Reduced toxoplasmastatic activity of monocytes and monocyte-derived macrophages from AIDS patients is mediated via prostaglandin E2

Fg, Delemarre; Stevenhagen, A.; Fp, Kroon; My, van Eer; Pl, Meenhorst; R, van Furth

doi:10.1097/00002030-199505000-00005

Cited by 15 publications

(10 citation statements)

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“…The involvement of PGE2 in the toxoplasmastatic activity of monocytes has been demonstrated earlier. Incubation of monocytes with PGE2 gave a dose-dependent increase in intracellular replication of T. gondii [25]. The inhibitory effect of GM-CSF on the expression of IL-2 receptors (IL-2R) by IFN-7-activated monocytes [26] most probably depends on a similar mechanism, as we found for the antimicrobial activity, i.e.…”

Section: Discussionmentioning

confidence: 54%

Granulocyte-macrophage colony-stimulating factor (GM-CSF) reduces toxoplasmastatic activity of human monocytes via induction of prostaglandin E2 (PGE2)

Delemarre

Stevenhagen

Furth

1995

Clinical and Experimental Immunology

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SUMMARYIn this study we investigated the effect of human GM-CSF on the toxoplasmastatic activity and release of H2O2 and PGE2 by human monocytes. Incubation of monocytes from healthy controls with GM-CSF resulted in a dose-dependent reduction of toxoplasmastatic activity and a decrease in H2O2 production. Furthermore GM-CSF-treated monocytes released more PGE2 than untreated cells. To investigate the role of PGE2 in the reduced toxoplasmastatic activity of GM-CSF-treated monocytes, these cells were incubated with indomethacin. This resulted in a reduction of PGE2 release and restoration of toxoplasmastatic activity of monocytes treated with GM-CSF. GM-CSF reduces the toxoplasmastatic activity of monocytes via production of PGE2.

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Section: Discussionmentioning

confidence: 54%

Granulocyte-macrophage colony-stimulating factor (GM-CSF) reduces toxoplasmastatic activity of human monocytes via induction of prostaglandin E2 (PGE2)

Delemarre

Stevenhagen

Furth

1995

Clinical and Experimental Immunology

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“…Many of these changes can be attributed to alterations in mediator production including cytokines (2) and eicosanoids (3,4). Prostaglandins (PG) 1 are one such group of mediators that are modulated in HIV infection (5,6). In patients with AIDS, serum levels of PGE 2 are significantly increased relative to serum levels of PGE 2 in normal controls (6).…”

mentioning

confidence: 99%

“…Prostaglandins (PG) 1 are one such group of mediators that are modulated in HIV infection (5,6). In patients with AIDS, serum levels of PGE 2 are significantly increased relative to serum levels of PGE 2 in normal controls (6). Augmented levels of PG are also found in cerebral spinal fluid of AIDS patients (7,8).…”

mentioning

confidence: 99%

Peroxisome Proliferator-activated Receptor γ Agonists Inhibit HIV-1 Replication in Macrophages by Transcriptional and Post-transcriptional Effects

Hayes¹,

Lane²,

King³

et al. 2002

Journal of Biological Chemistry

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“…In this connection, it is important to note that the cAMP/PKA pathway is overactive and the production of IL-12 is suppressed in a number of virus-induced pathological conditions such as HIV infection. (25,26) Several human demyelinating disorders have a known viral etiology: subacute sclerosing panencephalitis as a late complication of measles virus infection of childhood, (27) progressive multifocal leukoencephalopathy caused by the JC papovavirus, (28) encephalopathy and myelopathy (neuro-AIDS) caused by human immunodeficiency virus, (29) and human T-lymphotropic virus type 1 associated myelopathy/tropical spastic paraparesis. (30) Although the association of a virus with multiple sclerosis (MS) has not been confirmed, based on detection of virions, viral nucleic acids, or viral proteins in CNS or the presence of antiviral antibodies in serum and/or CSF, several viruses have been suggested to play a role in MS. (31)(32)(33) A common viral structure that is almost universally recognized by eukaryotic cells is dsRNA (Ͼ100 bp).…”

Section: Production Of Tnf-a (% Of Control)mentioning

confidence: 99%

Generation of Functional Blocking Monoclonal Antibodies Against Mouse Interleukin-12 p40 Homodimer and Monomer

Dasgupta

Bandopadhyay²,

Pahan³

2008

Hybridoma

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The role of interleukin (IL)-12 (p40:p35) and IL-23 (p40:p19) is becoming clear in immune response and inflammation. However, biological functions of IL-12 p40 homodimer (p40(2)) and monomer (p40) remain poorly understood due to the lack of specific monoclonal antibodies (MAb). Earlier we have demonstrated that both p40(2) and p40 activate microglia and macrophages to induce the expression of iNOS and TNF-alpha. To facilitate the studies on p40(2) and p40 further, we here describe the production of neutralizing MAb against mouse p40(2) and p40 for the first time after immunization of Armenian hamsters with recombinant p40(2). Antibodies produced from clones a3-1d and d7-12c specifically recognized p40(2) but not p40, IL-12, and IL-23. These MAbs also inhibited p40(2)- but not p40-, IL-12-, and IL-23-induced production of inflammatory molecules and activation of NF-kappaB. On the other hand, antibodies produced from clones a3-3a and a3-7g specifically recognized p40 and inhibited p40- but not p40(2)-, IL-12-, and IL-23-induced production of inflammatory molecules and activation of NF-kappaB. While MAbs a3-1d and d7-12c were used to establish p40(2)-specific ELISA, we utilized MAbs a3-3a and a3-7g to develop p40-specific ELISA. Interestingly, the production of p40(2) and p40 but not IL-12 in mouse peritoneal macrophages and primary microglia was an immediate early response to bacterial lipopolysaccharides. Furthermore, double-stranded RNA, the active component of a viral infection, induced the production of p40(2) and p40 but not IL-12 in macrophages and microglia. These results indicate the presence of different regulatory mechanisms for the production of IL-12p40(2)/p40 and IL-12p70.

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Reduced toxoplasmastatic activity of monocytes and monocyte-derived macrophages from AIDS patients is mediated via prostaglandin E2

Cited by 15 publications

References 0 publications

Granulocyte-macrophage colony-stimulating factor (GM-CSF) reduces toxoplasmastatic activity of human monocytes via induction of prostaglandin E2 (PGE2)

Granulocyte-macrophage colony-stimulating factor (GM-CSF) reduces toxoplasmastatic activity of human monocytes via induction of prostaglandin E2 (PGE2)

Peroxisome Proliferator-activated Receptor γ Agonists Inhibit HIV-1 Replication in Macrophages by Transcriptional and Post-transcriptional Effects

Generation of Functional Blocking Monoclonal Antibodies Against Mouse Interleukin-12 p40 Homodimer and Monomer

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