- Setting the Stage for a Successful Launch Into the Microbiome Space
- The Skin Microbiome in Relation to the Clothing Microbiome
- Microbiome host interaction: Influence of FLG Loss-Of-Function Mutations in Host-Microbe Interactions During Atopic Skin Inflammation
- Developing Beneficial Bacteria as Topical Therapeutics to Treat Skin Diseases
- How Phage Capsids Can Be Engineered for Gene Therapy of the Microbiome
- Restoring Healthy Skin Ecology with Microbial Ensembles
- Biofilm Production & Inflammatory Skin Molecules Support the Growth & Persistence of Cutibacterium acnes in Acne Vulgaris
Biofilm Production & Inflammatory Skin Molecules Support the Growth & Persistence of Cutibacterium acnes in Acne Vulgaris
Enea Gino Di Domenico, San Gallicano IRCCS
The study (Biofilm Production and Inflammatory Skin Molecules Support the Growth and Persistence of Cutibacterium acnes in Acne Vulgaris) presented by Enea Di Domenico, researcher at the San Gallicano dermatological institute in Rome, showed that the microbiome at the level of inflammatory lesions (papules and pustules) of patients with severe acne shows a significant reduction in microbial diversity compared to that observed in non-inflammatory acne lesions and skin of healthy subjects. Furthermore, it was found that C. acnes, although present in abundance in the skin of healthy patients, undergoes hyperproliferation at the level of inflammatory lesions compared to non-inflammatory lesions and the skin of healthy controls. The study also highlights that clinical isolates of C. acnes are capable of forming highly structured biofilms, promoting lesion chronicization and antibiotic tolerance. Finally, the presence of IL-α and VEGF levels, significantly higher in the skin of patients with acne than in healthy subjects, has been shown to be a key factor in favoring the proliferation of C. acnes.
The skin of subjects with severe acne shows a chronic inflammatory condition characterized by an overproduction of various inflammatory molecules. In particular, the study demonstrated that IL-1α and VEGF are able to induce a significant increase in the growth of C. acnes isolates. These observations indicate that inflammatory cytokines can selectively promote the growth of C. acnes, inducing a dysbiotic state of the skin microbiota. Consequently, it is not the presence of C. acnes that contributes to the onset of acne but rather its overproliferation to the detriment of other commensal species. The molecular mechanism responsible for the growth response of C. acnes to inflammatory molecules remains to be defined, also considering that in eukaryotic cells, the transduction of cytokine signals follows specific pathways that are putatively absent in bacteria. Although more research is needed to elucidate these mechanisms, the study results suggest that specific molecules produced on the skin of people with acne may selectively promote the growth of biofilm-producing C. acnes by causing alteration of the skin microbiota, promoting greater persistence and tolerance to antimicrobials by this microorganism.
