Ribavirin attenuates the respiratory immune responses to influenza viral infection in mice

Liao, Shang-hui; Li, Yun; Lai, Yunfeng; Liu, Geoffrey; Zhang, Fengxue; Xu, Pao

doi:10.1007/s00705-017-3291-7

Cited by 14 publications

(10 citation statements)

References 43 publications

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“…Ribavirin may yield anti-inflammatory effects by modulating micro-and astrogliosis, as it does in experimental autoimmune encephalomyelitis rat models [53,54]. Moreover, TLR4 levels, which are related to nociception, is one of Ribavirin putative targets in other immunological responses [23,[55][56][57]. Lastly, it is important to remark that 100 mg/kg of Acamprosate has no effects alleviating pain [51], and that we administered it at 8 mg/kg, which reinforces the synergistic effect of NeuroHeal towards this pathophysiological phenomenon.…”

Section: Discussionmentioning

confidence: 99%

NeuroHeal Treatment Alleviates Neuropathic Pain and Enhances Sensory Axon Regeneration

Casas

2020

Cells

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Peripheral nerve injury (PNI) leads to the loss of motor, sensory, and autonomic functions, and often triggers neuropathic pain. During the last years, many efforts have focused on finding new therapies to increase axonal regeneration or to alleviate painful conditions. Still only a few of them have targeted both phenomena. Incipient or aberrant sensory axon regeneration is related to abnormal unpleasant sensations, such as hyperalgesia or allodynia. We recently have discovered NeuroHeal, a combination of two repurposed drugs; Acamprosate and Ribavirin. NeuroHeal is a neuroprotective agent that also enhances motor axon regeneration after PNI. In this work, we investigated its effect on sensory fiber regeneration and PNI-induced painful sensations in a rat model of spare nerve injury and nerve crush. The follow up of the animals showed that NeuroHeal treatment reduced the signs of neuropathic pain in both models. Besides, the treatment favored sensory axon regeneration, as observed in dorsal root ganglion explants. Mechanistically, the effects observed in vivo may improve the resolution of cell-protective autophagy. Additionally, NeuroHeal treatment modulated the P2X4-BDNF-KCC2 axis, which is an essential driver of neuropathic pain. These data open a new therapeutic avenue based on autophagic modulation to foster endogenous regenerative mechanisms and reduce the appearance of neuropathic pain in PNI.

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Section: Discussionmentioning

confidence: 99%

NeuroHeal Treatment Alleviates Neuropathic Pain and Enhances Sensory Axon Regeneration

Casas

2020

Cells

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“…Total RNA was reverse transcribed into cDNA using PrimeScript™ 1st Strand cDNA Synthesis Kit (Takara, Japan) according to the Manufacturer's protocol. M gene of A/FM/1/47 H1N1 was carried out as mentioned before [27]. IFV quantity of PCR products were analyzed in the light of the mode for normalized expression (2 −△△ct ) [28].…”

Section: Reverse Transcription and Real-time Quantitative Pcrmentioning

confidence: 99%

Effect of αvβ3 Blockade Against Acute Lung Injury Induced by Influenza A Virus and Its Mechanism

Wang

Zeng

Liu

et al. 2021

Preprint

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Integrin αvβ3 is a heterodimer formed by αv and β3 subunits that is expressed in pulmonary endothelial cells, alveolar epithelial cells, interstitial cells and macrophages. Integrin αvβ3 not only has a common role of integrin family molecules in inflammation and tissue fibrosis, but also mediates the adsorption and penetration of various viruses into susceptible cells. Nevertheless, there are few studies on the effect of αvβ3 on acute lung injury (ALI) induced by influenza virus and its mechanism. Here, the effects of αvβ3 blockade [Cyclo(RGDyK)] against ALI induced by influenza A virus (IAV) in vitro and in vivo and its possible mechanism were studied. A549 cells and mice were infected with influenza virus A/FM/1/47 to induce ALI in vitro and in vivo. The results showed that Cyclo(RGDyK) reduced the ALI induced by IAV, alleviated pulmonary edema, improved lung histopathological changes and alleviated the accumulation of inflammatory cells in the lung. Cyclo(RGDyK) had inhibitory effect on cells and mice infected by IAV. Cyclo(RGDyK) (150 µg/kg) showed effective antiviral activity in vivo. Cyclo(RGDyK) had 70% protective effect against IAV and effectively reduced virus titer and inflammation in lung tissue. Cyclo(RGDyK) exhibited significantly anti-inflammatory and anti-fibrotic effect on improving the pneumonia and degree of pulmonary fibrosis and reducing the levels of pulmonary fibrotic markers (LN, HA, PCIII, IV-C, TGF-β1, and α-SMA). Additionally, Cyclo(RGDyK) inhibited expression of αvβ3,TGF-β1, HIF-1α, NF-κB, and p38 MAPK in the cells and mice lung tissues. The results showed that Cyclo(RGDyK) had a protective effect on ALI in mice infected with IAV and inhibited the progress of lung inflammation and fibrosis, which may be concern with its regulation of αvβ3/TGF-β1/HIF-1α signaling pathway.

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“…As an RNA polymerase inhibitor, RBV is a well-characterized and broad-spectrum antiviral drug against various RNA and DNA viruses, including influenza A and influenza B viruses. 7 It was approved by Dovepress Dovepress 5788 lin et al the American Food and Drug Administration for treatment against influenza virus or respiratory syncytial virus infection through nebulizer inhalation in 1986 and hepatitis C virus infection combined with interferon in 2001. 8 Nanomaterials have been studied or applied as carriers of drugs in the biomedical field because of their special physical and chemical properties compared with normal materials, such as the small particle size that contributes to the stable nanostructure and enables easy entrance into cells.…”

Section: Introductionmentioning

confidence: 99%

Restriction of H1N1 influenza virus infection by selenium nanoparticles loaded with ribavirin via resisting caspase-3 apoptotic pathway

Lin¹,

Li²,

Gong³

et al. 2018

IJN

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IntroductionRibavirin (RBV) is a broad-spectrum antiviral drug. Selenium nanoparticles (SeNPs) attract much attention in the biomedical field and are used as carriers of drugs in current research studies. In this study, SeNPs were decorated by RBV, and the novel nanoparticle system was well characterized. Madin-Darby Canine Kidney cells were infected with H1N1 influenza virus before treatment with RBV, SeNPs, and SeNPs loaded with RBV (Se@RBV).Methods and resultsMTT assay showed that Se@RBV nanoparticles protect cells during H1N1 infection in vitro. Se@RBV depressed virus titer in the culture supernatant. Intracellular localization detection revealed that Se@RBV accumulated in lysosome and escaped to cytoplasm as time elapsed. Furthermore, activation of caspase-3 was resisted by Se@RBV. Expressions of proteins related to caspase-3, including cleaved poly-ADP-ribose polymerase, caspase-8, and Bax, were downregulated evidently after treatment with Se@RBV compared with the untreated infection group. In addition, phosphorylations of phosphorylated 38 (p38), JNK, and phosphorylated 53 (p53) were inhibited as well. In vivo experiments indicated that Se@RBV was found to prevent lung injury in H1N1-infected mice through hematoxylin and eosin staining. Tunel test of lung tissues present that DNA damage reached a high level but reduced substantially when treated with Se@RBV. Immunohistochemical test revealed an identical result with the in vitro experiment that activations of caspase-3 and proteins on the apoptosis pathway were restrained by Se@RBV treatment.ConclusionTaken together, this study elaborates that Se@RBV is a novel promising agent against H1N1 influenza virus infection.

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Ribavirin attenuates the respiratory immune responses to influenza viral infection in mice

Cited by 14 publications

References 43 publications

NeuroHeal Treatment Alleviates Neuropathic Pain and Enhances Sensory Axon Regeneration

NeuroHeal Treatment Alleviates Neuropathic Pain and Enhances Sensory Axon Regeneration

Effect of αvβ3 Blockade Against Acute Lung Injury Induced by Influenza A Virus and Its Mechanism

Restriction of H1N1 influenza virus infection by selenium nanoparticles loaded with ribavirin via resisting caspase-3 apoptotic pathway

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