ArticleInfection and immunity1996
H2O2 induces monocyte apoptosis and reduces viability of Mycobacterium avium-M. intracellulare within cultured human monocytes.
Article in Infection and immunity, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 82 citations in OpenAlex.
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- Nitric oxide not apoptosis mediates differential killing of Mycobacterium bovis in bovine macrophages.PloS one · 2013Article
- Mycobacterium tuberculosis infection induces non-apoptotic cell death of human dendritic cells.BMC microbiology · 2011Article
- How tumour necrosis factor blockers interfere with tuberculosis immunity.Clinical and experimental immunology · 2010Review
- HIV-1 transforms the monocyte plasma membrane proteome.Cellular immunology · 2009Article
- Mycobacteria and innate cells: critical encounter for immunogenicity.Journal of biosciences · 2008Review
- Tactics of Mycobacterium avium subsp. paratuberculosis for intracellular survival in mononuclear phagocytes.Journal of veterinary science · 2008Review
- Phagocytosis of Borrelia burgdorferi, the Lyme disease spirochete, potentiates innate immune activation and induces apoptosis in human monocytes.Infection and immunity · 2008Article
- Bystander macrophage apoptosis after Mycobacterium tuberculosis H37Ra infection.Infection and immunity · 2008Article
- A caspase-independent pathway mediates macrophage cell death in response to Mycobacterium tuberculosis infection.Infection and immunity · 2007Article
- Apoptosis-inducing factor participation in bovine macrophage Mycobacterium bovis-induced caspase-independent cell death.Infection and immunity · 2007Article
- Mycobacterium tuberculosis pathogenesis and molecular determinants of virulence.Clinical microbiology reviews · 2003Review
- H2O2 production by cells on titanium and polystyrene surfaces using an in vivo model of exudate and surface related cell function.Journal of materials science. Materials in medicine · 2002Article
- Use of Hoechst 33342 staining to detect apoptotic changes in bovine mononuclear phagocytes infected with Mycobacterium avium subsp. paratuberculosis.Clinical and diagnostic laboratory immunology · 2001Article
- Redox and activation status of monocytes from human immunodeficiency virus-infected patients: relationship with viral load.Journal of virology · 1999Article
- Tumor necrosis factor alpha is a determinant of pathogenesis and disease progression in mycobacterial infection in the central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Apoptosis of Mycobacterium avium-infected macrophages is mediated by both tumour necrosis factor (TNF) and Fas, and involves the activation of caspases.Clinical and experimental immunology · 1999Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium avium-M. intracellulare, an intracellular parasite of mononuclear phagocytes, rarely causes disease in immunocompetent individuals. In contrast, in human immunodeficiency virus type 1-infected patients, M. avium-M. intracellulare can infect almost every tissue and organ. This suggests that immunocompetent individuals have a protective mechanism to control or prevent the infection. How mycobacterial may be killed by the host immune response is unclear. We have recently reported that induction of apoptosis of Mycobacterium bovis BCG-infected macrophages with ATP4- was associated with killing of the intracellular mycobacteria. In the present study, a long-term culture of M. avium-M. intracellulare-infected monocytes was used to further evaluate the interaction between M. avium-M. intracellulare and primary human monocytes. In our system, M. avium-M. intracellulare parasitized the human monocytes and appeared to replicate slowly over 14 days within the host cells. To examine the role of apoptotic mechanisms in survival or death of intracellular mycobacteria, M. avium-M. intracellulare-infected human monocytes were treated with a monoclonal antibody to Fas receptor (APO-1/CD95) or with various concentrations of H2O2. Although both of these exogenous agents induced monocyte apoptosis, optimal killing (65% reduction in CFU) of intracellular M. avium-M. intracellulare was observed only when M. avium-M. intracellulare-infected cells were treated with 10 mM H2O2. Fas-induced apoptosis did not affect M. avium-M. intracellulare viability. Our results suggest that not all stimuli of monocyte apoptosis induce killing of intracellular M. avium-M. intracellulare. Since release of H2O2 following phagocytosis of mycobacteria has been documented, H2O2-induced apoptotic death of M. avium-M. intracellulare-infected monocytes and its association with killing of the intracellular bacilli may be a physiological mechanism of host defense against M. avium-M. intracellulare.
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