scholarly journals Reduced Expression of Interleukin-8 Receptors A and B on Polymorphonuclear Neutrophils from Persons with Human Immunodeficiency Virus Type 1 Disease and Pulmonary Tuberculosis

1998 ◽  
Vol 177 (4) ◽  
pp. 921-930 ◽  
Author(s):  
S. Meddows-Taylor ◽  
D. J. Martin ◽  
C. T. Tiemessen
Keyword(s):  
Human Immunodeficiency Virus ◽  
Pulmonary Tuberculosis ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Interleukin 8 ◽  
Polymorphonuclear Neutrophils ◽  
Immunodeficiency Virus

scholarly journals Defective Neutrophil Degranulation Induced by Interleukin-8 and Complement 5a and Down-Regulation of Associated Receptors in Children Vertically Infected with Human Immunodeficiency Virus Type 1

2001 ◽  
Vol 8 (1) ◽  
pp. 21-30 ◽  
Author(s):  
Stephen Meddows-Taylor ◽  
Louise Kuhn ◽  
Tammy M. Meyers ◽  
Gayle Sherman ◽  
Caroline T. Tiemessen
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Severe Disease ◽  
Interleukin 8 ◽  
Polymorphonuclear Neutrophils ◽  
Control Group ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT The polymorphonuclear neutrophils (PMNs) of patients infected with human immunodeficiency virus type 1 (HIV-1) show impaired microbicidal responses. The present study assessed the functional integrity of PMN degranulation responses and the expression of specific receptors that mediate these responses in a group of children vertically infected with HIV-1. PMN degranulation in response to interleukin-8 (IL-8) and complement 5a (C5a) was measured in a group of HIV-1-infected children with mild and severe clinical disease and in an uninfected control group. In addition, the expression of CXCR1, CXCR2, and CD88 on whole-blood PMNs was quantified by flow cytometry. Although CXCR1 expression was found to be largely unaltered in the HIV-1-infected children relative to that in the control children, the intensity of CXCR2 expression was significantly reduced in those with severe disease. Furthermore, there was a significant reduction in the percentage of cells expressing CD88 and in the intensity of CD88 fluorescence in the HIV-1-infected children compared to that in control children, with CD88 fluorescence intensity more significantly reduced in the presence of severe disease. PMNs from a large proportion of the HIV-1-infected children either showed reciprocal degranulation responses or were unresponsive to IL-8 and C5a, whereas the PMNs from the uninfected children showed positive responses. Inefficient agonist-induced degranulation may contribute to the increased susceptibility of HIV-1-infected children to secondary microbial infections. Furthermore, reduced expression of CXCR2 and CD88 may be suggestive of defects in other functions of PMNs from HIV-1-infected children.

scholarly journals Induction of the Chemokines Interleukin-8 and IP-10 by Human Immunodeficiency Virus Type 1 Tat in Astrocytes

2000 ◽  
Vol 74 (19) ◽  
pp. 9214-9221 ◽  
Author(s):  
O. Kutsch ◽  
J.-W. Oh ◽  
A. Nath ◽  
E. N. Benveniste
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Interleukin 8 ◽  
Mrna Induction ◽  
Immunodeficiency Virus ◽  
The Brain ◽  
Hiv 1

ABSTRACT A finding commonly observed in human immunodeficiency virus type 1 (HIV-1)-infected patients is invasion of the brain by activated T cells and infected macrophages, eventually leading to the development of neurological disorders and HIV-1-associated dementia. The recruitment of T cells and macrophages into the brain is likely the result of chemokine expression. Indeed, earlier studies revealed that levels of different chemokines were increased in the cerebrospinal fluid of HIV-1-infected patients whereas possible triggers and cellular sources for chemokine expression in the brain remain widely undefined. As previous studies indicated that HIV-1 Tat, the retroviral transactivator, is capable of inducing a variety of cellular genes, we investigated its capacity to induce production of chemokines in astrocytes. Herein, we demonstrate that HIV-1 Tat72aa is a potent inducer of MCP-1, interleukin-8 (IL-8), and IP-10 expression in astrocytes. Levels of induced IP-10 protein were sufficiently high to induce chemotaxis of peripheral blood lymphocytes. In addition, Tat72aa induced IL-8 expression in astrocytes. IL-8 mRNA induction was seen less then 1 h after Tat72aastimulation, and levels remained elevated for up to 24 h, leading to IL-8 protein production. Tat72aa-mediated MCP-1 and IL-8 mRNA induction was susceptible to inhibition by the MEK1/2 inhibitor UO126 but was only modestly decreased by the inclusion of the p38 mitogen-activated protein kinase (MAPK) inhibitor SB202190. In contrast, Tat-mediated IP-10 mRNA induction was suppressed by SB202190 but not by the MEK1/2 inhibitor UO126. These findings indicate that MAPKs play a major role in Tat72aa-mediated chemokine induction in astrocytes.

scholarly journals Interleukin-8 Stimulates Human Immunodeficiency Virus Type 1 Replication and Is a Potential New Target for Antiretroviral Therapy

2001 ◽  
Vol 75 (17) ◽  
pp. 8195-8202 ◽  
Author(s):  
Brian R. Lane ◽  
Karin Lore ◽  
Paul J. Bock ◽  
Jan Andersson ◽  
Michael J. Coffey ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Lymphocytes ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Lymphoid Tissue ◽  
Interleukin 8 ◽  
Therapeutic Uses ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Production of the C-X-C chemokines interleukin-8 (IL-8) and growth-regulated oncogene alpha (GRO-α) in macrophages is stimulated by exposure to human immunodeficiency virus type 1 (HIV-1). We have demonstrated previously that GRO-α then stimulates HIV-1 replication in both T lymphocytes and macrophages. Here we demonstrate that IL-8 also stimulates HIV-1 replication in macrophages and T lymphocytes. We further show that increased levels of IL-8 are present in the lymphoid tissue of patients with AIDS. In addition, we demonstrate that compounds which inhibit the actions of IL-8 and GRO-α via their receptors, CXCR1 and CXCR2, also inhibit HIV-1 replication in both T lymphocytes and macrophages, indicating potential therapeutic uses for these compounds in HIV-1 infection and AIDS.

scholarly journals Impaired Interleukin-8-Induced Degranulation of Polymorphonuclear Neutrophils from Human Immunodeficiency Virus Type 1-Infected Individuals

1999 ◽  
Vol 6 (3) ◽  
pp. 345-351 ◽  
Author(s):  
Stephen Meddows-Taylor ◽  
Desmond J. Martin ◽  
Caroline T. Tiemessen
Keyword(s):  
Human Immunodeficiency Virus ◽  
Pulmonary Tuberculosis ◽  
Whole Blood ◽  
Interleukin 8 ◽  
Polymorphonuclear Neutrophils ◽  
Dependent Manner ◽  
Immunodeficiency Virus ◽  
Microbial Infections ◽  
Hiv 1

ABSTRACT Degranulation of peripheral blood polymorphonuclear leukocytes (PMNLs) was monitored in human immunodeficiency virus (HIV) type 1 (HIV-1)-infected individuals with or without pulmonary tuberculosis (HIV/TB and HIV groups, respectively) by measuring the release of β-glucuronidase induced by interleukin-8 (IL-8). This was increased in a dose-dependent manner in the control groups consisting of healthy blood donors and patients with pulmonary tuberculosis. In contrast, PMNLs from the HIV and HIV/TB groups responded reciprocally in the same assay; that is, higher IL-8 input concentrations resulted in the release of less enzyme than lower IL-8 input concentrations. The degranulation response of PMNLs from HIV-1-infected individuals was similarly altered for another agonist,N-formyl-methionyl-leucyl-phenylalanine, suggesting that impairment of the nonoxidative armature of PMNL was a more generalized phenomenon. However, impaired IL-8-induced degranulation was found to be associated with the reduced expression of both IL-8 receptors, A and B, on whole-blood PMNLs from HIV-1-infected patients compared with that on whole-blood PMNLs from healthy persons. The density of IL-8RA, in particular, was most reduced on the surfaces of PMNLs from those patients with the poorest degranulation in response to IL-8. Inefficient agonist-induced degranulation may contribute to the increased susceptibility of HIV-1-infected persons to secondary microbial infections, this being further exacerbated in HIV/TB patients who, in addition, display defects in phagocytosis and oxidative burst.

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