We are analyzing https://link.springer.com/article/10.1007/s10753-021-01466-3.

Title:
PI3K/AKT/mTOR and TLR4/MyD88/NF-κB Signaling Inhibitors Attenuate Pathological Mechanisms of Allergic Asthma | Inflammation
Description:
Abstract Asthma is an inflammatory airway disease wherein bronchoconstriction, airway inflammation, and airway obstruction during asthma attacks are the main problems. It is recognized that imbalance of Th1/Th2 and Th17/Treg is a critical factor in asthma pathogenesis. Manipulation of these with signaling molecules such as mTOR, PI3K, Akt, and MyD88 can control asthma. Mouse model of allergic asthma was produced and treated with ketamine, metformin, metformin and ketamine, triciribine, LY294002, and torin2. MCh challenge test, BALf
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Keywords {🔍}

article, asthma, google, scholar, cas, journal, signaling, allergic, inflammation, airway, metformin, cells, athari, factor, wang, immunology, medicine, mtor, ketamine, pathway, cell, access, kinase, liu, pikaktmtor, expression, targeting, rapamycin, privacy, cookies, content, research, shamsadin, zhao, myd, torin, rorγt, protein, receptor, differentiation, nuclear, chen, sciences, data, information, publish, search, tlrmydnfκb, april, seyyed,

Topics {✒️}

nuclear factor kappa-light-chain-enhancer tlr4/myd88/nf-κb signal pathway tlr4/myd88/nf-κb signaling serine/threonine-specific protein kinase pi3k-akt-mtor signaling pathway pi3k/akt/mtor signaling pathway month download article/chapter amp-activated protein kinase streptozotocin-induced diabetic rats conjugated alpha-alumina nanoparticle ltβ receptor-mediated signaling thioacetamide-induced hepatic fibrosis pi3k/akt/mtor pathway attenuate asthma pathology akt/mtor pathway activation targeting cell signaling regulate treg/th17 balance glucocorticoid-resistant chronic asthma house dust mite mtor signaling pathway related subjects targeted therapy 4 article inflammation aims privacy choices/manage cookies experimental allergic asthma full article pdf targeting microrna-17/ rorγt severe asthma exacerbation 5-induced lung injury pi3k/akt/mtor data-mining algorithm mehrabi nasab allergic airway inflammation severe pediatric asthma assess key factors phosphatidylinositol-3-kinase qrt regulates th17 differentiation myd88 gene expressions lung cancer treatment cys-lt level t-box expressed high endothelial venules alae el koraichi increased treg response childhood allergic asthma author yongming zhang transcription t-bet transforming growth factor nano-drug additional information publisher

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         description:Asthma is an inflammatory airway disease wherein bronchoconstriction, airway inflammation, and airway obstruction during asthma attacks are the main problems. It is recognized that imbalance of Th1/Th2 and Th17/Treg is a critical factor in asthma pathogenesis. Manipulation of these with signaling molecules such as mTOR, PI3K, Akt, and MyD88 can control asthma. Mouse model of allergic asthma was produced and treated with ketamine, metformin, metformin and ketamine, triciribine, LY294002, and torin2. MCh challenge test, BALf's Eos Count, the IL-4, 5, INF-γ, eicosanoid, total IgE levels were determined. The MUC5a, Foxp3, RORγt, PI3K, mTOR, Akt, PU.1, and MyD88 gene expressions and histopathology study were done. Asthma groups that were treated with all six components had reduced Penh value, total IgE, IL-4 and IL-5 levels, MUC5a, RORγt, MyD88 and mTOR expression, goblet cell hyperplasia, and mucus hyper-secretion. The eosinophil percentage and Cys-LT level were decreased by metformin and ketamine, triciribine, LY294002, and torin2. The level of IFN-γ was increased in triciribine, LY294002, and torin2. Metformin, metformin and ketamine, triciribine, LY294002, and torin2 reduced Akt and PI3K expression, peribronchial and perivascular inflammation, and increased expression of Foxp3. Torin2 had an effect on PU.1 expression. Inhibition of PI3K/AKT/mTOR and TLR4/MyD88/NF-κB signaling with targeted molecules can attenuate asthma pathology and play an important role in airways protection.
         datePublished:2021-04-16T00:00:00Z
         dateModified:2021-04-16T00:00:00Z
         pageStart:1895
         pageEnd:1907
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            signaling
            Th
            treatment
            target therapy
            Immunology
            Rheumatology
            Pharmacology/Toxicology
            Pathology
            Internal Medicine
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      headline:PI3K/AKT/mTOR and TLR4/MyD88/NF-κB Signaling Inhibitors Attenuate Pathological Mechanisms of Allergic Asthma
      description:Asthma is an inflammatory airway disease wherein bronchoconstriction, airway inflammation, and airway obstruction during asthma attacks are the main problems. It is recognized that imbalance of Th1/Th2 and Th17/Treg is a critical factor in asthma pathogenesis. Manipulation of these with signaling molecules such as mTOR, PI3K, Akt, and MyD88 can control asthma. Mouse model of allergic asthma was produced and treated with ketamine, metformin, metformin and ketamine, triciribine, LY294002, and torin2. MCh challenge test, BALf's Eos Count, the IL-4, 5, INF-γ, eicosanoid, total IgE levels were determined. The MUC5a, Foxp3, RORγt, PI3K, mTOR, Akt, PU.1, and MyD88 gene expressions and histopathology study were done. Asthma groups that were treated with all six components had reduced Penh value, total IgE, IL-4 and IL-5 levels, MUC5a, RORγt, MyD88 and mTOR expression, goblet cell hyperplasia, and mucus hyper-secretion. The eosinophil percentage and Cys-LT level were decreased by metformin and ketamine, triciribine, LY294002, and torin2. The level of IFN-γ was increased in triciribine, LY294002, and torin2. Metformin, metformin and ketamine, triciribine, LY294002, and torin2 reduced Akt and PI3K expression, peribronchial and perivascular inflammation, and increased expression of Foxp3. Torin2 had an effect on PU.1 expression. Inhibition of PI3K/AKT/mTOR and TLR4/MyD88/NF-κB signaling with targeted molecules can attenuate asthma pathology and play an important role in airways protection.
      datePublished:2021-04-16T00:00:00Z
      dateModified:2021-04-16T00:00:00Z
      pageStart:1895
      pageEnd:1907
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      keywords:
         inflammation
         asthma
         signaling
         Th
         treatment
         target therapy
         Immunology
         Rheumatology
         Pharmacology/Toxicology
         Pathology
         Internal Medicine
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            name:Tehran University of Medical Sciences
            address:
               name:Department of Cardiology, School of Medicine, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
               type:PostalAddress
            type:Organization
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      affiliation:
            name:Zhengzhou University People’s Hospital, Henan University People’s Hospital
            address:
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      name:Department of Respiratory and Critical Care Medicine, Henan Provincial People’s Hospital, Zhengzhou University People’s Hospital, Henan University People’s Hospital, Zhengzhou, China
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