Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats injected with peptidoglycan-polysaccharide polymers derived from group A streptococcal cell walls (PG-APS) develop a chronic, remittant, erosive synovitis. Spleen cells from injected rats failed to proliferate when stimulated in vitro by Con A or PHA, unless nylon wool adherent cells were first removed. The suppression could also be reversed by removing phagocytic cells which had ingested carbonyl iron. Cells from control rats were suppressed in vitro by co-culture with unfractionated or nylon wool-adherent cells from PG-APS injected rats, and the suppressor activity was still expressed after exposure of the suppressor cells to 3,000 rad of irradiation. Addition of catalase and indomethacin to cultures only partially reversed the suppression. T lymphocytes from rats given a single arthropathic dose of PG-APS remained suppressed for at least 86 days after injection. Cells from rats given a low, non-arthropathic dose of PG-APS did not become suppressed. Cells from the Buffalo rat, which is resistant to development of PG-APS-induced chronic arthritis, showed less suppression than cells from the susceptible Lewis and Sprague-Dawley rat strains.
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PMID:Immunosuppressive macrophages induced by arthropathic peptidoglycan-polysaccharide polymers from bacterial cell walls. 306 53

We investigate whether the previously shown contact system activation plays a pathogenetic role in a rat model of acute inflammation induced by peptidoglycan-polysaccharide (PG-APS) using a new specific plasma kallikrein inhibitor, Bz-Pro-Phe-boroArg-OH (P8720). Group I (control) received neither PG-APS nor inhibitor. Group II (disease-treated) received PG-APS intraperitoneally (IP) and P8720 orally. Group III (disease-untreated) received PG-APS IP. Anemia was evident at 49 h in group III but was not present (P < 0.01) in groups I and II. Spleen weight was significantly decreased in group II compared to group III. Acute arthritis progressively developed in group III from 27 to 49 h, but P8720 decreased the joint swelling in group II by 61% (P < 0.0005). We observed a significant fall in prekallikrein and factor XI (P < 0.01) in groups II and III but not in group I. The decrease in the functional levels of high molecular weight kininogen (P < 0.05) observed in group III were prevented by P8720 in group II. The changes in T-kininogen and alpha 1-inhibitor 3 acute-phase proteins were partially prevented by P8720. We conclude that the inflammatory reactions leading to arthritis and anemia, as well as the acute-phase reaction, are due in part to contact activation, and that specific kallikrein inhibitors may have therapeutic potential.
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PMID:Inhibition of plasma kallikrein prevents peptidoglycan-induced arthritis in the Lewis rat. 789 18