Staphylococcus aureus (S. aureus) is a Gram-positive bacterium that causes a wide cluster of human illnesses. It is commonly found in the anterior nares and on the skin with no evident damage. However, after entering the circulatory system, it can disperse and colonize basically all organs, bringing about fatal illnesses with up to 50% death rate. Inside tissues, S. aureus is quickly perceived by host pattern recognition receptors, and polymorphonuclear cells where powerful antibacterial functions are enlisted. S. aureus is notorious in resisting the antimicrobial actions of polymorphonuclear cells, requiring extra immune cells to control the disease. For example, Methicillin-resistant Staphylococcus aureus (MRSA) is highly resistant to treatment with antibiotics resulting in high mortality.
Macrophages are proficient phagocytes that have antibacterial action, and they encourage the enrolment of immune cells, organize adaptive immunity, and advance the goals of inﬂammation and wound healing. For the most part, they are grouped into two functional states; M1 macrophages which work against microbial action and M2 macrophages which are involved in immune regulation and wound mending. S. aureus can subvert macrophage actions by a few mechanisms, and an appealing procedure to diminish the disease intensity is to regulate macrophages in a way that would improve bacterial susceptibility to killing and advance the goal of inﬂammation resolution. Probiotics are microorganisms that can be utilized to beneﬁt the host, however, the exact mechanism by which probiotics work remain for the most part obscure.
To this end, Loyola University Chicago scientists Dr. Wonbeom Paik, Dr. Francis Alonzo III and Professor Katherine Knight conducted a study to see if exopolysaccharide could protect from systemic infection induced by S. aureus. Their research work is published in journal Infection and Immunity.
The research team observed that exopolysaccharide-treated mice infected with a strain of S. aureus didn’t adversely lose weight and also showed improved survival rates compared to phosphate buffered saline-treated infected control mice. Remarkably, even a single dose of exopolysaccharide day one before infection was sufficient to prevent weight loss. It was also noticed that the number of S. aureus CFU was reduced in the spleen and the liver 8-fold and 3-fold, respectively.
Furthermore, when macrophages was isolated from the peritoneal cavity of exopolysaccharide-treated mice, and incubated with serum-opsonized S. aureus, it was observed that by the 5th hour, the numbers of S. aureus CFU were significantly lower in cultures of cells from exopolysaccharide -treated mice, indicating that cells from these mice restrict growth of internalized S. aureus more than cells from control mice. It was also discovered that exopolysaccharide-induced macrophages inhibit S. aureus growth through reactive oxygen species, like that of proinﬂammatory M1 macrophages.
In a nut shell the study by Loyola University Chicago researchers successfully showed that B. subtilis derived exopolysaccharide shields mice from fatal S. aureus disease and that this protection is likely because of the decrease in bacterial burden and constraint of inﬂammation by macrophages that both stifle S. aureus replication through reactive oxygen species and limit T cell activation. They also demonstrated that this bolster of antimicrobial defenses and limitation of inflammation permits exopolysaccharide to counteract parts of S. aureus pathogenesis to improve infection outcomes, and that more research on the auxiliary and practical properties of exopolysaccharide is needed to fully understand its capacity as an immunomodulatory particle. This study opens the door to conduct more experiments to see whether probiotic products of B. subtilis are able to destroy S. aureus infections in humans and reduce MRSA infection rates in hospitals.
Palk. W., Alonzo, F., III., Knight, K., L., Probiotic Exopolysaccharide Protects against Systematic Staphylococcus aureus Infection, Inducing Dual-Functioning Macrophages That Restrict Bacterial Growth and Limit Inflammation InfectImmun 87:e00791-18.https://doi.org/10.1128/IAI.00791-18Go To InfectImmun