Publications by authors named "Liz Simon"

Background: Increased survival, prolonged antiretroviral treatment (ART), and lifestyle choices, including alcohol misuse, increase the risk for comorbid conditions, including cardiometabolic comorbidities among people with HIV (PWH). Published studies indicate that dysregulated adipose tissue phenotype, particularly of the visceral adipose depot, contributes to metabolic dysregulation. Using a nonhuman primate model of simian immunodeficiency virus (SIV) infection, we previously demonstrated that chronic binge alcohol (CBA) administration to ART-treated rhesus macaques decreases whole-body glucose-insulin dynamics, increases omental adipose tissue (OmAT) collagen content, decreases OmAT adipocyte size, and alters pancreatic endocrine function.

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Human immunodeficiency virus (HIV) infection produces neurological comorbidities including HIV-associated neurocognitive disorder (HAND) and chronic pain. HIV also increases the risk of developing an alcohol use disorder (AUD). With the rising prevalence of AUD in women and people with HIV (PWH), understanding the neurobiological impact of alcohol in these populations is important.

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Millions of Americans live with chronic inflammatory pain conditions, and the prevalence of these conditions increases with age and is higher in females. Still, it is poorly understood how sex, age and peripheral gene expression affect the trajectory of chronic inflammatory pain conditions. We used the inflammatory agent, Complete Freund's Adjuvant (CFA), to systematically test sex and age effects on mechanical and thermal sensitivity in adolescent and adult male and female Wistar rats over 3 weeks (Experiment 1 [onset]) or 11 weeks (Experiment 2 [recovery]).

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Background: People with HIV (PWH) are at increased risk for cardiometabolic comorbidities. We have reported that lifetime alcohol use among people with HIV (PWH) is associated with increased risk for metabolic syndrome. Dysfunctional adipose tissue and altered circulating adipokines mediate metabolic dysregulation.

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Chronic alcohol use leads to metabolic dysfunction in adipose tissue. The underlying mechanisms and the contribution of alcohol-induced adipose tissue dysfunction to systemic metabolic dysregulation are not well understood. In our previous studies, we found that chronic alcohol feeding induces mesenteric lymphatic leakage, perilymphatic adipose tissue (PLAT) inflammation, and local insulin resistance in rats.

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Article Synopsis
  • People with existing health issues, like metabolic problems, face higher risks for severe complications from SARS-CoV-2, and a high fat, high sugar diet (HFSD) and alcohol use may raise virus entry-related factors in cells.
  • A study on SIV-infected macaques found that those on an HFSD had significantly higher levels of the ACE2 receptor in lung and pancreatic tissues compared to those on a standard diet, while alcohol consumption did not affect these levels.
  • The findings suggest that a poor diet might heighten the risk for infections like COVID-19 by increasing key receptor expressions, highlighting the link between diet quality and virus susceptibility.
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  • This study investigates how chronic binge alcohol (CBA) affects liver metabolism in female rhesus macaques infected with SIV and treated with antiretroviral therapy (ART), focusing on their diet.
  • Researchers compared the liver characteristics of macaques on CBA versus a control group for 14.5 months, measuring gene and protein expression related to metabolism.
  • The findings indicate that CBA macaques showed increased expression of enzymes linked to glucose and lipid metabolism without signs of fat buildup (steatosis) or blood sugar issues, suggesting potential future health risks with poorer diets or environmental factors.
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  • Alcohol misuse in people with HIV and chronic binge alcohol in SIV-infected macaques lead to increased physical frailty and impaired muscle function, with specific microRNAs (myomiRs) involved in this impairment.
  • Previous research found that myomiRs are expressed differently in muscle from alcohol-administered macaques, impacting the differentiation of muscle stem cells (myoblasts).
  • The current study showed that delivering extracellular vesicle (EV)-carried miR-206 improves myoblast differentiation and muscle cell growth, suggesting EVs could be a potential treatment to enhance muscle function in individuals affected by alcohol-related issues.
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Alcohol misuse and HIV independently induce myopathy. We previously showed that chronic binge alcohol (CBA) administration, with or without simian immunodeficiency virus (SIV), decreases differentiation capacity of male rhesus macaque myoblasts. We hypothesized that short-term alcohol and CBA/SIV would synergistically decrease differentiation capacity and impair bioenergetic parameters in female macaque myoblasts.

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Article Synopsis
  • Alcohol-related myopathy occurs early in alcohol users and worsens with long-term abuse, affecting skeletal muscle mass and function through various complex mechanisms.
  • This evidence-based review analyzed peer-reviewed studies from January 2012 to November 2022, focusing on the acute and chronic impacts of alcohol on skeletal muscle, yielding 96 relevant research papers out of 708 initial studies.
  • The findings highlight that alcohol use reduces protein synthesis, increases protein degradation, and disrupts mitochondrial functions, but there is a lack of comprehensive studies on the specific mechanisms involved.
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Background: Effective antiretroviral therapy (ART) in people living with HIV (PLWH) has improved life expectancy and increased risk of age-associated cardiometabolic comorbidities. At-risk alcohol use is more frequent among PLWH and increases the risk of health challenges. PLWH with at-risk alcohol use are more likely to meet criteria for prediabetes/diabetes and this is associated with impaired whole-body glucose-insulin dynamics.

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Article Synopsis
  • * Mitochondria are important for various cellular functions beyond energy production, such as immune activation and nutrient sensing; however, alcohol impairs their function, leading to the generation of harmful reactive oxygen species (ROS) and accumulation of dysfunctional mitochondria.
  • * This review explores how alcohol-induced mitochondrial dysfunction disrupts immunometabolism, both in terms of immune cell influence on tissue metabolism and immune cell energy usage, ultimately contributing to tissue injury.
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Article Synopsis
  • People with HIV often engage in risky alcohol use, which can accelerate neurocognitive decline, although the mechanisms behind this association (HIV-associated neurocognitive disorder - HAND) are still being studied.
  • Research has indicated that chronic binge alcohol consumption in SIV-infected macaques leads to behavioral issues and neuroinflammation, with some effects mitigated by antiretroviral therapy (ART).
  • The study explored how gene expression related to opioid, tachykinin, and endocannabinoid systems varied in both the frontal cortex and peripheral blood, revealing complex interactions between SIV, alcohol use, and ART, but did not find consistent changes between blood and brain gene expressions.
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People living with HIV (PLWH) represent a vulnerable population to adverse musculoskeletal outcomes due to HIV infection, antiretroviral therapy (ART), and at-risk alcohol use. Developing measures to prevent skeletal degeneration in this group requires a grasp of the relationship between alcohol use and low bone mass in both the PLWH population and its constituents as defined by sex, age, and race. We examined the association of alcohol use with serum biochemical markers of bone health in a diverse cohort of PLWH enrolled in the New Orleans Alcohol Use in HIV (NOAH) study.

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Our studies in chronic binge alcohol (CBA) -treated simian immunodeficiency virus (SIV)-infected macaques and in people living with HIV (PLWH) show significant alterations in metabolic homeostasis. CBA promotes a profibrotic phenotype in adipose tissue and skeletal muscle (SKM) and decreases adipose-derived stem cell and myoblast differentiation, making adipose and SKM potential drivers in metabolic dysregulation. Furthermore, we have shown that the differential expression of microRNAs (miRs) in SKM contributes to impaired myoblast differentiation potential.

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Article Synopsis
  • Antiretroviral therapy has significantly improved life expectancy for people living with HIV (PLWH), but they still face higher risks of age-related health issues, such as frailty.
  • A study involving 341 participants found that specific body composition metrics, like fat-free mass and waist-to-hip ratio, are linked to frailty risk, but not all measures had the same impact depending on factors like substance use and physical activity.
  • The results indicated that muscle strength and recent alcohol use were important moderators in the relationship between body composition and frailty, with variations based on individual characteristics such as strength levels and body mass index (BMI).
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At-risk alcohol use is associated with multisystemic effects and end-organ injury, and significantly contributes to global health burden. Several alcohol-mediated mechanisms have been identified, with bioenergetic maladaptation gaining credence as an underlying pathophysiological mechanism contributing to cellular injury. This evidence-based review focuses on the current knowledge of alcohol-induced bioenergetic adaptations in metabolically active tissues: liver, cardiac and skeletal muscle, pancreas, and brain.

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Article Synopsis
  • Effective antiretroviral therapy has made HIV a manageable chronic disease, particularly impacting those over 50, with HIV targeting specific immune cells (CD4 T cells) that express co-receptors CCR5 and CXCR4.
  • Research on male rhesus macaques shows that chronic binge alcohol consumption increases the percentage of gut CD4 T cells expressing the co-receptor CXCR4 and that hormone loss may raise levels of activated T cells.
  • The study found that combining chronic binge alcohol and ovariectomy in SIV-infected female macaques resulted in higher levels of activated CD4 T cells and disrupted mitochondrial homeostasis, offering insights into alcohol's effects on viral expression in these cells.
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On November 19th, 2021, the annual Alcohol and Immunology Research Interest Group (AIRIG) meeting was held at Loyola University Chicago Health Sciences Campus in Maywood, Illinois. The 2021 meeting focused on how alcohol misuse is linked to immune system derangements, leading to tissue and organ damage, and how this research can be translated into improving treatment of alcohol-related disease. This meeting was divided into three plenary sessions: the first session focused on how alcohol misuse affects different parts of the immune system, the second session presented research on mechanisms of organ damage from alcohol misuse, and the final session highlighted research on potential therapeutic targets for treating alcohol-mediated tissue damage.

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CD4 T cell differentiation to pro-inflammatory and immunosuppressive subsets depends on immunometabolism. Pro-inflammatory CD4 subsets rely on glycolysis, while immunosuppressive Treg cells require functional mitochondria for their differentiation and function. Previous pre-clinical studies have shown that ethanol (EtOH) administration increases pro-inflammatory CD4 T cell subsets; whether this shift in immunophenotype is linked to alterations in CD4 T cell metabolism had not been previously examined.

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At-risk alcohol use is a major contributor to the global health care burden and leads to preventable deaths and diseases including alcohol addiction, alcoholic liver disease, cardiovascular disease, diabetes, traumatic injuries, gastrointestinal diseases, cancers, and fetal alcohol syndrome. Excessive and frequent alcohol consumption has increasingly been linked to alcohol-associated tissue injury and pathophysiology, which have significant adverse effects on multiple organ systems. Extensive research in animal and in vitro models has elucidated the salient mechanisms involved in alcohol-induced tissue and organ injury.

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At-risk alcohol use is a significant risk factor associated with multisystemic pathophysiological effects leading to multiorgan injury and contributing to 5.3% of all deaths worldwide. The alcohol-mediated cellular and molecular alterations are particularly salient in vulnerable populations, such as people living with HIV (PLWH), diminishing their physiological reserve, and accelerating the aging process.

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Progression of chronic infections to end-stage diseases and poor treatment results are frequently associated with alcohol abuse. Alcohol metabolism suppresses innate and adaptive immunity leading to increased viral load and its spread. In case of hepatotropic infections, viruses accelerate alcohol-induced hepatitis and liver fibrosis, thereby promoting end-stage outcomes, including cirrhosis and hepatocellular carcinoma (HCC).

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People living with HIV (PLWH) have increased prevalence of comorbid conditions including insulin resistance and at-risk alcohol use. Circulating microRNAs (miRs) may serve as minimally invasive indicators of pathophysiological states. We aimed to identify whether alcohol modulates circulating miR associations with measures of glucose/insulin dynamics in PLWH.

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Aims: To assess whether binge drinking and heavy alcohol use are associated with increased sugar and fat consumption among a Southern cohort of people living with HIV (PWH).

Methods: This was a cross-sectional analysis of PWH enrolled in the New Orleans Alcohol use in HIV (NOAH) Study (n = 215). Binge and heavy drinking were identified through a 30-day Alcohol Timeline-Followback and dietary intake was assessed through a 24-hour dietary recall.

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