Systems-based approach to examine the cytokine responses in primary mouse lung macrophages infected with low pathogenic avian Influenza virus circulating in South East Asia

Taye, Biruhalem; Chen, Hui; Myaing, Myint Zu; Tan, Boon Huan; Maurer‐Stroh, Sebastian; Sugrue, Richard J.

doi:10.1186/s12864-017-3803-6

Cited by 3 publications

(2 citation statements)

References 93 publications

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“…Transcriptomic data showed metabolic genes, including Irg1, Ca2, Pfkfb3, and Hk2, among the top 100 most upregulated genes in alveolar MØ after IAV infection. This result was consistent with in vitro MØ studies in which IAV induced the expression of glycolytic metabolic genes concomitant to increased extracellular acidification associated with glycolysis 225. Switching from OXPHOS to glycolysis facilitates ROS production mediated by dedicated enzymes, such as NADPH oxidases.…”

supporting

confidence: 89%

Fueling influenza and the immune response: Implications for metabolic reprogramming during influenza infection and immunometabolism

Bahadoran

Bezavada

Smallwood

2020

Immunological Reviews

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The metabolic impact of influenza A virus (IAV) infections on immune cells remains largely uncharacterized. However, much is known about the metabolism of IAV infection and immunometabolism. Thus, we will consider four main factors: the metabolic requirements of influenza virus, metabolic reprogramming of immune cells that are mobilized to fight IAV infection, the impact of systemic or local metabolism on the infection and immune response, and vice versa. We will also address the interplay of metabolism and cytokines with a focus on those relevant to IAV infections. Finally, we will limit information on immunometabolism to key cell types critical to fighting IAV infection. We will relate this information to the unique metabolic demands on immune cells and discuss how their translocation through nutrient diverse and changing environments may affect their functions in IAV infection. | ME TABOLIS M AND THE LUNG MICROENVIRONMENT | Steady-state metabolismUnder aerobic conditions, cells sustain themselves catabolically using glycolytic carbons to fuel the tricarboxylic acid (TCA) cycle. AbstractRecent studies support the notion that glycolysis and oxidative phosphorylation are rheostats in immune cells whose bioenergetics have functional outputs in terms of their biology. Specific intrinsic and extrinsic molecular factors function as molecular potentiometers to adjust and control glycolytic to respiratory power output. In many cases, these potentiometers are used by influenza viruses and immune cells to support pathogenesis and the host immune response, respectively. Influenza virus infects the respiratory tract, providing a specific environmental niche, while immune cells encounter variable nutrient concentrations as they migrate in response to infection. Immune cell subsets have distinct metabolic programs that adjust to meet energetic and biosynthetic requirements to support effector functions, differentiation, and longevity in their ever-changing microenvironments. This review details how influenza coopts the host cell for metabolic reprogramming and describes the overlap of these regulatory controls in immune cells whose function and fate are dictated by metabolism. These details are contextualized with emerging evidence of the consequences of influenzainduced changes in metabolic homeostasis on disease progression. K E Y W O R D Shost pathogen, immune response, Immunometabolism, Influenza, metabolism, viral infection, virus | 141 BAHADORAN et Al.

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supporting

confidence: 89%

Fueling influenza and the immune response: Implications for metabolic reprogramming during influenza infection and immunometabolism

Bahadoran

Bezavada

Smallwood

2020

Immunological Reviews

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“…Following infection with various IAV strains, excessive levels of inflammatory mediators and widespread tissue damage can be observed in the lung, a target tissue for respiratory viruses ( Jang et al, 2012 ; Burggraaf et al, 2014 ; Herold et al, 2015 ; Taye et al, 2017 ). Moreover, several studies have shown that neurotropic and even non-neurotropic IAV infections lead to the release of inflammatory mediators in the brain ( Jang et al, 2012 ; Jurgens et al, 2012 ; Hosseini et al, 2018 ; Düsedau et al, 2021 ).…”

Section: Resultsmentioning

confidence: 99%

Influenza vaccine is able to prevent neuroinflammation triggered by H7N7 IAV infection

et al. 2023

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Influenza A virus (IAV) subtypes are a major cause of illness and mortality worldwide and pose a threat to human health. Although IAV infection is considered a self-limiting respiratory syndrome, an expanded spectrum of cerebral manifestations has been reported following IAV infection. Neurotropic IAVs, such as the H7N7 subtype, are capable of invading the central nervous system (CNS) and replicating in brain cells, resulting in microglia-induced neuroinflammation. Microglial cells, the brain’s resident immune cells, are instrumental in the inflammatory response to viral infection. While activation of microglia is important to initially contain the virus, excessive activation of these cells leads to neuronal damage. Previous studies have shown that acute and even long-term IAV-induced neuroinflammation leads to CNS damage. Therefore, the search for possible preventive or therapeutic strategies is of great importance. In this study, we investigated the potential effect of vaccination against acute neuroinflammation induced by H7N7 infection and subsequent neuronal damage in the hippocampus, a particularly vulnerable brain region, comparing young and aged mice. Immunosenescence is one of the striking pathophysiological changes during mammalian aging that leads to “inflammaging” and critically limits the protection by vaccines in the elderly. The results suggest that formalin-inactivated H7N7 vaccine has a preventive effect against the inflammatory responses in the periphery and also in the CNS after H7N7 infection. Cytokine and chemokine levels, increased microglial density, and cell volume after H7N7 infection were all attenuated by vaccination. Further structural analysis of microglial cells also revealed a change in branching complexity after H7N7 infection, most likely reflecting the neuroprotective effect of the vaccination. In addition, synapse loss was prevented in vaccinated mice. Remarkably, engulfment of post-synaptic compartments by microglia can be proposed as the underlying mechanism for spine loss triggered by H7N7 infection, which was partially modulated by vaccination. Although young mice showed better protection against neuroinflammation and the resulting deleterious neuronal effects upon vaccination, a beneficial role of the vaccine was also observed in the brains of older mice. Therefore, vaccination can be proposed as an important strategy to prevent neurological sequelae of H7N7 infection.

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Memory effect of arsenic-induced cellular response and its influences on toxicity of titanium dioxide nanoparticle

Liu

et al. 2019

Sci Rep

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Toxicity of arsenic (As) has been widely characterized. However, few studies focus on whether cell responses induced by As at nontoxic concentration could be inherited and further change cell tolerance to another pollutant. In this study, human A549 and HeLa cells were exposed to As at nontoxic concentrations for 10 or 15 passages, then the cells were recovered in the cell medium without As. At 25th passage, residual As in both type of cells was completely removed through the recovery process. And no abnormity in cell viability was identified in both type of cells between control and As-treated groups. Above results indicated that As exposure-recovery treatment had limited influence on phenotype of the cells. However, gene expression profiles determined by high-throughput sequencing showed that As exposure-recovery treatment induced similar expression modification of genes related to inflammation, oxidative stress and epigenetic modulation in the A549 and HeLa cells after recovery of 10 or 15 passages, indicating that As-induced cellular responses have been partially memorized at transcriptional level. The memory effect might play key roles in increased tolerance of the A549 and HeLa cells to adverse effects (cell viability, intracellular reactive oxygen species (ROS) generation and plasma membrane damage) induced by titanium dioxide nanoparticles (as representative pollutant). This study shed new lights on toxic effects induced by As at nontoxic concentration, which is useful for risk assessment of combined effects of As and other pollutants.

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Systems-based approach to examine the cytokine responses in primary mouse lung macrophages infected with low pathogenic avian Influenza virus circulating in South East Asia

Cited by 3 publications

References 93 publications

Fueling influenza and the immune response: Implications for metabolic reprogramming during influenza infection and immunometabolism

Fueling influenza and the immune response: Implications for metabolic reprogramming during influenza infection and immunometabolism

Influenza vaccine is able to prevent neuroinflammation triggered by H7N7 IAV infection

Memory effect of arsenic-induced cellular response and its influences on toxicity of titanium dioxide nanoparticle

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