Macrophage Polarization in AIDS: Dynamic Interface between Anti-Viral and Anti-Inflammatory Macrophages during Acute and Chronic Infection

Burdo, Tricia H.; Walker, Joshua; Williams, Kenneth C.

doi:10.4172/2155-9899.1000333

Cited by 22 publications

(19 citation statements)

References 82 publications

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“…Macrophage polarization is relevant in HIV infection where acute and chronic inflammation, characterized by different macrophage polarization states, are present at different stages of disease (47). Disease progression is associated with a shift in the cytokine environment from a type-1 inflammatory environment to a type-2 immunosuppressive environment (48–50) and is posited to drive the shift from HIV infection-driven M1 polarization of macrophages (51) toward an M2 polarization state (47, 52). The effects of M1 and M2 polarization in vivo are varied, with each stimulating pathways that both benefit and inhibit host defenses, as discussed extensively (52).…”

Section: Monocyte/macrophage Biologymentioning

confidence: 99%

The HIV Reservoir in Monocytes and Macrophages

Jaworowski²,

2019

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In people living with HIV (PLWH) who are failing or unable to access combination antiretroviral therapy (cART), monocytes and macrophages are important drivers of pathogenesis and progression to AIDS. The relevance of the monocyte/macrophage reservoir in PLWH receiving cART is debatable as in vivo evidence for infected cells is limited and suggests the reservoir is small. Macrophages were assumed to have a moderate life span and lack self-renewing potential, but recent discoveries challenge this dogma and suggest a potentially important role of these cells as long-lived HIV reservoirs. This, combined with new HIV infection animal models, has led to a resurgence of interest in monocyte/macrophage reservoirs. Infection of non-human primates with myeloid-tropic SIV implicates monocyte/macrophage activation and infection in the brain with neurocognitive disorders, and infection of myeloid-only humanized mouse models are consistent with the potential of the monocyte/macrophage reservoir to sustain infection and be a source of rebound viremia following cART cessation. An increased resistance to HIV-induced cytopathic effects and a reduced susceptibility to some antiretroviral drugs implies macrophages may be relevant to residual replication under cART and to rebound viremia. With a reappraisal of monocyte circulation dynamics, and the development of techniques to differentiate between self-renewing tissue-resident, and monocyte-derived macrophages in different tissues, a new framework exists to contextualize and evaluate the significance and relevance of the monocyte/macrophage HIV reservoir. In this review, we discuss recent developments in monocyte and macrophage biology and appraise current and emerging techniques to quantify the reservoir. We discuss how this knowledge influences our evaluation of the myeloid HIV reservoir, the implications for HIV pathogenesis in both viremic and virologically-suppressed PLWH and the need to address the myeloid reservoir in future treatment and cure strategies.

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Section: Monocyte/macrophage Biologymentioning

confidence: 99%

The HIV Reservoir in Monocytes and Macrophages

Jaworowski²,

2019

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“…Chronic HIV-1-associated immune activation also leads to altered secretion of pro-and anti-inflammatory cytokines, chemokines, and ultimately, dysregulation of the host immune system. In addition, HIV-infected macrophages have been implicated in the elimination of effector CD8+ T cells (Alfano et al, 2013;Burdo et al, 2015;Cassol et al, 2010;Shi & Pamer, 2011;Sica et al, 2015). In summary, M1 and M2 macrophages clearly play an important role in early, late and chronic HIV and SIV function and finally tissue pathology.…”

Section: Viral Infectionmentioning

confidence: 99%

Section: Viral Infectionmentioning

confidence: 99%

“…Polarized activation of macrophages has been associated with HIV, SIV, Kaposi's sarcoma-associated herpesvirus The most prominent dysfunction in individuals with advanced HIV is defect in migration of circulating monocytes in response to chemoattractants (Burdo et al, 2015). Monocytes as well as lung alveolar macrophages isolated from HIV infected patients have also shown reduced phagocytic activity, decreased both phagosome-lysosome fusion, and intracellular killing of opportunistic pathogens (Burdo et al, 2015;Cassol et al, 2010). These functional defects result in the inefficient control of infection with opportunistic pathogens infection, enhancement of viral replications, further macrophage activation and finally disease pathogenesis.…”

Section: Viral Infectionmentioning

confidence: 99%

“…A good example of macrophage polarization, and function by viral pathogen are showed by human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infection (Alfano, Graziano, Genovese, & Poli, 2013;Burdo et al, 2015;Cassol, Cassetta, Alfano, & Poli, 2010). The polarization of macrophages toward the M1 phenotype is important for efficient anti-viral immune responses (Burdo et al, 2015). Polarized activation of macrophages has been associated with HIV, SIV, Kaposi's sarcoma-associated herpesvirus The most prominent dysfunction in individuals with advanced HIV is defect in migration of circulating monocytes in response to chemoattractants (Burdo et al, 2015).…”

Section: Viral Infectionmentioning

confidence: 99%

See 2 more Smart Citations

Macrophage plasticity, polarization, and function in health and disease

Shapouri‐Moghaddam

Mohammadian

Vazini

et al. 2018

Journal Cellular Physiology

3,117

2,541

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Macrophages are heterogeneous and their phenotype and functions are regulated by the surrounding micro-environment. Macrophages commonly exist in two distinct subsets: 1) Classically activated or M1 macrophages, which are pro-inflammatory and polarized by lipopolysaccharide (LPS) either alone or in association with Th1 cytokines such as IFN-γ, GM-CSF, and produce pro-inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, IL-12, IL-23, and TNF-α; and 2) Alternatively activated or M2 macrophages, which are anti-inflammatory and immunoregulatory and polarized by Th2 cytokines such as IL-4 and IL-13 and produce anti-inflammatory cytokines such as IL-10 and TGF-β. M1 and M2 macrophages have different functions and transcriptional profiles. They have unique abilities by destroying pathogens or repair the inflammation-associated injury. It is known that M1/M2 macrophage balance polarization governs the fate of an organ in inflammation or injury. When the infection or inflammation is severe enough to affect an organ, macrophages first exhibit the M1 phenotype to release TNF-α, IL-1β, IL-12, and IL-23 against the stimulus. But, if M1 phase continues, it can cause tissue damage. Therefore, M2 macrophages secrete high amounts of IL-10 and TGF-β to suppress the inflammation, contribute to tissue repair, remodeling, vasculogenesis, and retain homeostasis. In this review, we first discuss the basic biology of macrophages including origin, differentiation and activation, tissue distribution, plasticity and polarization, migration, antigen presentation capacity, cytokine and chemokine production, metabolism, and involvement of microRNAs in macrophage polarization and function. Secondly, we discuss the protective and pathogenic role of the macrophage subsets in normal and pathological pregnancy, anti-microbial defense, anti-tumor immunity, metabolic disease and obesity, asthma and allergy, atherosclerosis, fibrosis, wound healing, and autoimmunity.

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Tumor hijacks macrophages and microbiota through extracellular vesicles

Jiang

Mei

et al. 2022

Exploration

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The tumor microenvironment (TME) is a biological system with sophisticated constituents. In addition to tumor cells, tumor‐associated macrophages (TAMs) and microbiota are also dominant components. The phenotypic and functional changes of TAMs are widely considered to be related to most tumor progressions. The chronic colonization of pathogenic microbes and opportunistic pathogens accounts for the generation and development of tumors. As messengers of cell‐to‐cell communication, tumor‐derived extracellular vesicles (TDEVs) can transfer various malignant factors, regulating physiological and pathological changes in the recipients and affecting TAMs and microbes in the TME. Despite the new insights into tumorigenesis and progress brought by the above factors, the crosstalk among tumor cells, macrophages, and microbiota remain elusive, and few studies have focused on how TDEVs act as an intermediary. We reviewed how tumor cells recruit and domesticate macrophages and microbes through extracellular vehicles and how hijacked macrophages and microbiota interact with tumor‐promoting feedback, achieving a reciprocal coexistence under the TME and working together to facilitate tumor progression. It is significant to seek evidence to clarify those specific interactions and reveal therapeutic targets to curb tumor progression and improve prognosis.

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Macrophage Polarization in AIDS: Dynamic Interface between Anti-Viral and Anti-Inflammatory Macrophages during Acute and Chronic Infection

Cited by 22 publications

References 82 publications

The HIV Reservoir in Monocytes and Macrophages

The HIV Reservoir in Monocytes and Macrophages

Macrophage plasticity, polarization, and function in health and disease

Tumor hijacks macrophages and microbiota through extracellular vesicles

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