# Insights into microbial dysbiosis and Cutibacterium acnes CAMP factor interactions in acne vulgaris

## TL;DR

This study investigates how changes in skin microbes and specific factors from Cutibacterium acnes contribute to acne, offering new insights into potential treatments.

## Contribution

The study identifies CAMP2 and CAMP5 as key inflammatory factors and shows how anti-IL-8 treatment can reduce acne-related inflammation.

## Key findings

- Microbial dysbiosis, especially in comedones, is significantly linked to acne development.
- CAMP2 and CAMP5 from Cutibacterium acnes show high inflammatory and haemolytic activity in keratinocytes.
- Topical anti-IL-8 treatment reduces inflammation and CAMP expression in a murine model.

## Abstract

Acne vulgaris is a common skin condition marked by the formation of comedones, papules, pustules and nodules, with its underlying causes still not fully understood. This study explores the impact of microbial dysbiosis and virulence factors on acne development. Through high-throughput 16S rRNA sequencing, we identified significant disruptions in the skin microbiome, particularly in comedones. Key virulence factors of Cutibacterium acnes, known as Christie–Atkins–Munch-Peterson (CAMP) factors, were assessed using both in vitro and in vivo models. Among these, CAMP2 and CAMP5 demonstrated the highest inflammatory and haemolytic activities in keratinocytes. Topical anti-IL-8 treatment in a murine model effectively reduced inflammation and suppressed CAMP expression. Structural analysis of CAMP3 uncovered distinct pathogenic features that, alongside CAMP5, were found to aggravate acne-like inflammation and sebaceous gland atrophy. These findings advance our understanding of the interplay between microbial dysbiosis and CAMP factors in acne pathogenesis, offering potential avenues for therapeutic intervention.