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

Spleen cells from newborn to 2-day-old, but not 3-day-old or older, rats suppress the activity of cells from adult animals in xenogeneic local graft-versus-host (GVH) assay. The duration of neonatal suppressor cell activity can be significantly prolonged by treating newborn rats with exogenous prostaglandin E2 (PGE2), and the suppression was completely abolished by administration of PGE inhibitor indomethacin. The results thus demonstrate an involvement of PGE2 in the mechanism of action of neonatal suppressor cells and may explain some discrepancies concerning the nature of natural suppressor cells present in newborn animals.
 ...
PMID:The role of prostaglandin E in the natural suppressor activity of spleen cells from newborn rats. 297 33

Spleen cells from F344 male rats showed decreased DNA synthetic responsiveness [( 3H]thymidine incorporation) with age to the T cell mitogen phytohemagglutinin (PHA). Decreased proliferative responses were associated with decreased production of interleukin-2 (IL-2) and could be partially restored by providing exogenous IL-2. Responses of spleen cells from aged rats could also be enhanced by removal of Sephadex G-10 adherent cells. Furthermore, co-culture of adherent cell-containing spleen cells from aged rats with nonadherent spleen cells from young rats resulted in suppression of responses. Purified peritoneal exudate macrophages (PEM) from aged rats showed potent regulatory effects on PHA responses of young and old nonadherent spleen cells resulting in suppression above 2.5% macrophage/nonadherent spleen cell ratios. PEM from young rats enhanced the response of young T cells but failed to affect the response of aged T cells. T cell proliferation in the presence of prostaglandin (PGE1) showed age-dependent differences in regulation such that at 10(-6) to 10(-7) M young responses were enhanced and old responses were suppressed. These results suggest that decreased responsiveness of T cells to PHA with age is a complex phenomenon involving changes in both production of regulatory mediators by T cells (IL-2) and macrophages (PGE) as well as changes in T cell responsiveness to these signals.
 ...
PMID:Cellular immunosenescence in F344 rats: decline in responsiveness to phytohemagglutinin involves changes in both T cells and macrophages. 660 4

It has been suggested that the arteriolar vasodilatation and hyperdynamic circulation observed in rats with partial portal vein ligation (PPVL) is caused by increased splanchnic and systemic delivery of vasodilator substances. The aims of our study were to determine organ-specific generation of prostaglandin E(2) (PGE(2)) in rats with PPVL during the evolution of portal hypertension. Rats with PPVL and sham-operated (S) rats were studied in the first, third, fourth and 14th postoperative days. They were anesthetized and splenic pulp pressure and blood pressure were measured. Spleen, colon and lungs were removed and the splenic, pulmonary and mucosal colonic PGE(2) were determined. All PPVL rats developed sequential hemodynamic changes compatible with evolving portal hypertension. Splenic pulp pressure was higher in PPVL rats compared with S rats during all days of the study. Within the group of PPVL the splenic pulp pressure was higher in the first postoperative day and decreased in the ensuing days. No changes in splenic and colonic PGE(2) generation were noted during the study period. Pulmonary PGE(2) generation increased significantly in the first postoperative day in PPVL rats compared with S rats. However, similar increase was observed on the third postoperative day in S rats. PGE(2) probably has no role in splanchnic hemodynamic changes during evolution of portal hypertension. Pulmonary PGE(2) generation may increase as a response to increased portal pressure, or to abdominal surgery.
 ...
PMID:Longitudinal prostaglandin E(2) generation in various organs during evolution of experimental portal hypertension. 1240 32