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)

Cell-mediated immunity is clearly the critical host defense mechanism against human Coxiella burnetii infection (Q fever); the role of specific antibody is unclear. By using a mouse macrophage tumor cell line, J774, persistently infected with C. burnetii phase I organisms, in a standard 51Cr-release cytotoxicity assay, we explored the possibility that antibody-dependent cellular cytotoxicity may be immune mechanism in Q fever. After 16 h of incubation in the presence of immune sera from Q fever hepatitis or endocarditis patients, nonimmune human peripheral blood effector cells specifically lysed infected J774 target cells; no 51Cr release was seen in the presence of nonimmune sera or uninfected target cells. An effector/target ratio of at least 5:1 was required, and monocytes were more efficient effector cells than lymphocytes. Cytotoxicity was blocked by preincubation of effector cells with purified aggregated human immunoglobulin G, indicating the role of Fc receptor-bearing effector cells. Two nonphagocytic lymphoid tumor cell targets, passively coated with C. burnetii, did not induce substantial immune-specific cytolysis, suggesting that bystander lysis does not explain the observation of specific lysis. Although antibody-dependent cellular cytotoxicity may participate in primary defense, alternatively, it may facilitate the dissemination of C. burnetii or surreptitiously participate in granuloma formation.
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PMID:Antibody-dependent cellular cytotoxicity of Coxiella burnetii-infected J774 macrophage target cells. 669 Apr 2

The authors developed monoclonal antibodies to Coxiella burnetti, the agent of Q fever. The selected monoclonal antibody, Cox1D8, did not cross-react with other bacteria and was used for early detection of C burnetti in shell vial cell cultures and for staining C burnetii in paraffin embedded tissues. Formalin or Bouin fixation did not alter the reactivity of the antigen with the antibody. This monoclonal antibody could be useful in the pathologic diagnosis of Q fever hepatitis and endocarditis.
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PMID:Monoclonal antibodies to Coxiella burnetii for antigenic detection in cell cultures and in paraffin-embedded tissues. 813 88

We report about a 42-year-old farmer with leucocytosis, elevation of transaminases and liver cirrhosis as an underlying condition. The diagnosis of Q fever hepatitis was made through liver biopsy and serology. Under therapy with doxycycline, transaminases initially increased again; after switching to ciprofloxacin, the patient could be discharged 3 weeks after admission. Q fever is caused by Coxiella burnetii. The most frequent acute manifestation is a self-limiting flu-like illness. Chronic Q fever mostly presents as endocarditis. The diagnosis is made through histology ("doughnut" granulomas), PCR, serology (acute: anti-phase II antibodies, chronic: anti-phase I antibodies) and culture. Standard therapy is doxycycline.
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PMID:[A 42-year-old farmer with nonspecific leucocytosis and elevated transaminases. Acute septic reaction in Coxiella burnetii infection]. 1830 71