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

Meddows‐Taylor, Stephen; Martin, Des; Tiemessen, Caroline T.

doi:10.1086/515232

Cited by 46 publications

(48 citation statements)

References 28 publications

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“…Based on in vitro experiments, the prevailing view is that neutrophil biology including chemotaxis (4,6), oxidant production, and bacterial killing (4) are affected in HIV infections, such that the innate immune response dominated by these leukocytes is depressed. Although a key feature of the innate immune response is the rapid recruitment of neutrophils, to date a systematic assessment of the potentially affected mechanisms in this multistep process has not been evaluated in lentiviral infections.…”

Section: Figurementioning

confidence: 99%

“…Although neither HIV nor FIV is thought to infect neutrophils (the primary leukocytes involved in innate immunity), there is a growing body of literature to suggest impairment of neutrophil function from HIV-infected patients in response to bacterial infections despite the preservation of absolute neutrophil counts with advanced immunosuppression. In fact, in the case of HIV, isolated neutrophils have been shown to have decreased oxidant production (3), protease release (3), bacterial killing (4), phagocytosis (5), and chemotaxis (4,6). Although the increased susceptibility to infections in HIV-and FIV-infected patients may be related to impaired antimicrobial functions related to bacterial killing (oxidant production, protease release, phagocytosis), it might also be associated with impaired neutrophil recruitment (rolling, adhesion, or emigration).…”

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confidence: 99%

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In Vivo Impairment of Neutrophil Recruitment during Lentivirus Infection

Kubes

Heit

Marle

et al. 2003

The Journal of Immunology

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Evidence indicates that the lentivirus, HIV, infection affects neutrophil response to bacteria and bacterial products in vitro. We used a novel model of rapid onset immunosuppression following infection with a similar lentivirus, feline immunodeficiency virus (FIV), in cats to examine neutrophil function within the microvasculature in vivo and to determine the steps that are impaired in the neutrophil recruitment cascade. In uninfected cats and cats infected neonatally with FIV, the mesentery was exteriorized, but remained autoperfused during intravital microscopy for 4 h. When the tissue was superfused with 10 μg/ml of LPS for 4 h, intravital microscopy displayed a profound increase in neutrophil rolling at both 8 and 12 wk of age in uninfected cats. At 12 wk of age, FIV-infected animals showed a profound decrease in the number of rolling neutrophils. In vitro studies revealed that neutrophils from infected and uninfected animals rolled equally well on surrogate selectin substrata. In addition, in vivo neutrophil adhesion and emigration out of the vasculature were severely reduced, and in vitro neutrophil chemotaxis from FIV-infected animals was significantly impaired in response to fMLP or IL-8. However, FIV infection of neutrophils could not be detected. In summary, in vivo lentivirus infection with immunosuppression leads to a severe impairment in neutrophil rolling, adhesion, and emigration in response to bacterial stimulants potentially involving both endothelial and neutrophil dysfunction. These in vivo studies also indicate that neutrophil dysfunction should be taken into account when treating infections and tissue injury.

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Section: Figurementioning

confidence: 99%

mentioning

confidence: 99%

In Vivo Impairment of Neutrophil Recruitment during Lentivirus Infection

Kubes

Heit

Marle

et al. 2003

The Journal of Immunology

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“…64 Another study demonstrated significant reduction in the expression of both receptors on neutrophils in persons with pulmonary TB and/or HIV infection. 65 Since neutrophils are known to play a protective nonphagocytic role in the initial host defense mechanisms against M. tuberculosis, 66,67 reduced expression of these receptors could impair the chemotactic response of neutrophils to IL-8 and hence the immune response in mycobacterial infection. These findings also highlight the importance of these receptors in neutrophil functions.…”

Section: Decay Of Ldmentioning

confidence: 99%

Extent and distribution of linkage disequilibrium around the SLC11A1 locus

2003

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The SLC11A1 (or NRAMP1) locus on human chromosome 2q35 encodes for the protein solute carrier family 11, member 1. It is expressed in macrophages and involved in the early stages of macrophage priming and activation. Different association studies have shown that the SLC11A1 gene affects susceptibility to infectious diseases and autoimmune inflammatory diseases. Although functional SLC11A1 polymorphisms may account for its role in affecting the susceptibility to these diseases, the positive association can also be because of flanking polymorphisms showing linkage disequilibrium (LD) with this locus. This is the first systematic study to investigate the LD pattern within and around the gene. LD was investigated by genotyping 17 genetic markers in a Chinese population (n ¼ 360). The results indicate that LD is maintained at least 110 kb both upstream and downstream of the locus. The complex LD pattern demands that association studies with SLC11A1 should be carried out with both 5 0 and 3 0 markers. The strong LD between IL8RB and the 5 0 SLC11A1 markers also dictates that IL8RB be tested for association with these diseases. Thus, positive association with SLC11A1 should be interpreted cautiously, and IL8RB should also be considered as a potential candidate susceptibility gene unless proven otherwise.

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“…gp41 has been detected in brain tissues of patients affected by AIDS dementia (22) and Abs recognizing various epitopes of gp41 appear at early stages of HIV infection (61). Moreover, it has been reported that monocytes and neutrophils from HIV-1-infected patients responded poorly to a variety of chemoattractants, including FMLP (62)(63)(64)(65)(66). The interaction of gp41 peptides with FPRs on human basophils might be of clinical relevance in patients with HIV-1 infection.…”

Section: Increasing Evidence Indicates That Human Fc⑀rimentioning

confidence: 99%

HIV-1 Envelope gp41 Peptides Promote Migration of Human FcεRI+ Cells and Inhibit IL-13 Synthesis Through Interaction with Formyl Peptide Receptors

Paulis

Florio

Prevete

et al. 2002

The Journal of Immunology

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We evaluated the effects of synthetic peptides (2017, 2019, 2020, 2021, 2023, 2027, 2029, 2030, 2031, and 2035) encompassing the structure of HIV-1MN envelope gp41 on both chemotaxis of human basophils and the release of preformed mediators (histamine) and of cytokines (IL-13). Peptides 2019 and 2021 were potent basophil chemoattractants, whereas the other peptides examined were ineffective. Preincubation of basophils with FMLP or gp41 2019 resulted in complete desensitization to a subsequent challenge with homologous stimulus. Incubation of basophils with low concentration (5 × 10−7 M) of FMLP, which binds with high affinity to N-formyl peptide receptor (FPR), but not to FPR-like 1, did not affect the chemotactic response to a heterologous stimulus (gp41 2019). In contrast, a high concentration (10−4 M) of FMLP, which binds also to FPR-like 1, significantly reduced the chemotactic response to gp41 2019. The FPR antagonist cyclosporin H inhibited chemotaxis induced by FMLP, but not by gp41 2019. None of these peptides singly induced the release of histamine or cytokines (IL-4 and IL-13) from basophils. However, low concentrations of peptides 2019 and 2021 (10−8–10−6 M) inhibited histamine release from basophils challenged with FMLP but not the secretion caused by anti-IgE and gp120. Preincubation of basophils with peptides 2019 and 2021 inhibited the expression of both IL-13 mRNA, and the FMLP-induced release of IL-13 from basophils. These data highlight the complexity of the interactions between viral and bacterial peptides with FPR subtypes on human basophils.

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

Cited by 46 publications

References 28 publications

In Vivo Impairment of Neutrophil Recruitment during Lentivirus Infection

In Vivo Impairment of Neutrophil Recruitment during Lentivirus Infection

Extent and distribution of linkage disequilibrium around the SLC11A1 locus

HIV-1 Envelope gp41 Peptides Promote Migration of Human FcεRI+ Cells and Inhibit IL-13 Synthesis Through Interaction with Formyl Peptide Receptors

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