ArticleInfection and immunity1993
Bacterial cell wall polymers (peptidoglycan-polysaccharide) cause reactivation of arthritis.
Article in Infection and immunity, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 29 citations in OpenAlex.
- Peptidoglycan in osteoarthritis synovial tissue is associated with joint inflammation.Arthritis research & therapy · 2024Article
- Article
- Helicobacter pylori expresses an autolytic enzyme: gene identification, cloning, and theoretical protein structure.Journal of bacteriology · 2002Article
- The morphological transition of Helicobacter pylori cells from spiral to coccoid is preceded by a substantial modification of the cell wall.Journal of bacteriology · 1999Article
- Detection of muramic acid in a carbohydrate fraction of human spleen.Infection and immunity · 1995Article
- PPD and hsp65 induced monoarthritis initiates spontaneous recurrent flares in Lewis rats.Annals of the rheumatic diseases · 1995Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Intraperitoneal (i.p.) injection of peptidoglycan-polysaccharide derived from group A streptococci (PG-APS) causes chronic arthritis with spontaneous remissions and exacerbations. We hypothesized that, following i.p. injection, PG-APS released from hepatic stores mediated spontaneous recurrences of arthritis. We tested whether transplanted livers with large amounts of PG-APS were able to reactivate quiescent arthritis. Saline-loaded (group 1) or PG-APS-loaded (group 2) livers were transplanted into rats which had been injected intra-articularly 10 days earlier with PG-APS in one joint and saline in the other. A comparison was made with the arthritis that occurred in rats injected i.p. with PG-APS which did not receive transplants (group 3). Arthritis was monitored by serial measurement of joint diameters. Transplantation of saline-loaded livers (group 1) caused no reactivation of arthritis. However, transplantation of PG-APS-loaded livers (group 2) reactivated arthritis (P < 0.0001). Injection of PG-APS i.p. (group 3) induced the most-severe arthritis. PG-APS levels in plasma decreased with time, and PG-APS accumulated in the spleen in groups 2 and 3. Plasma and hepatic levels of PG-APS in rats injected i.p. with PG-APS were greater than levels in rats transplanted with PG-APS-loaded livers, which in turn were greater than levels in rats with saline-loaded livers. Plasma tumor necrosis factor did not correlate with recurrence of arthritis. Transplantation with PG-APS-loaded livers induced reactivation of arthritis in preinjured joints. The extent of arthritis was proportional to hepatic PG-APS content. Reactivation of arthritis may be mediated by slow release of liver-sequestered PG-APS or cytokines (not tumor necrosis factor) released by the liver.
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Registered trials
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