The Role of Inflammatory Pathways in Acne Development
Acne starts when hair follicles get clogged, but inflammation plays a big part in turning that into red bumps, pimples, and cysts. Bacteria like Cutibacterium acnes, once called Propionibacterium acnes, live in the skin’s oil glands and trigger strong immune reactions that make things worse.
Inside the skin, four main processes team up to cause acne. Follicles overproduce skin cells that stick together, blocking pores. Oil glands make too much sebum, creating a perfect spot for bacteria to grow. The bacteria then release signals that spark inflammation. This inflammation feeds back into more cell buildup and oil production, making a vicious cycle.
Cutibacterium acnes is a key player. It prompts skin cells and immune cells to pump out pro-inflammatory chemicals like IL-1, IL-8, IL-12, and TNF-alpha. These chemicals call in neutrophils and other immune fighters, which release reactive oxygen species and damage the follicle wall. That spills bacteria, oil, and dead cells into deeper skin layers, forming painful nodules and pus-filled spots.
Several pathways drive this inflammation. The NF-kappaB pathway is central. It senses stress or bacteria and turns on genes for more inflammatory signals like IL-1beta, IL-6, IL-8, TNF-alpha, and COX-2. Cutibacterium acnes activates NF-kappaB through Toll-like receptor 2, or TLR2, on immune and skin cells. This TLR2/MyD88/NF-kappaB chain ramps up cytokines that swell the skin and worsen blockages.
IL-1 signaling pulls in neutrophils and keeps the fire burning. Leukotriene B4 adds to the damage by drawing more immune cells. Even oil from glands helps. Changes in sebum, like more squalene and less linoleic acid, create a pro-inflammatory environment that boosts bacterial growth and cytokine release.
The skin’s immune system gets involved too. Sebaceous glands make antimicrobial peptides and link to stress hormones, amplifying the response. Inflammasomes, groups of proteins in skin cells, also activate and release more IL-1beta when bacteria poke them.
This inflammation does not just react; it sustains acne. Inflammatory signals mess with skin cell growth and oil production, keeping pores clogged. Breaking these pathways, like blocking NF-kappaB or TLR2, can calm the skin and clear lesions.
Sources
https://www.anecochem.com/newsInfo-261.html
https://pmc.ncbi.nlm.nih.gov/articles/PMC12735603/
https://pmc.ncbi.nlm.nih.gov/articles/PMC12729757/
https://faseb.onlinelibrary.wiley.com/doi/full/10.1096/fj.202501944R
