PubMed · 15010635
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Larry E Millikan. Acne.. https://doi.org/10.1111/j.1540-9740.2004.03137.x
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A major consequence of microbial infection is the tissue injury that results from the host inflammatory response. In acne, inflammation is due in part to the ability of Propionibacterium acnes to activate TLR2. Because all-trans retinoic acid (ATRA) decreases inflammation in acne, we investigated whether it regulates TLR2 expression and function. Treatment of primary human monocytes with ATRA led to the down-regulation of TLR2 as well as its coreceptor CD14, but not TLR1 or TLR4. The ability of a TLR2/1 ligand to trigger monocyte cytokine release was inhibited by pre- and cotreatment with ATRA; however, TLR4 activation was affected by cotreatment only. ATRA also down-regulated monocyte cytokine induction by P. acnes. These data indicate that ATRA exerts an anti-inflammatory effect on monocytes via two pathways, one specifically affecting TLR2/1 and CD14 expression and one independent of TLR expression. Agents that target TLR expression and function represent a novel strategy to treat inflammation in humans.
New research has refined our understanding of the immunopathophysiology of acne. Various immune factors, including both innate and adaptive immune responses, have been implicated in the pathophysiology of inflammatory acne. Topical retinoids such as tretinoin, adapalene, and tazarotene, exhibit immunomodulatory effects that may help to explain their efficacy in the resolution of inflammatory lesions.
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