Host DNA released by NETosis promotes rhinovirus-induced type-2 allergic asthma exacerbation.

Toussaint M,et al.

Nat Med. 2017 Jun;23(6):681-691.

Speaker:  Yu-Ting Shao (邵郁婷)             Time:14:00-15:00, Nov. 15, 2017

Commentator: Ching-Chuan Liu,Ph.D.(劉清泉 老師)          Place: Room 601

Abstract:

  Patients at risk for asthma, or with existing asthma, viral respiratory tract infections can have a profound effect on the expression of disease or loss of control. Viral respiratory tract infections, most frequently with rhinovirus, are the predominant microorganisms associated with asthma exacerbations. While Th2-mediated responses are clearly implicated in exacerbations, it is unclear how responses to rhinovirus infection interact with Th2 immunity to enhance disease in allergic asthma to cause exacerbations. In the data, we can see that airway neutrophilia is increased during virus-induced exacerbations. Neutrophils can undergo a process called NETosis that  release NETs into the extracellular space.NETs contain dsDNA and histone and nonhistone proteins. Some viruses can induce NETosis and it can be sensed by the adaptive or innate immunity to induce type-2 immune system.The injection of mouse genomic dsDNA alone is sufficient to induce many features of rhinovirus-induced type-2 immune responses and asthma pathology.On the other hand, blocking neutrophil elastase inhibits NETosis or using DNase degrades NETs can both protect mice from type-2 immunopathology. Authors report that rhinovirus infection is a potent inducer of NETs, and the release of dsDNA,has a central role to induce type-2 cytokine induction and exacerbation severity

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