echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Biochemistry News > Biotechnology News > Molecular mechanisms for the co-regulation of acute lung infection damage in the lost nerve-spleen

    Molecular mechanisms for the co-regulation of acute lung infection damage in the lost nerve-spleen

    • Last Update: 2020-09-06
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    On April 11th Cell Discovery, an international academic journal, published online the latest research results of the Su-Yu Research Group of the Pasteur Institute in Shanghai, Chinese Academy of Sciences, "The molecular mechanism of the vagal circuits to co-regulate acute lung infection injury" (Signals of vagal circuits with AKT1 in alpha7 nAChR-CD11b-cells lessen E.coli or LPS-acute.
    Acute lung injury can be induced by infection (bacteria, viruses, etc.), acid inhalation, trauma and other factors, and the pathology is manifested in severe inflammatory reactions in the lungs, inflammation cell immersion, lung endothion and endothelphel cell damage, and imbalance of the gas and blood barrier.
    patients with acute lung injuries still have mortality rates of more than 30 to 40 percent, even if they have severe supportive therapies.
    how the nervous system regulates infection, inflammation and immunity is a new interdisciplinary research hotspot, and many important scientific questions need to be answered.
    control of the inflammatory response of the classic ecstrophic nerve is achieved through choline's anti-inflammatory pathline.
    The path is believed to activate alpha7 nAChR (a subtype of ACh subject) by the ecstasy nerve release passer acetylcholine (ACh), inhibit the activation of the nucleokine kB (NF-kB) of inflammatory cells, especially monocytes/macrophages, and reduce the production of inflammatory factors such as tumor necrosis factors (TNF-alpha) and high-migration family protein 1 (HMGB1).
    spleen is the functional hub of the path.
    because the spleen butt circulation has a filter effect on the whole body blood, so this regulation plays an important role in explaining the systemic inflammatory response.
    is an open organ to the outside world, lung infection, inflammation of the inflammatory factors, generally do not enter the body circulation.
    , the arc of inflammation of the pulmonary side-sensing nerve is essential for the identification of lung pathogens and the control of infection and inflammation.
    the theory of neuro-inflammatory reflex arc of pulmonary by-intersection refers to the fact that the ecstratic nerve can dominate the far airway, or even the anticul bubble, and dominate the airway sensor.
    to rely on airway sensors or pathogens to identify changes in the sensor's perception of pathogens and inflammation in the lungs.
    the sensory nuclea (NTS) that can be transmitted to the bridge brain through the lost nerve.
    this integration, ACh is secreted through the pulmonary fanatic nerve, activating the inflammatory cell alpha7 nAChR in the lungs, inhibiting NF-kB activation and lowering the level of inflammatory cytokines, reducing inflammation and damage to the lungs.
    therefore cutting off the lost nerve and knocking out alpha7 nAChR can aggravate acute lung damage induced by polysaccharides (LPS) or E. coli (E.coli).
    Su Wei has been engaged in the study of the mechanism of the regulation of acute lung injury by the ecstratic nerve.
    He put forward the theory that the neuro-inflammatory reflex arc of pulmonary by-cross-sensing nerve regulates the immunity of lung infections, and led the research team of Ph.D. students Zhao Caixuan and Yang Xi, with the help of Michael A. Matthay, a professor at the University of California, San Francisco, to discover the signaling mechanism of the ecstransic nerve-spleen to co-regulate acute lung infection and inflammatory response (see figure above).
    team found that LPS or E. coli-induced acute lung injury mouse models that removed the lost nerve can significantly increase the spleen alpha7 nAChR-CD11b-plus cells (CD11b is the surface marker of inflammatory cells-monocytes and neutral granulocytes) swimming out and increasing the collection of lung alpha7 nAchR-CD11b-plus cells, increasing the inflammatory response of the lungs.
    the application of alpha7 nAChR astigids to mice corrects the effects of ecstransic nerve excision, inhibits spleen swelling and lung collection of alpha7 nAchR-CD11b-cells, and reduces the inflammatory response of the lungs.
    the ecstasy nerve can promote the serine 473 phosphorylation of alpha7 nAchR-CD11b-cell protein kinase B (AKT1) by activating alpha7 nAChR and inhibiting the spleen swelling of these cells.
    the alpha7 nAchR-CD11b-cells of the bone marrow are not affected by this mechanism.
    Again, knocking out Akt1 can reduce spleen alpha7 nAChR-CD11b-cells in acute lung injury, but instead increase lung alpha-7 nAChR-CD11b-plus cells, promoting neutral granulocytosis and aggravating LPS and E. coli-induced acute lung injury.
    the ecstasy nerve excision and knock-off alpha7 nAChR and CD11b can reduce lung collection of spleen and bronchial alveo scuffles (BAL) Ly6CintGr1hi neutoprine cells and Ly6Chi monocytes AKT1 serine 473 phosphate, promote neutopophilus and monocytes to E. coli damaged lungs, plus severe E. coli and LPS induced acute lung damage.
    thus the ecstasy nerve promotes alpha7 nAchR-CD11b-cell AKT1 phosphorylation, inhibits spleen inflammatory cell mobilization and lung collection, and reduces E. coli and LPS-induced acute lung damage.
    the development of acute lung injury by regulating AKT1 phosphorylation through alpha7 nAChR, which provides a new theoretical basis for the treatment of acute lung injury.
    .
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.