Intradermal injection of Propionibacterium acnes: a model of inflammation relevant to acne.

The intradermal injection of 140 micrograms of Propionibacterium acnes (CN 6134) into the ears of female Sprague-Dawley rats produced a chronic inflammation with formation of acneiform lesions. Inflammation was characterized by more than a doubling of ear thickness at 24 h and a peak of 3-4 times control levels at day 21. At 42 days post injection ears were still 3 times normal thickness. Histologically there was early polymorph accumulation giving way to macrophages and lymphocytes by day 7. Pilosebaceous follicles overlying the inflamed area lost their sebaceous glands and became hyperplastic cords of cells that grew down and encapsulated inflammatory loci. By day 9 many of these follicles had become secondary comedones. Three isolates of P. acnes from inflammatory acne lesions and 4 of 5 isolates from non-acne patients produced results similar to that of the strain CN 6134. In these cases the number of histologically evident secondary comedones was correlated with ear thickness. In contrast, samples of Streptococcus lactis, Escherichia coli B, and Staphylococcus epidermidis failed to produce this combination of chronic inflammation and high lesion count. Benzoyl peroxide, tetracycline, erythromycin, phenidone, naproxen, and cis and trans retinoic acid were inactive as inhibitors of P. acnes CN 6134-induced ear thickening. The corticosteroid fluocinolone acetonide produced dramatic suppression of inflammation, but upon cessation of treatment the ears returned to inflamed levels. The specificity for P. acnes, the formation of acneiform lesions, and the recalcitrance of the inflammation suggest our model is indeed relevant to acne.