How is pathophysiology of acne vulgaris?

• Sebaceous gland (hyperseborrhea) • Keratinocytes of the follicle (Follicular differentiation -> Keratinization) • Bacteria: Cutibacterium acnes, Staphylococcus epidermidis • Microbiome • Innate immunity (1st line defense) • Genetic predisposition Cutibacterium is an inhabitant of normal human skin and sebaceous follicles, density of colonization increases at puberty and associates w/inflammatory lesions, they modulate expression of immune markers, there is diversity in types predominant ones are IA1, CC18, A1