Staphylococcus aureus (S. aureus) is one of the most common pathogen causing
septic arthritis. To colonize the joints and establish
septic arthritis this bacterium needs to resist the host innate immune responses.
Lysozyme secreted by neutrophils and macrophages is an important defense
protein present in the joint synovial fluids. S. aureus is known to be resistant to
lysozyme due to its
peptidoglycan modification by O-acetylation of N-acetyl
muramic acid. In this study we have investigated the role of O-acetylated
peptidoglycan in
septic arthritis. Using mouse models for both local and hematogenous S. aureus
arthritis we compared the onset and progress of the disease induced by O-acetyl
transferase mutant and the parenteral wild type SA113 strain. The
disease progression was assessed by observing the clinical parameters including
body weight,
arthritis, and functionality of the affected limbs. Further X-ray and histopathological examinations were performed to monitor the
synovitis and bone damage. In local S. aureus
arthritis model, mice inoculated with the ΔoatA strain developed milder disease (in terms of knee swelling, motor and movement functionality) compared to mice inoculated with the wild type SA113 strain. X-ray and histopathological data revealed that ΔoatA infected mice knee joints had significantly lesser joint destruction, which was accompanied by reduced bacterial load in knee joints. Similarly, in hematogenous S. aureus
arthritis model, ΔoatA mutant strain induced significantly less severe clinical
septic arthritis compared to its parental strain, which is in accordance with radiological findings. Our data indicate that
peptidoglycan O-acetylation plays an important role in S. aureus mediated
septic arthritis.