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Asthma and allergy

An IFNγ bias in severe asthma

Nature Reviews Immunology volume 15, pages 466–467 (2015)Cite this article

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An analysis of bronchoalveolar lavage (BAL) fluid showed that the percentage of IFNγ+CD4+ T cells and IL-17+CD4+ T cells was higher in individuals with severe asthma than in those with mild–moderate asthma. Furthermore, IFNγ levels were higher in samples from individuals with severe asthma, whereas interleukin-5 (IL-5) and IL-17 levels were similar between the two groups, and IL-13 production was enhanced only in individuals with mild–moderate asthma.

Next, the authors sought to develop a new mouse model of severe asthma. Bacterial airway infections have been linked with treatment-resistant severe asthma in humans and therefore, the authors hypothesized that the bacterial second messenger cyclic diguanylate (c-di-GMP), which induces TH1 and TH17 cell responses, could be used as part of a model of severe asthma. In this regard, mice were first sensitized and then challenged with house dust mite (HDM) allergen with or without c-di-GMP. Similar to severe asthma in humans, mice that received c-di-GMP had heightened airway hyperreactivity (AHR) and neutrophil-dominant airway inflammation, and these mice responded poorly to treatment with the corticosteroid dexamethasone. Furthermore, the lungs of these c-di-GMP-treated 'severe asthma mice' (SA mice) had high levels of IFNγ and IL-17.

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References

  1. Raundhal, M. et al. High IFN-γ and low SLPI mark severe asthma in mice and humans. J. Clin. Invest. http://dx.doi.org/10.1172/JCI80911 (2015)

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  1. Olive Leavy
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Fahy, J. V. Type 2 inflammation in asthma — present in most, absent in many. Nat. Rev. Immunol. 15, 57–65 (2015)

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Leavy, O. An IFNγ bias in severe asthma. Nat Rev Immunol 15, 466–467 (2015). https://doi.org/10.1038/nri3891

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