ArticleMediators of inflammation1995
Defective production of interferon-gamma and tumour necrosis factor-alpha by AIDS mononuclear cells after in vitro exposure to Rhodococcus equi.
Article in Mediators of inflammation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Rhodoccocus Equi Pneumonia and Paradoxical Immune Reconstitution Inflammatory Syndrome in a Patient with Acquired Immune Deficiency Syndrome (AIDS).The American journal of case reports · 2017Article
- Disseminated Rhodococcus equi infection in HIV infection despite highly active antiretroviral therapy.BMC infectious diseases · 2011Article
- Rhodococcus equi and Arcanobacterium haemolyticum: two "coryneform" bacteria increasingly recognized as agents of human infection.Emerging infectious diseasesReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The production of interferon-gamma and tumour necrosis factor-alpha was evaluated in the peripheral blood mononuclear cells (PBMCs) from healthy donors and AIDS patients after Rhodococcus equi infection in vitro. PBMCs from healthy donors secreted elevated levels of IFN-gamma and TNF-alpha when challenged in vitro with killed R. equi, whereas the release of both cytokines was impaired in supernatant cultures from AIDS patients. We conclude that the failure of IFN-gamma generation in AIDS patients in response to R. equi is not antigen-specific but it may reflect the global impairment of T-cell function. In such patients, however, the infection with R. equi, a facultative intracellular pathogen which survives and replicates within macrophages, may be responsible for the impairment in the TNF-alpha release, possibly enhancing the HIV-induced macrophage dysftmction.
Identifiers
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Registered trials
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