Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immune protection from endocarditis caused by Streptococcus defectivus was examined by using a rabbit model. Previously we had demonstrated that immunization with nutritionally variant streptococci (NVS, now referred to as Streptococcus, species defectivus and adjacens) protected rabbits against endocarditis when they were challenged with the homologous strain. However, when high-titer immune globulin was transferred to nonimmunized rabbits, no protection was achieved. In the present study, immunosuppressive treatments were given to previously immunized rabbits, and alterations in the level of protection were determined by using the rabbit endocarditis model. Control-immunized rabbits as well as immunized rabbits receiving cyclosporin A or methylprednisolone treatments were protected from S. defectivus endocarditis at levels between 50% and 67%. Rabbits in each of these groups cleared S. defectivus organisms from the circulation by 3 hours after infection. Nitrogen mustard-treated rabbits (immunized or nonimmunized), however, were unable to clear S. defectivus organisms as efficiently (almost 100 times as many organisms in the blood when compared with other groups) by 3 hours, and all were susceptible to endocarditis. These data suggest that circulating phagocytes such as monocytes and granulocytes function to a certain extent in protection against S. defectivus endocarditis. Moreover, when neutrophils were transfused into granulocytopenic and monocytopenic rabbits, efficient clearance was prolonged, indicating that polymorphonuclear leukocytes were involved in the later (greater than 1 hour after infection) phase of protection.
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PMID:Evaluation of the immune response in protection against experimental Streptococcus defectivus endocarditis. 201 95

Intravegetation host inflammatory cell function may play a role in the more salutary clinical outcomes in human right- vs. left-sided endocarditis. To study this in vivo, 90 rabbits with tricuspid Pseudomonas aeruginosa endocarditis received either no therapy (controls), nitrogen mustard (HN2) to induce combined granulocytopenia + monocytopenia, etoposide (VP-16-213) to induce selective monocytopenia, or dexamethasone. Intravegetation inflammatory cell influxes were scored on a semiquantitative histopathologic scale. In VP-16-213 and dexamethasone recipients and tricuspid endocarditis controls, gradual decreases in mean intravegetation bacterial densities were observed over a 13-day infection period; in contrast, HN2 treatment was associated with a significant increase in intravegetation bacterial densities by day 13 of infection (p less than 0.001 vs. other tricuspid endocarditis groups). Histopathologically, vegetations from untreated controls and dexamethasone recipients showed granulocyte influxes during infection, while HN2 treatment resulted in predominantly granulocyte depletion within infected tricuspid vegetations; VP-16-213 caused mononuclear cell depletion at this site. This study supports the concept that the granulocyte plays a critical role in modulating spontaneous endocardial clearances of bacteria in experimental tricuspid endocarditis.
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PMID:Pathogenic effects of monocytopenia, granulocytopenia and dexamethasone on the course of experimental Pseudomonas aeruginosa endocarditis in rabbits. 250 46