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Inflammasome and Lung Pathologies

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Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

Nonregulated inflammation in the lung often leads to chronic inflammatory diseases such as asthma, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis. Interleukin-1α (IL-1α) and interleukin-1β (IL-1β) are potent mediators of innate immunity and IL-1β is processed by large multiprotein complexes called inflammasomes. Using a mice model of lung inflammatory diseases, it was shown that acute cigarette smoke exposure induces inflammasome-dependent IL-1β maturation and ASC-associated protein complex is necessary to lung emphysema. Moreover, bleomycin- or crystalline silica particle-induced pulmonary inflammation and fibrosis are Nlrp3 inflammasome dependent. Nlrp3-containing inflammasome appears to be an essential mediator for allergic lung inflammation. Pulmonary exposure to nanomaterials may lead to pulmonary inflammation and fibrosis. Inhalation of nano-TiO2 provokes lung inflammation which is strongly dependent on IL-1α.

Nlrp3 inflammasome appears as a corner stone in pulmonary inflammatory diseases, but growing evidences suggest that IL-1α plays an important role through the common IL-1 receptor.

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Acknowledgments

I thank Dr Valérie Quesniaux, the director of the UMR6218 IEM unit for comments and discussions, and Pr François Erard for critically reviewing the manuscript and for helpful discussion.

I would like to thank Jürg Tschopp, Vincent Lagente, and François Huaux for fruitfull collaborations.

The work was supported by the Key-Obs SAS, Orleans, the “Conseil Général du Loiret” (PhD fellowship) and the Agence Nationale pour la Recherche (ANR).

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Correspondence to Isabelle Couillin .

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Ryffel, B., Togbe, D., Couillin, I. (2011). Inflammasome and Lung Pathologies. In: Couillin, I., Pétrilli, V., Martinon, F. (eds) The Inflammasomes. Progress in Inflammation Research. Springer, Basel. https://doi.org/10.1007/978-3-0348-0148-5_11

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