Interferon regulated gene (IRG) expression-signature in a mouse model of chikungunya virus neurovirulence

Nair, Sreeja R.; Abraham, Rachy; Sundaram, Sankar; Sreekumar, Easwaran

doi:10.1007/s13365-017-0583-3

Cited by 24 publications

(25 citation statements)

References 65 publications

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“…Lower expression of Ralgapa2 , an inhibitor of GLUT4 translocation , represents a mechanism by which absence of MyD88 in muscle may have prevented the inhibition of GLUT4 translocation that occurs with inactivity. Very little information is known about the gene 9930111J21Rik2 , but it appears to be immune related and regulated by interferon . As mentioned previously, the interaction between estrogen and inflammation, specifically interferon gamma , make the robust decreases in 9930111J21Rik2 expression an intriguing mechanism for how ablation of muscle MyD88 signaling may have protected female mice from the negative metabolic consequences of inactivity.…”

Section: Discussionmentioning

confidence: 99%

Absence of MyD88 from Skeletal Muscle Protects Female Mice from Inactivity‐Induced Adiposity and Insulin Resistance

Mahmassani

Reidy

McKenzie

et al. 2020

Obesity

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Objective Inactivity and inflammation are linked to obesity and insulin resistance. It was hypothesized that MyD88 (mediates inflammation) knockout from muscle (MusMyD88−/−) would prevent, whereas miR146a−/− (MyD88 inhibitor) would exacerbate, inactivity‐induced metabolic disturbances. Methods Cre‐control, MusMyD88−/−, and miR146a−/− mice were given running wheels for 5 weeks to model an active phenotype. Afterward, half were placed into a small mouse cage (SMC) to restrict movement for 8 days. Body composition, muscle (3H)2‐deoxyglucose uptake, visceral fat histology, and tissue weight (hind limb muscles, visceral fat, and liver) were assessed. In skeletal muscle and visceral fat, RNA sequencing and mitochondrial function were performed on female MusMyD88−/− and Cre‐control SMC mice. Results The SMC induced adiposity, hyperinsulinemia, and muscle insulin‐stimulated glucose uptake, which was worsened in miR146a−/− mice. In females, MusMyD88−/− mice were protected. Female MusMyD88−/− mice during the SMC period (vs. Cre‐control) exhibited higher Igf1 and decreased Ip6k3 and Trim63 muscle expression. Visceral fat transcript changes corresponded to improved lipid metabolism, decreased adipose expansion (Gulp1↑, Anxa2↓, Ehd1↓) and meta‐inflammation (Hmox1↓), and increased beiging (Fgf10↑). Ralgapa2, negative regulator of GLUT4 translocation, and inflammation‐related gene 993011J21Rik2 were decreased in both muscle and fat. Conclusions Whole‐body miR146a−/− exacerbated inactivity‐induced fat gain and muscle insulin resistance, whereas MusMyD88−/− prevented insulin resistance in female mice.

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Section: Discussionmentioning

confidence: 99%

Absence of MyD88 from Skeletal Muscle Protects Female Mice from Inactivity‐Induced Adiposity and Insulin Resistance

Mahmassani

Reidy

McKenzie

et al. 2020

Obesity

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“…A possible mechanism for the upregulation of RTP4 in DRG neurons during neuropathic pain could involve "interferon (IFN)." This is because the RTP4 gene can be upregulated by type I IFN (IFN-α, IFN-β, IFN -ε, IFN-κ, IFN-ω, IFN-δ, IFN-ζ, and IFN-τ) leading to RTP4 being referred to as "IFN stimulated gene" (Schoggins et al, 2011;Hoyo-Becerra et al, 2015;Nair et al, 2017;Dang et al, 2018). Peripheral immune responding cell such as plasmacytoid dendritic cells or macrophages and the central glial cells like astrocytes or microglia have been identified as main producers of type I IFNs after viral infection, and the IFNs have been shown to affect neuronal survival, neurite outgrowth leading to modulation of the glutamatergic neurotransmission under some pathological conditions including multiple sclerosis and Alzheimer's disease (reviewed in Blank and Prinz, 2017).…”

Section: Possible Physiological Role Of Rtp4 In Pain Perception -The mentioning

confidence: 99%

“…Although RTP4 was initially characterized as a GPCR chaperone protein as described above (Saito et al, 2004;Behrens et al, 2006;Mainland and Matsunami, 2012), more recent publications clearly revealed its significant role in regulation of immune responses such as IFN-related antiviral immunity (Schoggins et al, 2011;Nair et al, 2017;Dang et al, 2018;Zarei Ghobadi et al, 2019;He et al, 2020). Thus, it is suggested that RTP4 could be induced by type I IFNs and work as a negative regulator of interferons pathways.…”

Section: Possible Physiological Role Of Rtp4 In Pain Perception -The mentioning

confidence: 99%

“…Interestingly, recent studies reveal that RTP4 expression is induced upon immune stimulation in vitro (Schoggins et al, 2011;Hoyo-Becerra et al, 2015;Nair et al, 2017;Dang et al, 2018); this suggests an effect on neuronal immune-related pathological states including neuropathic pain. In this review, we outline the possible role of the MOPr-DOPr heteromer and RTP4 in pain with an emphasis on neuropathic pain.…”

Section: Introductionmentioning

confidence: 99%

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The Possible Role of MOPr-DOPr Heteromers and Its Regulatory Protein RTP4 at Sensory Neurons in Relation to Pain Perception

Fujita

2020

Front. Cell. Neurosci.

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Heteromers between mu opioid receptor (MOPr) and delta opioid receptor (DOPr) (i.e., MOPr-DOPr heteromer) have been found to be expressed in different brain regions, in the spinal cord, and in dorsal root ganglia. Recent studies on this heteromer reveal its important pathophysiological function in pain regulation including neuropathic pain; this suggests a role as a novel therapeutic target in chronic pain management. In addition, receptor transporter protein 4 (RTP4) has been shown to be involved in the intracellular maturation of the MOPr-DOPr heteromers. RTP4 appears to have unique distribution in vivo being highly expressed in sensory neurons and also macrophages; the latter are effector cells of the innate immune system that phagocytose foreign substances and secrete both pro-inflammatory and antimicrobial mediators; this suggests a possible contribution of RTP4 to neuronal immune-related pathological conditions such as neuropathic pain. Although RTP4 could be considered as an important therapeutic target in the management of pain via MOPr-DOPr heteromer, a few reports have supported this. This review will summarize the possible role or functions of the MOPr-DOPr heteromer and its regulatory molecule RTP4 in pain modulation at sensory neurons.

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“…Following alphavirus detection and subsequent induction of the IFN pathway, IFN binds to cell surface receptors initiating the canonical JAK-STAT signalling cascade that leads to the transcriptional regulation of IFN-stimulated genes (ISGs). Large scale overexpression screening, RNAseq and microarray analysis has identified numerous ISGs with antiviral activity specific to alphaviruses [51,52,53,54,55,56]. Using the prototype arthritogenic alphavirus SINV as a model of IFN induction, antiviral activity against infection was shown to be only partially dependent on the combined contribution of the two major dsRNA-triggered antiviral pathways, the coupled 2’,5’-oligoadenylate (2-5A) synthetase (OAS)/RNase L pathway and dsRNA-dependent protein kinase PKR pathway [55].…”

Section: Innate Immune Response To Acute Arthritogenic Alphavirus mentioning

confidence: 99%

Arthritogenic Alphavirus-Induced Immunopathology and Targeting Host Inflammation as A Therapeutic Strategy for Alphaviral Disease

Mostafavi

Abeyratne

Zaid

et al. 2019

Viruses

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Arthritogenic alphaviruses are a group of medically important arboviruses that cause inflammatory musculoskeletal disease in humans with debilitating symptoms, such as arthralgia, arthritis, and myalgia. The arthritogenic, or Old World, alphaviruses are capable of causing explosive outbreaks, with some viruses of major global concern. At present, there are no specific therapeutics or commercially available vaccines available to prevent alphaviral disease. Infected patients are typically treated with analgesics and non-steroidal anti-inflammatory drugs to provide often inadequate symptomatic relief. Studies to determine the mechanisms of arthritogenic alphaviral disease have highlighted the role of the host immune system in disease pathogenesis. This review discusses the current knowledge of the innate immune response to acute alphavirus infection and alphavirus-induced immunopathology. Therapeutic strategies to treat arthritogenic alphavirus disease by targeting the host immune response are also examined.

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Interferon regulated gene (IRG) expression-signature in a mouse model of chikungunya virus neurovirulence

Cited by 24 publications

References 65 publications

Absence of MyD88 from Skeletal Muscle Protects Female Mice from Inactivity‐Induced Adiposity and Insulin Resistance

Absence of MyD88 from Skeletal Muscle Protects Female Mice from Inactivity‐Induced Adiposity and Insulin Resistance

The Possible Role of MOPr-DOPr Heteromers and Its Regulatory Protein RTP4 at Sensory Neurons in Relation to Pain Perception

Arthritogenic Alphavirus-Induced Immunopathology and Targeting Host Inflammation as A Therapeutic Strategy for Alphaviral Disease

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