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Impact of cell wall peptidoglycan O-acetylation on the pathogenesis of Staphylococcus aureus in septic arthritis.

Journal article
Authors Gaurav Baranwal
Majd Mohammad
Anders Jarneborn
Bommana Raghunath Reddy
Archana Golla
Sumana Chakravarty
Lalitha Biswas
Friedrich Götz
Sahadev Shankarappa
Tao Jin
Raja Biswas
Published in International journal of medical microbiology : IJMM
Volume 307
Issue 7
Pages 388-397
ISSN 1618-0607
Publication year 2017
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 388-397
Language en
Keywords S. aureus, O-Acetylation, Peptidoglycan, Lysozyme, Septic arthritis
Subject categories Rheumatology and Autoimmunity, Infectious Medicine, Microbiology


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.

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