Inhibiting Adenosine Receptor Signaling Promotes Accumulation of Effector CD4+ T Cells in the Lung Parenchyma During Severe Tuberculosis

Amaral, Eduardo Pinheiro; Salles, Érika Machado de; Bomfim, Caio César Barbosa; Salgado, Rafael Moysés; Almeida, Fabrício Moreira; Souza, Paula Carolina de; Álvarez, José María; Hirata, Mário Hiroyuki; Lassounskaia, Elena; Lima, Maria Regina D'Império

doi:10.1093/infdis/jiy586

Cited by 15 publications

(16 citation statements)

References 45 publications

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“…Chen, 2013; S. R. Ma et al, 2017). Briefly, proinflammatory ATP released from injured and necrotic cells to the extracellular space is sequentially converted into adenosine monophosphate (AMP) and adenosine by surface‐expressing CD39 (ENTPDase‐1) and CD73 (NT5E), which drives a shift from an ATP‐driven proinflammatory environment to an anti‐inflammatory milieu induced by adenosine (Amaral et al, 2019; Antonioli, Pacher, Vizi, & Hasko, 2013; Roberts, Stagg, & Dwyer, 2014). Adenosine mediates immunoregulatory effects by binding to adenosine receptors (A1R, A2AR, A2BR, and A3R) on the surface of various immune cells such as T, B, and natural killer (NK) cells (Bastid et al, 2015; Clayton, Al‐Taei, Webber, Mason, & Tabi, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…(ENTPDase-1) and CD73 (NT5E), which drives a shift from an ATPdriven proinflammatory environment to an anti-inflammatory milieu induced by adenosine (Amaral et al, 2019;Antonioli, Pacher, Vizi, & Hasko, 2013;Roberts, Stagg, & Dwyer, 2014). Adenosine mediates immunoregulatory effects by binding to adenosine receptors (A1R, A2AR, A2BR, and A3R) on the surface of various immune cells such as T, B, and natural killer (NK) cells (Bastid et al, 2015;Clayton, Al-Taei, Webber, Mason, & Tabi, 2011).…”

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confidence: 99%

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The role of the CD39–CD73–adenosine pathway in liver disease

Wang

Gao

Zhou

et al. 2020

Journal Cellular Physiology

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Extracellular adenosine triphosphate (ATP) is a danger signal released by dying and damaged cells, and it functions as an immunostimulatory signal that promotes inflammation. The ectonucleotidases CD39/ectonucleoside triphosphate diphosphohydrolase-1 and CD73/ecto-5′-nucleotidase are cell-surface enzymes that breakdown extracellular ATP into adenosine. This drives a shift from an ATP-driven proinflammatory environment to an anti-inflammatory milieu induced by adenosine. The CD39-CD73-adenosine pathway changes dynamically with the pathophysiological context in which it is embedded. Accumulating evidence suggests that CD39 and CD73 play important roles in liver disease as critical components of the extracellular adenosinergic pathway. Recent studies have shown that the modification of the CD39-CD73-adenosine pathway alters the liver's response to injury. Moreover, adenosine exerts different effects on the pathophysiology of the liver through different receptors. In this review, we aim to describe the role of the CD39-CD73-adenosine pathway and adenosine receptors in liver disease, highlighting potential therapeutic targets in this pathway, which will facilitate the development of therapeutic strategies for the treatment of liver disease.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

The role of the CD39–CD73–adenosine pathway in liver disease

Wang

Gao

Zhou

et al. 2020

Journal Cellular Physiology

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“…The coffee or caffeine consumption has many other effects on the liver and lung. We summarize these emerging findings in the Table 2 [6,28,29,30,31,32,33,34,35,36,37,38,39,40,41] and Table 3 [24,26,42,43,44,45,46,47,48,49,50].…”

Section: Discussionmentioning

confidence: 99%

Effects of Caffeine Treatment on Hepatopulmonary Syndrome in Biliary Cirrhotic Rats

Chang

Chuang

Tsai

et al. 2019

IJMS

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Hepatopulmonary syndrome (HPS) is a lethal complication of cirrhosis characterized by hypoxia and overt intrapulmonary shunting. In this study, we investigated the effect of caffeine in rats with common bile duct ligation (CBDL)-induced liver cirrhosis and HPS. CBDL rats were randomly allocated to receive caffeine or vehicle for 14 days. On the 28th day after CBDL, mortality rate, hemodynamics, liver, and renal biochemistry parameters and arterial blood gas analysis were evaluated. Lung and liver were dissected for the evaluation of inflammation, angiogenesis and protein expressions. In another series with parallel groups, the intrapulmonary shunting was determined. Caffeine significantly reduced portal pressure (caffeine vs. control: 10.0 ± 3.7 vs. 17.0 ± 8.1 mmHg, p < 0.05) in CBDL rats. The mortality rate, mean arterial pressure, biochemistry data and hypoxia were similar between caffeine-treated and control groups. Caffeine alleviated liver fibrosis and intrahepatic angiogenesis but intrapulmonary inflammation and angiogenesis were not ameliorated. The hepatic VEGF/Rho-A protein expressions were down-regulated but the pulmonary inflammation- and angiogenesis-related protein expressions were not significantly altered by caffeine. Caffeine did not reduce the intrapulmonary shunting, either. Caffeine has been shown to significantly improve liver fibrosis, intrahepatic angiogenesis and portal hypertension in cirrhotic rats, however, it does not ameliorate HPS.

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“…The Beijing complex, of which the MTB strain MIRU-VNTR 42425 is an example, has been associated with severe outcomes, extrapulmonary infection [19], and hypervirulence [20]. This strain complex is also highly prevalent in extensively and multiple drug (X/MDR) TB cases, suggesting development of resistance may be associated with the pathogenic characteristics, immune evasion, and aggressive nature of the infection [21,22,23,24].…”

Section: Discussionmentioning

confidence: 99%

Severe Clinical Outcomes of Tuberculosis in Kharkiv Region, Ukraine, Are Associated with Beijing Strains of Mycobacterium tuberculosis

et al. 2019

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Genotypic variation in Beijing lineages of Mycobacterium tuberculosis (MTB), the causative agent of tuberculosis (TB), has been associated with hyper virulence and the spread of extensively and multiple drug (X/MDR) resistant MTB strains in Eastern Europe, Central Asia, and East Asia. The clinical outcomes of 215 new cases of TB among the population of the Kharkiv region of Eastern Ukraine were analyzed to uncover factors associated with severe infection. Infecting MTB strains were profiled by 5 locus exact tandem repeats (ETRs) and 15 locus mycobacterial interspersed repetitive unit-variable number tandem repeat (MIRU-VNTR) genotyping. Among diverse MTB genotypes discovered in Ukraine, the Beijing genotype (MIRU-VNTR 42425) was significantly associated with risk factors for severe outcomes of disease in the study population, including TB/HIV co-infection and treatment failure. Strain replacement (superinfection) was observed in 10 patients, suggesting repeated exposure to novel MTB strains in hospital or community settings. Inclusion of MTB genotyping data may identify at-risk patients and improve treatment adherence to prevent X/MDR development for effective public health response against tuberculosis in Ukraine.

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Inhibiting Adenosine Receptor Signaling Promotes Accumulation of Effector CD4+ T Cells in the Lung Parenchyma During Severe Tuberculosis

Cited by 15 publications

References 45 publications

The role of the CD39–CD73–adenosine pathway in liver disease

The role of the CD39–CD73–adenosine pathway in liver disease

Effects of Caffeine Treatment on Hepatopulmonary Syndrome in Biliary Cirrhotic Rats

Severe Clinical Outcomes of Tuberculosis in Kharkiv Region, Ukraine, Are Associated with Beijing Strains of Mycobacterium tuberculosis

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