in acne and natural immune-mediated inflammatory response in acne P. acnes induces and activates TLR2 and TLR4, causing the production of a series of pro-inflammatory factors, such as IL1, TNFα, prostaglandins, leukotrienes and chemokines (IL8), and is also a mechanism for amplifying the inflammatory response. p. acnes is responsible for the inflammatory response through its effects on keratinogenic cells, sebaceous gland cells TLR2/4 expression, regulating IL1?, TNF? and other pro-inflammatory mediators production, which is involved in the inflammatory response process. 2015 National Academic Conference on Integrative Dermatology and Venereology Acne Treatment Re-conceptualization Tetracycline as an antimicrobial drug in the first line of acne treatment was considered effective in the treatment of acne as early as the 1950s. However, subsequent studies have found that tetracyclines resistant to P. acnes in vitro are also effective in acne patients, while subantibacterialdose tetracyclines are also effective in treating acne, and their mechanism of action is through their specific anti-inflammatory effects. Tetracycline inhibits the release of chemokines from P. acnes, thereby inhibiting protein synthesis, and also inhibits the production of reactive oxygen species (ROS) by P. acnes-induced neutrophils. The amount of subtilisin also reduced the number of acne, indicating that it also has an effect on non-inflammatory acne, and the mechanism may work by inhibiting cytokines IL1α, MMP9, etc. It was also found that chemically modified tetracyclines (CMT) had no bactericidal effect after the removal of structures targeting bacterial ribosomes and protein synthesis, but also inhibited the expression of inflammatory factors IL8 and MMP1, thus suppressing the inflammatory response caused by P. acnes. Toossi et al. compared 50 patients given 40 mg/d or 100 mg/d of doxycycline respectively and showed significant improvement in lesions at 3 months, but there was no statistical difference in efficacy between the two. side effects were significantly less in the small dose group compared to the high dose group. Therefore, using the anti-inflammatory effect of tetracyclines, we can use them as monotherapy or maintenance treatment, thus reducing the use of full-dose antibiotics and avoiding or reducing the development of drug resistance. Acne treatment goals: prevention of recurrence and reduction of scarring Parinitha et al. treated 50 patients with moderate to severe acne with a low dose of 0.3 to 0.4 mg/(kg?d) of isotretinoin for 3 months and followed up for 6 months and found an efficiency of 90%, although 98% of the patients still had labyrinthitis, but to a lesser extent, and the recurrence rate after 6 months was only 4%. The lower dose of isotretinoin 0.15-0.28 mg/(kg?d) could also achieve a significant efficiency of 87.54%. A review of the previous literature on the treatment of acne with low doses of isotretinoin showed that an effective rate of 69-99% could be achieved. The efficacy of high-dose treatment can be achieved at a cumulative dose of ≥120 mg/kg with a small dose of isotretinoin, and it is the small dose that significantly reduces side effects, increases patient compliance, and enables a full course of treatment, thus reducing scar formation and recurrence rates.