The skin disease acne vulgaris is characterized by chronic inflammation affecting up to 85–100% in adolescence, 10% of which is severe and 30% is moderate [1,2]. Without proper control, this condition may lead to permanent disfigurement and even severe social and psychological problems. Cutibacterium acnes (C. acnes) causes the acne inflammatory response, which is crucial to the pathological alterations of acne, by changing the composition of sebum and inducing a number of immunological responses [3,4]. The inflammatory cascade of C. acnes may cause skin irritation and acne scar formation.

Inflammation is a sophisticated defense mechanism against a wide range of hazardous stimuli, such as infections and irritants, but an overly aggressive inflammatory response causes damage to one's own tissues. Numerous studies have investigated the control of inflammatory signaling pathways in different disorders, focusing on potential molecular targets for anti-inflammatory therapy to counteract the harmful consequences of inflammation [5], [6], [7]. The generation of pro-inflammatory cytokines is the most important biochemical mechanism by which the inflammatory response is mediated. There are several inflammatory factors associated with acne lesions, including tumor necrosis factor alpha (TNF-α), interleukin 8 (IL-8), and interleukin 6 (IL-6) [8,9]. Phosphorylation of molecules involved in the MAPK and NF-κB signaling cascade can promote the production of inflammatory factors. It is essential to target the NF-κB and MAPK pathways to inhibit the expression of inflammatory mediators in anti-inflammatory medications.

The active ingredient in turmeric, curcumin, is a polyphenolic curcuminoid that has been proven to have antioxidant, anti-inflammatory, anti-apoptotic, and antibacterial activities [10,11]. According to research on anti-inflammatory diseases, curcumin can reduce inflammation in a variety of conditions, including neuritis, fatty liver inflammation, arthritis, and nephritis, by inhibiting the NF-κB pathway and brain hypoxic injury, brain trauma, epilepsy, and acute vasculitis by inhibiting the MAPK pathway [12], [13], [14], [15]. Only our preliminary work on the ability of curcumin to prevent an inflammatory response by THP-1 cells to C. acnes stimulation via the NF-κB pathway exists in curcumin research in acne [16]. We believe that curcumin is a good candidate for preventing C. acnes-induced inflammatory response that leads to acne.

Treatment based on photosensitizers, light sources, and molecular oxygen has been used to treat a wide range of disorders, including cancer and non-cancerous diseases, with few side effects [17,18]. Photodynamic treatment techniques are becoming widely accepted in the field of acne treatment. Several studies have shown that curcumin combined with phototherapy can reduce the activity of several pathogenic bacteria, including C. acnes [19], Streptococcus pyogenes [20], and Aeromonas gingivalis [21]. Another study discovered that the combination of curcumin and blue light reduced inflammatory response by reducing Staphylococcus aureus infection in the epidermis of diabetic mice [22]. However, there has been no research on the effectiveness of curcumin photodynamics in reducing acne inflammation.

In this investigation, we sought to determine how curcumin, either alone or in conjunction with blue light, inhibits the production of inflammatory factors by C. acnes biofilm in human keratinocytes. Curcumin alone or curcumin-PDT inhibition via NF-κB and MAPKs may provide an attractive new approach to limit the generation of inflammatory molecules for treatment of acne.