Abstract
Aim
Cutibacterium acnes is involved in chronic/low-grade pathologies such as prosthetic joint infection (PJI) or sarcoidosis. During these diseases, granulomatous structures are frequently observed. In this study, we induced a physiological granulomatous reaction in response to different well-characterized clinical C. acnes isolates in order to investigate the cellular process during the granulomatous formation.
Method
An acne C. acnes ATCC6919 isolate (clonal complex (CC) 18, phylotype IA1), a PJI C. acnes BL clinical isolate (CC36, phylotype IB) and a sarcoidosis C. acnes S8 strain (CC28, phylotype IA2) were included and co-culture with PBMC. Cellular aggregation was followed daily using light microscopy. At various time points of incubation (day 3 and day 7), granuloma structures were processed for microscopic observation, colony forming unit enumeration after Triton ×100 lysis to release the internalized bacteria (bacterial load within the granulomas), as well as for flow cytometric analysis (detection of CD4, CD8 and NK lymphocytes).
Results
All C. acnes isolates generated granulomatous structures in our experimental conditions. The bacterial burden was better controlled by granulomas induced by sarcoidosis C. acnes isolate. PJI C. acnes isolate, belonging to CC36, promoted the recruitment of CD8+ lymphocytes inside the granuloma. At the opposite, acne and sarcoidosis C. acnes isolates, belonging, respectively, to phylotype IA1/CC18 and phylotype IA2/CC28 generated a higher number of granuloma and promoted the recruitment of CD4+ lymphocytes inside the granuloma.
Conclusions
Our results provide new arguments supporting the role of C. acnes in the development of infections and new explanations concerning the mechanisms underlying PJI due to C. acnes.
This model appears to be a possible alternative assay to animal models for studying the immune response to C. acnes infection.
