section 3:Acne is a common skin disease affecting up to 80% of adolescents and young adults, and is characterized by the formation of comedones, papules, pustules, and nodules on the face, neck, chest, and back. The pathogenesis of acne is complex and involves several molecular mechanisms, including increased sebum production, altered keratinization, bacterial colonization, and inflammation.The main molecular players in acne pathogenesis are androgens, sebum, Propionibacterium acnes, toll-like receptor (TLR) signaling, and pro-inflammatory cytokines. Androgens, such as testosterone, stimulate the sebaceous glands to produce excess sebum, which then accumulates in hair follicles and contributes to comedone formation. The overproduction of sebum also alters the skin microenvironment and promotes the growth of P. acnes, a commensal bacterium that can become pathogenic and exacerbate inflammation.acnes stimulates the TLR2 and TLR4 receptors on immune cells, leading to the activation of inflammatory pathways and the release of pro-inflammatory cytokines, such as interleukin-1β (IL-1β), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α). These cytokines recruit and activate immune cells, such as neutrophils and monocytes, which then contribute to the formation of papules, pustules, and nodules through the release of enzymes and reactive oxygen species.Additionally, alterations in keratinocyte differentiation and desquamation have been observed in acne. Specifically, increased expression of keratin 17 (K17) and decreased expression of involucrin (IVL) have been reported in acne lesions, indicating a disruption in normal epidermal differentiation.In summary, acne is a complex skin disease that involves multiple molecular mechanisms, including androgen-mediated sebum production, P. acnes colonization, TLR signaling, cytokine release, and alterations in keratinocyte differentiation. Understanding the molecular pathophysiology of acne is crucial for the development of effective treatments and prevention strategies. Question 1.[Provide a self-generated graphical abstract summarising one method of treating acne. Ensure that you clearly demonstrate how the therapeutic intervention alters the behavior of the disease process you have described in section 3.
section 3:Acne is a common skin disease affecting up to 80% of adolescents and young adults, and is characterized by the formation of comedones, papules, pustules, and nodules on the face, neck, chest, and back. The pathogenesis of acne is complex and involves several molecular mechanisms, including increased sebum production, altered keratinization, bacterial colonization, and inflammation.The main molecular players in acne pathogenesis are androgens, sebum, Propionibacterium acnes, toll-like receptor (TLR) signaling, and pro-inflammatory cytokines. Androgens, such as testosterone, stimulate the sebaceous glands to produce excess sebum, which then accumulates in hair follicles and contributes to comedone formation. The overproduction of sebum also alters the skin microenvironment and promotes the growth of P. acnes, a commensal bacterium that can become pathogenic and exacerbate inflammation.acnes stimulates the TLR2 and TLR4 receptors on immune cells, leading to the activation of inflammatory pathways and the release of pro-inflammatory cytokines, such as interleukin-1β (IL-1β), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α). These cytokines recruit and activate immune cells, such as neutrophils and monocytes, which then contribute to the formation of papules, pustules, and nodules through the release of enzymes and reactive oxygen species.Additionally, alterations in keratinocyte differentiation and desquamation have been observed in acne. Specifically, increased expression of keratin 17 (K17) and decreased expression of involucrin (IVL) have been reported in acne lesions, indicating a disruption in normal epidermal differentiation.In summary, acne is a complex skin disease that involves multiple molecular mechanisms, including androgen-mediated sebum production, P. acnes colonization, TLR signaling, cytokine release, and alterations in keratinocyte differentiation. Understanding the molecular pathophysiology of acne is crucial for the development of effective treatments and prevention strategies.
Question 1.[Provide a self-generated graphical abstract summarising one method of treating acne. Ensure that you clearly demonstrate how the therapeutic intervention alters the behavior of the disease process you have described in section 3.
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