Mechanisms Underlying HIV-Associated Noninfectious Lung Disease

Presti, Rachel; Flores, Sonia C.; Palmer, Brent E.; Atkinson, Jeffrey J.; Lesko, Catherine R.; Lau, Bryan; Fontenot, Andrew P.; Roman, Jesse; McDyer, John F.; Twigg, Homer L.

doi:10.1016/j.chest.2017.04.154

Cited by 26 publications

(22 citation statements)

References 73 publications

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“…In recent years, the widespread use of ART has improved the survival of people with HIV [ 1 ], leading to the emergence of chronic inflammatory lung diseases as a noteworthy concern in this population [ 7 , 9 ]. COPD [ 9 , 11 , 12 , 117 ], lung cancer [ 10 , 118 ], pulmonary hypertension [ 13 ], and bronchial asthma [ 7 , 119 ] occur at high frequency among HIV-infected individuals. HIV infection induces a state of chronic inflammation characterized by persistent immune dysregulation [ 120 ], which likely induces the release of proinflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

HIV gp120 Induces the Release of Proinflammatory, Angiogenic, and Lymphangiogenic Factors from Human Lung Mast Cells

et al. 2020

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Human lung mast cells (HLMCs) express the high-affinity receptor FcεRI for IgE and are involved in chronic pulmonary diseases occurring at high frequency among HIV-infected individuals. Immunoglobulin superantigens bind to the variable regions of either the heavy or light chain of immunoglobulins (Igs). Glycoprotein 120 (gp120) of HIV-1 is a typical immunoglobulin superantigen interacting with the heavy chain, variable 3 (VH3) region of human Igs. The present study investigated whether immunoglobulin superantigen gp120 caused the release of different classes of proinflammatory and immunoregulatory mediators from HLMCs. The results show that gp120 from different clades induced the rapid (30 min) release of preformed mediators (histamine and tryptase) from HLMCs. gp120 also caused the de novo synthesis of cysteinyl leukotriene C4 (LTC4) and prostaglandin D2 (PGD2) from HLMCs. Incubation (6 h) of HLMC with gp120 induced the release of angiogenic (VEGF-A) and lymphangiogenic (VEGF-C) factors from HLMCs. The activating property of gp120 was mediated through the interaction with IgE VH3+ bound to FcεRI. Our data indicate that HIV gp120 is a viral superantigen, which induces the release of different proinflammatory, angiogenic, and lymphangiogenic factors from HLMCs. These observations could contribute to understanding, at least in part, the pathophysiology of chronic pulmonary diseases in HIV-infected individuals.

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Section: Discussionmentioning

confidence: 99%

HIV gp120 Induces the Release of Proinflammatory, Angiogenic, and Lymphangiogenic Factors from Human Lung Mast Cells

et al. 2020

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“…Alcohol downregulates the expression of GM-CSF receptors on the cell surface of the alveolar macrophages and impairs their immune function [ 38 ]. In HIV infection, alveolar macrophages are infected with HIV and infected cells have impaired phagocytic function as well as abnormal oxidative burst and cytokine secretion [ 39 ]. Thus, phagocytic ability of alveolar macrophages can be impaired in a different way.…”

Section: Origins Of Macrophagesmentioning

confidence: 99%

The Phagocytic Function of Macrophage-Enforcing Innate Immunity and Tissue Homeostasis

Hirayama

Iida

Nakase

2017

IJMS

655

325

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Macrophages are effector cells of the innate immune system that phagocytose bacteria and secrete both pro-inflammatory and antimicrobial mediators. In addition, macrophages play an important role in eliminating diseased and damaged cells through their programmed cell death. Generally, macrophages ingest and degrade dead cells, debris, tumor cells, and foreign materials. They promote homeostasis by responding to internal and external changes within the body, not only as phagocytes, but also through trophic, regulatory, and repair functions. Recent studies demonstrated that macrophages differentiate from hematopoietic stem cell-derived monocytes and embryonic yolk sac macrophages. The latter mainly give rise to tissue macrophages. Macrophages exist in all vertebrate tissues and have dual functions in host protection and tissue injury, which are maintained at a fine balance. Tissue macrophages have heterogeneous phenotypes in different tissue environments. In this review, we focused on the phagocytic function of macrophage-enforcing innate immunity and tissue homeostasis for a better understanding of the role of tissue macrophages in several pathological conditions.

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“…A recent study on HIV-associated noninfectious lung disease suggests development of COPD in HIV patients due to a progressive loss of CD4 cells, which yields a persistent inflammatory state from CD8 T cell overexpression. It also suggests that HIV viral protein can exert direct effect on endothelial cells leading to pulmonary artery hypertension [25]. In this new age of understanding of the disease, there has been insufficient investigation regarding its association with bronchiectasis.…”

Section: Discussionmentioning

confidence: 99%

Assessment of Bronchiectasis in HIV Patients among an Urban Population

Dronamraju

Singh

Poon

et al. 2020

Case Reports in Pulmonology

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Bronchiectasis is characterized by permanent destruction of the airways that presents with productive cough, as well as bronchial wall thickening and luminal dilatation on computed tomographic (CT) scan of the chest; it is associated with high mortality. Accumulating data suggests higher rates of bronchiectasis among the HIV-positive population. This case series involves 14 patients with bronchiectasis and HIV followed at two major urban institutions from 1999 to 2018. Demographics, clinical presentation, microbiology, radiographic imaging, and outcomes were collected and compiled. Mean age was 42 years (range 12-77 years). 36% had a CD4 count greater than 500 cells/mm3, 28% had a CD4 count between 200 and 500 cells/mm3, and 36% had AIDS. 43% were treated for Pneumocystis jiroveci pneumonia (PJP) and 50% for Mycobacterium avium complex (MAC) infection. 21% had COPD, 7% had asthma, and 7% had a history of pulmonary aspergillosis. Two patients were followed up by pulmonary services after diagnosis of bronchiectasis on CT. The timeline of the follow-up in these cases was within months and after three years respectively. It is posited that the prevalence of bronchiectasis in HIV patients may be underestimated. Improving recognition and management of bronchiectasis could help diminish rehospitalization rates.

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Mechanisms Underlying HIV-Associated Noninfectious Lung Disease

Cited by 26 publications

References 73 publications

HIV gp120 Induces the Release of Proinflammatory, Angiogenic, and Lymphangiogenic Factors from Human Lung Mast Cells

HIV gp120 Induces the Release of Proinflammatory, Angiogenic, and Lymphangiogenic Factors from Human Lung Mast Cells

The Phagocytic Function of Macrophage-Enforcing Innate Immunity and Tissue Homeostasis

Assessment of Bronchiectasis in HIV Patients among an Urban Population

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