Etiology & Pathophysiology Emotional stress influences the course of acne. Cutaneous neurogenic factors including neuropeptides, neuropeptide- degrading enzymes and neurotrophic factors, are associated with inflammation in the pathogenesis of acne. An increase in the number of mast cells around the sebaceous glands is also a factor. Substance P (SP)-immunoreactive nerve fibres are close to the sebaceous glands. SP, a neuropeptide, stimulates lipogenesis of the sebaceous glands, which may be followed by proliferation of Propionibacterium acnes (a gram-positive anaerobic bacillus rod). This paves the way for inflammatory reactions via the mast cells. Although Acne vulgaris is not life- threatening, it is very much a condition with serious psychological effects such as morbidity, decreased self- esteem, depression, and social withdrawal. In acne vulgaris abnormal keratinisation , - hormonal function , - bacterial growth , and i mmune hypersensitivity are involved. This is common during puberty when sebaceous glands are particularly active in pilosebaceous follicles of the head and chest. Over-production of sebum is stimulated by androgens and this increased production is associated with plugged follicle pores, which may become inflamed and develop into inflammatory acne. This inflammatory acne may be a direct response to the follicular inhabitant Propionibacterium acnes , which is a member of normal cutaneous flora. Stress stimulates the corticotropin-releasing hormone (CRH) system. Receptors of corticotropin-releasing factor (CRF) are present in human skin, as are mast cells. Stress-related crosstalk between mast cells, neurons and keratinocytes plays a significant role in all dermatological pathologies. CRH is capable to induce lipid synthesis, steroidogenesis and interact with testosterone and growth hormone. An overly- vigorous immune response to Propionibacterium acnes (P. acnes) is a fundamental problem in acne vulgaris. These bacteria secrete polypeptides, like extracellular enzymes, such as proteases, hyaluronidases and neuroaminidases, which can involve epithelium permeabilization and inflammatory infiltration. P. acnes produces both chemotactic- and pro- inflammatory cytokine inducing factors. Early-infiltrated lesions consist of polymorphonuclear cells. These cells attract T-helper cells of the CD4 phenotype, also known as T4 cells. Antibodies, specifically-aimed at P. acnes antigenic determinants, are IgG and IgA immunoglobulins. Since the Toll like receptor TLR2 plays a role in the aetiology of acne, its stimulation by P. acnes gives rise to the production of Interleukin-8 (IL-8)- and Interleukin-12 (IL-12) pro-inflammatory cytokines.

TARGETS Propionibacterium acnes bacteria Mast cells Corticotropin-releasing factor (CRF) Cytokines IL-8 and IL-12 Type1 5-α-reductase 5-Lipoxygenase Tyrosinase Reactive oxygen species (ROS)

COUNTERACTIONS Anti-bacterial Degranulation Inhibition Inhibition Inhibition Inhibition Inhibition Inhibition

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GOD’S HEAVENLY CHALLENGE… ACNE VULGARIS

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