The clostridia are a group of anaerobic spore-forming bacteria that are ubiquitously found in the environment and can cause significant disease in both humans and animals. The diseases caused by clostridial species are toxin mediated and can be fatal. The transmission and survival of these bacteria is facilitated through spores, which are metabolically inactive bacterial cell types that resist environmental stresses such as oxygen, antibiotic exposure, and UV radiation.
While spores are necessary for disease transmission and bacterial survival, their role in virulence has not been intensively studied. Previous work has shown that spores from Bacillus anthracis can bind the potent serine protease plasminogen (PLG) to their surface, leading to the degradation of C3b, a key immune complement protein, thus indicating that spores may play an active role during disease. Other bacterial species such as Staphylococcus aureus and Yersinia pestis are also capable of binding PLG to their surface. Since B. anthracis is closely related to members of the genus Clostridium, investigating if clostridial spores share this characteristic may provide information on their role during disease.
In this study, we examined the ability of spores and vegetative cells of Clostridium perfringens and Paeniclostridium (previously Clostridium) sordellii to bind human PLG to their surface via Western blot analysis and super resolution microscopy. We found that the spores, but not the vegetative cells, of C. perfringens and P. sordellii bound human PLG to their surface. Additionally, using cytokine arrays and an ELISA we found that plasmin, the active form of PLG, when bound to C. perfringens spores, appeared to have immunomodulatory effects on bone marrow derived macrophages. This study therefore provides evidence that clostridial spores may play a role in pathogenesis beyond disease initiation.