Analytical and quantitative cytopathology and histopathology · 2014
Toll-like receptor 2 and P. acnes: do they trigger initial acne vulgaris lesions?
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Bakry Ola Ahmed, Samaka Rehab Monir, Sebika Hend, Seleit Iman
Аннотация
OBJECTIVE: To elucidate the role of toll-like receptor 2 (TLR2) in the pathogenesis of acne vulgaris through its immunohistochemical localization in inflammatory and noninflammatory lesions of this disease entity.
STUDY DESIGN: Using standard immunohistochemical techniques, we examined 30 acne cases (involved and noninvolved skin) and the normal skin biopsies of 30 sex- and age-matched, healthy subjects representing the control group.
RESULTS: All examined cases showed positive TLR2 expression in epidermis, pilosebaceous units and dermal inflammatory infiltrate. There were statistically significant differences between acne-involved skin and normal skin and between acne-involved and noninvolved skin regarding TLR2 expression intensity in pilosebaceous units (p < 0.001 for both) and dermal inflammatory infiltrate (p < 0.001 for both). Intense TLR2 expression was in favor of inflammatory acne lesions in pilosebaceous units (p = 0.03) and dermal inflammatory infiltrate (p < 0.05). Intense TLR2 expression was also in favor of severe acne lesions in pilosebaceous units (p = 0.0002) and dermal inflammatory infiltrate (p = 0.001).
CONCLUSION: TLR2 is involved in the pathogenesis of inflammatory and noninflammatory acne lesions. This occurs through Propionibacterium acnes-mediated activation with the resultant release of inflammatory cytokines.
STUDY DESIGN: Using standard immunohistochemical techniques, we examined 30 acne cases (involved and noninvolved skin) and the normal skin biopsies of 30 sex- and age-matched, healthy subjects representing the control group.
RESULTS: All examined cases showed positive TLR2 expression in epidermis, pilosebaceous units and dermal inflammatory infiltrate. There were statistically significant differences between acne-involved skin and normal skin and between acne-involved and noninvolved skin regarding TLR2 expression intensity in pilosebaceous units (p < 0.001 for both) and dermal inflammatory infiltrate (p < 0.001 for both). Intense TLR2 expression was in favor of inflammatory acne lesions in pilosebaceous units (p = 0.03) and dermal inflammatory infiltrate (p < 0.05). Intense TLR2 expression was also in favor of severe acne lesions in pilosebaceous units (p = 0.0002) and dermal inflammatory infiltrate (p = 0.001).
CONCLUSION: TLR2 is involved in the pathogenesis of inflammatory and noninflammatory acne lesions. This occurs through Propionibacterium acnes-mediated activation with the resultant release of inflammatory cytokines.