Phagocytic Activity in Human Immunodeficiency Virus Type 1 Infection

Pugliese, A.; Vidotto, V.; Beltramo, Tiziana; Torre, Donato

doi:10.1128/cdli.12.8.889-895.2005

Cited by 34 publications

(40 citation statements)

References 100 publications

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“…In addition, more typical bacterial pathogens, such as Streptococcus pneumoniae, are also increased in patients with HIV/AIDS, reflecting a significant problem with airway host defense. The precise mechanisms underlying HIV-1-induced immune dysfunction within the lung are not known; however, HIV-1 can infect alveolar macrophages (6), and evidence suggests that phagocytosis and other innate immune functions are impaired in monocytes/macrophages from individuals infected with HIV-1 (7,8). Therefore, there are compelling reasons to identify the mechanisms by which alveolar macrophage immune function is impaired in chronic HIV-1 infection so that novel therapies designed to augment pulmonary host defenses can be developed.…”

mentioning

confidence: 99%

HIV-1–Transgene Expression in Rats Decreases Alveolar Macrophage Zinc Levels and Phagocytosis

Joshi

Raynor

Fan

et al. 2008

Am J Respir Cell Mol Biol

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mentioning

confidence: 99%

HIV-1–Transgene Expression in Rats Decreases Alveolar Macrophage Zinc Levels and Phagocytosis

Joshi

Raynor

Fan

et al. 2008

Am J Respir Cell Mol Biol

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“…It has been demonstrated that apoptosis could, in part, be responsible for HIV-related neutropenia [33], which could occur either spontaneously [8] or be triggered via death receptors such as Fas/FasL [9]. We have reported previously that spontaneous neutrophil death is not Fas/FasL-induced during HIV infection [9].…”

Section: Discussionmentioning

confidence: 95%

Mechanisms of neutrophil death in human immunodeficiency virus-infected patients: role of reactive oxygen species, caspases and map kinase pathways

Salmen¹,

Montes

Sóyano

et al. 2007

Clinical and Experimental Immunology

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SummaryNeutrophils from human immunodeficiency virus-positive (HIV + ) patients have an increased susceptibility to undergo programmed cell death (PCD), which could explain neutropenia during advanced disease. In this work, key steps of PCD have been evaluated in neutrophils from HIV + patients. The role of caspase-3, caspase-8, mitogen activated protein kinase (MAPK) and reactive oxygen species (ROS) was analysed. Spontaneous neutrophil death is dependent upon caspase-3 but independent of caspase-8, suggesting that the intrinsic pathway is involved as a pathogenic mechanism of PCD. Inhibition of ROS decreased spontaneous PCD and caspase-3 hydrolysis, connecting oxidative stress and caspase-3 activation with neutrophil PCD in HIVinfected patients. Additionally, an increased neutrophil death was observed in HIV + patients, following inhibition of p38 MAPK, suggesting a role for p38 MAPK in cell survival during the disease. We conclude that oxidative stress secondary to HIV infection can accelerate neutrophil death.

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“…For example, cellular activation and cytokine production, intracellular killing, and phagocytosis are altered or generally inhibited by HIV-1 [23]. This is particularly relevant because infected macrophages can remain in such a state for weeks and months, producing virus and acting as long-term HIV-1 cellular reservoirs [24].…”

Section: Discussionmentioning

confidence: 98%

Leishmania infantumPromastigotes Reduce Entry of HIV‐1 into Macrophages through a Lipophosphoglycan‐Mediated Disruption of Lipid Rafts

et al. 2008

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Visceral leishmaniasis is now recognized as an opportunistic disease in patients infected with human immunodeficiency virus type 1 (HIV-1). We report here that Leishmania infantum promastigotes enhance HIV-1 replication in monocyte-derived macrophages (MDMs) at late time points in the virus growth curve but also that, surprisingly, a reduction in HIV-1 production is seen during the initial days after infection. This early effect is caused by a Leishmania-mediated inhibition of virus entry into MDMs through the action of lipophosphoglycan (LPG), the major promastigote surface glycolipid. The impact of LPG in the observed phenomenon was confirmed using LPG-defective lpg1-/- knockout mutant promastigotes. Our results suggest that the LPG-mediated effect results from the disruption of lipid rafts. Altogether, these findings suggest that the presence of Leishmania within the same cellular microenvironment leads to 2 opposite, time-dependent effects on HIV-1 replication. Leishmania and HIV-1 can thus establish complex interactions in their common natural host cells.

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Phagocytic Activity in Human Immunodeficiency Virus Type 1 Infection

Cited by 34 publications

References 100 publications

HIV-1–Transgene Expression in Rats Decreases Alveolar Macrophage Zinc Levels and Phagocytosis

HIV-1–Transgene Expression in Rats Decreases Alveolar Macrophage Zinc Levels and Phagocytosis

Mechanisms of neutrophil death in human immunodeficiency virus-infected patients: role of reactive oxygen species, caspases and map kinase pathways

Leishmania infantumPromastigotes Reduce Entry of HIV‐1 into Macrophages through a Lipophosphoglycan‐Mediated Disruption of Lipid Rafts

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