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Results for “Immune dysfunction”

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At least 181 records · Page 10Linked to original sources
PubMed1986

Immune dysfunction in rabbits associated with chronic administration of enemas and rectal insemination.

NZ rabbits were treated with various combinations of enemas and intrarectal insemination (1 or 3 ml of semen a week) to investigate the effects of intestinal uptake and immunogenicity of seminal components and of an unrelated antigen, bovine serum albumin (BSA), given simultaneously. For 5 months the treatment was limited to enemas and/or semen, and total immunoglobulins and antisperm and antilymphocyte antibodies were determined. Then, without interruption of the treatments, the animals received two courses of three consecutive daily intrarectal administrations of BSA, and the humoral response was determined 7 days after each course of administration. Only 1 of 18 intrarectally inseminated animals responded with production of antisperm antibodies; none had antilymphocyte antibodies. Total immunoglobulins, however, were significantly increased in animals receiving enemas alone (p less than 0.02) or followed by insemination (p less than 0.05). The humoral response to BSA was significantly (p less than 0.01) enhanced by prior administration of enemas but was moderately reduced by simultaneous administration of semen, in a dose-related fashion.

Animals↗
PubMed1998

Endometriosis: abnormal endometrium and dysfunctional immune response.

This review highlights recent studies that illuminate the role of the immune system in endometriosis. The findings are discussed in the framework of a model which proposes that endometriosis reflects an immunological selection process. Endometrial cells, which are inherently resistant to apoptosis and immune-mediated elimination, acquire the capacity to utilize the products of an activated immune system to establish ectopic foci of disease. Cyclical inflammatory/immune cell stimulation that fails to eliminate ectopic endometrial implants results in progressive immunological derangement and associated pathophysiological changes which are characteristic of the disease.

Endometriosis↗
PubMed1989

Immune dysfunction in primary biliary cirrhosis. II. Increased production of prostaglandin E.

In a previous study we observed that after in vitro treatment with indomethacin, lymphocyte response to phytohaemagglutinin (PHA) in primary biliary cirrhosis (PBC) patients was higher than that of controls. We know that indomethacin also inhibits prostanoid production, and thus in the present work we directly measured prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) production by mononuclear cells and monocytes from 12 PBC patients, 11 control subjects, and three control disease patients (alcoholic cirrhosis, AC). PHA-stimulated enriched monocytes from PBC patients produced approximately threefold more PGE2 (after 48 h of culture) than did normal and AC monocytes (P less than 0.05). TXB2 production was similar in all groups studied. We also made cultures in which PBC-purified lymphocytes proliferated better than PBC mononuclear cells (i.e. lymphocytes plus monocytes). Thus, a monocyte population producing PGE2 could be responsible, at least in part, for the hyporesponsiveness to PHA observed in PBC patients.

Humans↗