ArticleInflammation2011
Possible protective role of chloramphenicol in TSST-1 and coagulase-positive Staphylococcus aureus-induced septic arthritis with altered levels of inflammatory mediators.
Article in Inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- A Review: Antimicrobial Therapy for Human Pythiosis.Antibiotics (Basel, Switzerland) · 2022Review
- Article
- Azithromycin in combination with riboflavin decreases the severity of Staphylococcus aureus infection induced septic arthritis by modulating the production of free radicals and endogenous cytokines.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013Article
- Effects of Low-Level Laser Therapy, 660 nm, in Experimental Septic Arthritis.ISRN rheumatology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chloramphenicol is mostly used against coagulase-negative Staphylococcus aureus, and its protective role against coagulase-positive S. aureus is not well studied. In our study, arthritis was induced in mice by S. aureus (Apollo Gleneagles 33 (AG-33) or American Type Culture Collection 25923 (ATCC-25923)) infection. Chloramphenicol was administered after 2 h of infection. Mice were killed at 1, 3, 5 days post-infection. Mice inoculated with pathogenic Staphylococci (AG-33) expressing coagulase and Toxic shock syndrome toxin-1 (TSST-1), displayed severe arthritis with enhanced bacterial burden in the spleen, cytokine production in serum and synovial tissue, neutrophil recruitment, and cyclooxegenase-2 expression in synovial tissue compared with ATCC-25923-infected groups. Severity of arthritis was regulated by chloramphenicol treatment. Our study suggests that alteration in the inflammatory cytokine levels and pronounced production of cyclooxygenase-2 play important roles in progression of arthritis which is regulated by application of chloramphenicol.
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Registered trials
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