Abstract:Given that infection with Mycobacterium tuberculosis (Mtb) is the leading cause of death amongst individuals living with HIV, understanding the complex mechanisms by which Mtb exacerbates HIV infection may lead to improved treatment options or adjuvant therapies. While it is well-understood how HIV compromises the immune system and leaves the host vulnerable to opportunistic infections such as Mtb, less is known about the interplay of disease once active Mtb is established. This review explores how glutathione… Show more
“…Moreover, there are specific host pathways, such as the PPARγ and LXR transcriptional regulators, that have revealed the mechanisms by which host immunity alters the bacterial microenvironment. One hallmark of tuberculosis infection is the accumulation of M.tb-infected foamy macrophages containing large lipid bodies ( Wong et al, 2020 ). In this review, we focus on emerging concepts and the current understanding of lipid utilization in M.tb, how the immune response modulates lipid homeostasis in both the bacterium and the host, and how these pathways are likely to be manipulated therapeutically.…”
Section: Diseases Related To Lipid Droplets and Immune Cellsmentioning
Lipid droplets (LDs) are commonly found in various biological cells and are organelles related to cell metabolism. LDs, the number and size of which are heterogeneous across cell type, are primarily composed of polar lipids and proteins on the surface with neutral lipids in the core. Neutral lipids stored in LDs can be degraded by lipolysis and lipophagocytosis, which are regulated by various proteins. The process of LD formation can be summarized in four steps. In addition to energy production, LDs play an extremely pivotal role in a variety of physiological and pathological processes, such as endoplasmic reticulum stress, lipid toxicity, storage of fat-soluble vitamins, regulation of oxidative stress, and reprogramming of cell metabolism. Interestingly, LDs, the hub of integration between metabolism and the immune system, are involved in antitumor immunity, anti-infective immunity (viruses, bacteria, parasites, etc.) and some metabolic immune diseases. Herein, we summarize the role of LDs in several major immune cells as elucidated in recent years, including T cells, dendritic cells, macrophages, mast cells, and neutrophils. Additionally, we analyze the role of the interaction between LDs and immune cells in two typical metabolic immune diseases: atherosclerosis and Mycobacterium tuberculosis infection.
“…Moreover, there are specific host pathways, such as the PPARγ and LXR transcriptional regulators, that have revealed the mechanisms by which host immunity alters the bacterial microenvironment. One hallmark of tuberculosis infection is the accumulation of M.tb-infected foamy macrophages containing large lipid bodies ( Wong et al, 2020 ). In this review, we focus on emerging concepts and the current understanding of lipid utilization in M.tb, how the immune response modulates lipid homeostasis in both the bacterium and the host, and how these pathways are likely to be manipulated therapeutically.…”
Section: Diseases Related To Lipid Droplets and Immune Cellsmentioning
Lipid droplets (LDs) are commonly found in various biological cells and are organelles related to cell metabolism. LDs, the number and size of which are heterogeneous across cell type, are primarily composed of polar lipids and proteins on the surface with neutral lipids in the core. Neutral lipids stored in LDs can be degraded by lipolysis and lipophagocytosis, which are regulated by various proteins. The process of LD formation can be summarized in four steps. In addition to energy production, LDs play an extremely pivotal role in a variety of physiological and pathological processes, such as endoplasmic reticulum stress, lipid toxicity, storage of fat-soluble vitamins, regulation of oxidative stress, and reprogramming of cell metabolism. Interestingly, LDs, the hub of integration between metabolism and the immune system, are involved in antitumor immunity, anti-infective immunity (viruses, bacteria, parasites, etc.) and some metabolic immune diseases. Herein, we summarize the role of LDs in several major immune cells as elucidated in recent years, including T cells, dendritic cells, macrophages, mast cells, and neutrophils. Additionally, we analyze the role of the interaction between LDs and immune cells in two typical metabolic immune diseases: atherosclerosis and Mycobacterium tuberculosis infection.
“…HIV may potentiate mycobacterial virulence factors and has a significant impact on the progression of TB ( 4 , 5 ). TB also promotes cellular susceptibility to HIV and drives HIV replication ( 5 , 6 ).…”
BackgroundTuberculosis (TB) is an important opportunistic infection in acquired immunodeficiency diseases (AIDS). Although the frequency of CD4+CD8+ double-positive (DP) T cells has been observed to increase in pathological conditions, their role (phenotypic and functional) is poorly described, especially in human immunodeficiency virus (HIV) infection with TB (HIV/TB (HT) coinfection).MethodsThe percentage and phenotypic and functional properties of peripheral blood DP T cells in patients with HT coinfection in comparison to uninfected controls and to patients with HIV or TB mono-infection were analyzed by direct intracellular cytokine staining (ICS).ResultsTotal and CD4lowCD8high DP T cells were significantly increased in patients with both HIV and TB mono-infection, especially in patients with HT coinfection. Compared with healthy controls (HCs), the percentage of DP T cells expressing chemokine receptor 5 (CCR5) in patients with HT coinfection was significantly higher. Compared with HCs and patients with TB, a lower percentage of tumor necrosis factor α (TNF-α) secreting DP T cells and a higher percentage of granzyme A-secreting DP T cells were observed in patients with HIV mono-infection and HT coinfection, respectively. In addition, DP T cells expressed more cytolytic markers (granzyme A and perforin) than CD4+ T cells, but similarly to CD8+ T cells in patients with HT coinfection.ConclusionsOur data suggested that HT coinfection resulted in a marked increase in DP T cells, especially the CD4lowCD8high subpopulation. DP T cells may be susceptible to HT coinfection, and have the same cytotoxic function as CD8+ T cells.
“…The syndemic interaction between the human immunodeficiency virus (HIV) and multidrugresistant tuberculosis (MDR-TB) epidemics has had deadly consequences around the world [1]. World health organization (WHO) has recommended the rapid molecular test called Xpert MTB/RIF assay which gives the results within two hours in addition to detecting rifampicin resistance and being more accurate than sputum smear microscopy for diagnosis [2].…”
Background: human immunodeficiency virus (HIV) infection triggers massive depletion of cluster of differentiation type 4 (CD4) T cells and is a known cause of developing active pulmonary tuberculosis (TB). Mycobacterium tuberculosis (Mtb) infection also has a negative impact on the immune response to HIV, accelerating the progression from HIV infection to AIDS. Aim of the work: is evaluation of plasma level of CD4 + and CD8 + T cells in multi drug resistant tuberculosis (MDR/ TB) co infected with HIV. Materials and methods: This is a case-control study. A total of 130 participants were consecutively selected for the study.
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