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Autor Thema: Viren-Infektionen verursachen Asthma / Crippling viral infections 'cause asthma'  (Gelesen 5433 mal)


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9 September 2012
Crippling viral infections 'cause asthma'

By James Gallagher Health and science reporter, BBC News

How could a virus increase the risk of asthma?

Viral infections in newborns "cripple" part of the immune system and increase the risk of asthma later in life, US researchers studying mice have said.

They showed infections by respiratory syncytial virus (RSV) stripped immune cells of their ability to calm down inflammation in the lung's airways.

They say their findings, published in the journal Nature Medicine, will help develop ways of preventing asthma.


The article in Nature:

Article preview

Nature Medicine | Article
Early infection with respiratory syncytial virus impairs regulatory T cell function and increases susceptibility to allergic asthma

    Nandini Krishnamoorthy,
    Anupriya Khare,
    Timothy B Oriss,
    Mahesh Raundhal,
    Christina Morse,
    Manohar Yarlagadda,
    Sally E Wenzel,
    Martin L Moore,
    R Stokes Peebles Jr,
    Anuradha Ray
    & Prabir Ray

    Nature Medicine     (2012)

Received    02 April 2012
Accepted    09 July 2012
Published online    09 September 2012


Immune tolerance is instituted early in life, during which time regulatory T (Treg) cells have an important role. Recurrent infections with respiratory syncytial virus (RSV) in early life increase the risk for asthma in adult life. Repeated infection of infant mice tolerized to ovalbumin (OVA) through their mother's milk with RSV induced allergic airway disease in response to OVA sensitization and challenge, including airway inflammation, hyper-reactivity and higher OVA-specific IgE, as compared to uninfected tolerized control mice. Virus infection induced GATA-3 expression and T helper type 2 (TH2) cytokine production in forkhead box P3 (FOXP3)+ Treg cells and compromised the suppressive function of pulmonary Treg cells in a manner that was dependent on interleukin-4 receptor ? (IL-4R?) expression in the host. Thus, by promoting a TH2-type inflammatory response in the lung, RSV induced a TH2-like effector phenotype in Treg cells and attenuated tolerance to an unrelated antigen (allergen). Our findings highlight a mechanism by which viral infection targets a host-protective mechanism in early life and increases susceptibility to allergic disease.

And the consequences for cancer development still is to be researched...
Würde ich von Licht leben,
müßte ich grün sein.