Improvement in neutrophil and monocyte function during highly active antiretroviral treatment of HIV-1-infected patients

Mastroianni, Claudio Maria; Lichtner, Miriam; Mengoni, Fabio; D’Agostino, Claudia; Forcina, Gabriele; d’Ettorre, Gabriella; Santopadre, Paola; Vullo, Vincenzo

doi:10.1097/00002030-199905280-00003

Cited by 73 publications

(52 citation statements)

References 35 publications

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“…It is well established that the phagocytic function of neutrophils and cells of the macrophage lineage is impaired in HIV-1-infected patients 8,9,12,13 . Both FcgR-and MR-mediated phagocytosis are inhibited, enabling the development of several opportunistic pathogens 12,46 .…”

Section: Discussionmentioning

confidence: 99%

“…The other key phagocytes such as monocytes and neutrophils are, respectively, poorly (o1%) or not virally infected in HIV-1 patients. Nevertheless, their phagocytic activity is also affected in these patients 12,13 . Altogether these observations indicate that a secreted HIV-1 virulence factor might be responsible for the decreased phagocytic activity of phagocytes.…”

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confidence: 99%

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HIV-1 Tat inhibits phagocytosis by preventing the recruitment of Cdc42 to the phagocytic cup

et al. 2015

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

HIV-1 Tat inhibits phagocytosis by preventing the recruitment of Cdc42 to the phagocytic cup

et al. 2015

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“…5,6 As neutrophils appear to play a crucial role in the control of the infectious process, one can hypothesize that a deficient migratory ability of neutrophils may aggravate infections. Indeed, impairment of neutrophil migration has been reported in leukemia, 7 diabetes, 8 and AIDS, 9 diseases associated with high susceptibility to infection. Furthermore, previous studies from our group showed that failure of neutrophil migration is observed in severe sepsis induced by cecal ligation and puncture and Staphylococcus aureus administration.…”

Section: Introductionmentioning

confidence: 99%

Impaired neutrophil chemotaxis in sepsis associates with GRK expression and inhibition of actin assembly and tyrosine phosphorylation

Arraes

Freitas

Silva

et al. 2006

Blood

138

106

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The deregulation of inflammatory response during sepsis seems to reflect the overproduction of mediators, which suppress leukocyte functions. We investigated the intracellular mechanisms underlying the inability of neutrophils from severe septic patients to migrate toward chemoattractants. Patients IntroductionSepsis is a complex clinical syndrome resulting from a damaging host response to infection. 1 In the United States, more than 700 000 patients per year develop sepsis, with mortality rates reported to vary between 30% and 70%, despite the best available supportive care. 2 Polymorphonuclear neutrophils (PMNs) play the first line in the host defense against microorganisms, being recruited to the inflammatory sites by chemoattractants such as leukotriene B 4 (LTB 4 ) and chemokines. 3,4 Once emigrated, these leukocytes are able to phagocytose and to generate large amounts of reactive oxygen and nitrogen species, such as hydrogen peroxide and nitric oxide, which are crucial products for the microbicidal activity of these cells. 5,6 As neutrophils appear to play a crucial role in the control of the infectious process, one can hypothesize that a deficient migratory ability of neutrophils may aggravate infections. Indeed, impairment of neutrophil migration has been reported in leukemia, 7 diabetes, 8 and AIDS, 9 diseases associated with high susceptibility to infection. Furthermore, previous studies from our group showed that failure of neutrophil migration is observed in severe sepsis induced by cecal ligation and puncture and Staphylococcus aureus administration. 10,11 In these lethal models, failure of neutrophil migration to the site of infection was accompanied by increased numbers of bacteria in the peritoneal fluid and blood. Conversely, in sublethal infection in which massive neutrophil migration was observed, bacterial infection was restricted to the peritoneal cavity, and the animals exhibited a low mortality rate. 10,11 More recently, we have also reported that blood neutrophils obtained from patients with sepsis failed to respond in vitro to the chemotactic stimuli FMLP and LTB 4 . This unresponsiveness was directly associated to a poor prognosis. 12 Evidence from literature suggests that the high levels of circulating cytokines/chemokines observed in severe sepsis may mediate the impairment of neutrophil migration, in addition to being involved in the deleterious physiopathologic findings of the disease, such as coagulation disorders, cardiovascular collapse, and organ failure. 13 The intravenous administration of tumor necrosis factor-␣ (TNF-␣) or interleukin-8 (IL-8) inhibited neutrophil migration to mouse peritoneal cavity and anti-TNF-␣ antibody partially prevented the inhibition of neutrophil migration in endotoxemia model. 14 However, the molecular mechanisms involved in the reduced ability of neutrophils to migrate during sepsis were not completely clarified.Independent of their chemical nature, most chemoattractants exert their action via binding to specific G protein-coupled receptors (GP...

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“…Mastroianni et al (62) found that highly active antiretroviral therapy (HAART) produces a significant improvement in chemotaxis and microbicidal activity of monocytic and neutrophil cells, contributing to cell-mediated immune responses against opportunistic agents (for instance, APC function). Consequently, a correct antiretroviral treatment, possibly associated with a suitable immunotherapy and/or growth factor treatment, may improve the monocyte/macrophage and neutrophil functions, together with some correlated activities of the immune system, as underlined by various authors (52,53,74) This contributes to the reduction in incidence of concomitant infections, especially those produced by opportunistic microorganisms such as the Mycobacterium avium complex, Pneumocystis carinii, Toxoplasma gondii, and Candida albicans.…”

Section: Effect Of Antiretroviral Therapy On Phagocytic Cell Functionmentioning

confidence: 99%

Phagocytic Activity in Human Immunodeficiency Virus Type 1 Infection

Pugliese

Vidotto

Beltramo

et al. 2005

Clin Vaccine Immunol

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Improvement in neutrophil and monocyte function during highly active antiretroviral treatment of HIV-1-infected patients

Abstract: The functional improvement of two critical components of innate antimicrobial immunity, such as neutrophils and monocytes, may contribute to the improved cell-mediated immune responses against opportunistic infections in HAART-treated patients.

Cited by 73 publications

References 35 publications

HIV-1 Tat inhibits phagocytosis by preventing the recruitment of Cdc42 to the phagocytic cup

HIV-1 Tat inhibits phagocytosis by preventing the recruitment of Cdc42 to the phagocytic cup

Impaired neutrophil chemotaxis in sepsis associates with GRK expression and inhibition of actin assembly and tyrosine phosphorylation

Phagocytic Activity in Human Immunodeficiency Virus Type 1 Infection

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