Abstract | OBJECTIVE: Permanent reduction in joint function is a severe postinfectious complication in patients with Staphylococcus aureus septic arthritis. We undertook this study to determine whether this reduction in joint function might be caused by persistent joint inflammation after the adequate eradication of bacteria by antibiotics. METHODS: RESULTS: CONCLUSION:
Antibiotic-killed S aureus induced and maintained joint inflammation mediated through TLR-2, TNFRI, and RAGE. The cross-talk between neutrophils and monocytes is responsible for this type of arthritis. Anti-TNF therapy might be used as a novel strategy, in combination with antibiotics, to treat staphylococcal septic arthritis.
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Authors | Abukar Ali, Xuefeng Zhu, Jakub Kwiecinski, Inger Gjertsson, Catharina Lindholm, Yoichiro Iwakura, Xiaoyang Wang, Nils Lycke, Elisabet Josefsson, Rille Pullerits, Tao Jin |
Journal | Arthritis & rheumatology (Hoboken, N.J.)
(Arthritis Rheumatol)
Vol. 67
Issue 1
Pg. 107-16
(Jan 2015)
ISSN: 2326-5205 [Electronic] United States |
PMID | 25302691
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2015 by the American College of Rheumatology. |
Chemical References |
- Anti-Bacterial Agents
- Receptor for Advanced Glycation End Products
- Receptors, Immunologic
- Receptors, Tumor Necrosis Factor, Type I
- Tlr2 protein, mouse
- Tnfrsf1a protein, mouse
- Toll-Like Receptor 2
- Cloxacillin
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Topics |
- Animals
- Anti-Bacterial Agents
(pharmacology)
- Arthritis, Experimental
(metabolism, microbiology, pathology)
- Arthritis, Infectious
(metabolism, microbiology, pathology)
- Cell Communication
(physiology)
- Cloxacillin
(pharmacology)
- Disease Models, Animal
- Female
- Mice
- Mice, Inbred BALB C
- Mice, Inbred C57BL
- Mice, Knockout
- Monocytes
(pathology)
- Neutrophils
(pathology)
- Receptor for Advanced Glycation End Products
- Receptors, Immunologic
(deficiency, genetics, metabolism)
- Receptors, Tumor Necrosis Factor, Type I
(deficiency, genetics, metabolism)
- Severity of Illness Index
- Staphylococcus aureus
(drug effects)
- Toll-Like Receptor 2
(deficiency, genetics, metabolism)
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