Actinomyces and CCL11 Linked to Idiopathic Pulmonary Fibrosis in New Research
Recent research has identified a potential causal link between the bacterium actinomyces and idiopathic pulmonary fibrosis (IPF), with CCL11 acting as a key mediator in this relationship. The study, published in Clinical Respiratory Journal, utilized a two-step, two-sample Mendelian randomization approach to investigate the role of gut microbiota and circulating inflammatory proteins in the advancement of IPF.
"these data indicated that CCL11 was a critical moderator in the causal pathway from Actinomyces to IPF," the authors wrote.
The findings build upon existing evidence suggesting Actinomyces' involvement in various diseases. A study published last year implicated Actinomyces and other opportunistic bacteria in severe COVID-19. CCL11, the researchers noted, has also been associated with eosinophilic inflammatory diseases. One study found that inhibiting CCL11 release from T helper 2 cells "could control the transition from an acute inflammatory response to chronic fibrosis."
The investigators emphasized the need for further research to determine how these findings regarding Actinomyces and CCL11 might translate into clinical applications.
The study did acknowledge several limitations. The datasets primarily comprised individuals of European descent, potentially limiting the generalizability of the results. Additionally, the authors noted that some single nucleotide polymorphisms associated with exposure factors could be influenced by unmeasured variables. The analysis focused on 211 bacteria and 91 circulating inflammatory proteins, utilizing approximately 14,000 bacterial samples and cases, which the researchers conceded could introduce bias.
While the study pinpointed Actinomyces-CCL11 as a significant connection to IPF, the authors suggest that other mediating factors likely remain undiscovered.