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CD1d-restricted invariant natural killer T (iNKT) cells play a critical role in the induction of airway hyperreactivity (AHR). After intranasal alpha-galactosylceramide (α-GalCer) administration, bronchoalveolar lavage fluid (BALF) proteins from mouse lung were resolved by two-dimensional differential gel electrophoresis (2D-DIGE), and identified by tandem mass spectroscopy. A lack of iNKT cells prevented the development of airway responses including AHR, neutrophilia and the production of the proinflammatory cytokines in lungs. Differentially abundant proteins in the BALF proteome of α-GalCer-treated wild type mice included lungkine (CXCL15), pulmonary surfactant-associated protein D (SFTPD), calcium-activated chloride channel regulator 1 (CLCA1), fragments of complement 3, chitinase 3-like proteins 1 (CH3LI) and 3 (CH3L3) and neutrophil gelatinase-associated lipocalin (NGAL). These proteins may contribute to iNKT regulated AHR via several mechanisms: altering leukocyte chemotaxis, increasing airway mucus production and possibly via complement activation.

Original publication

DOI

10.1371/journal.pone.0129446

Type

Journal article

Journal

PLoS One

Publication Date

2015

Volume

10

Keywords

Acute-Phase Proteins, Animals, Chemokines, CXC, Chemotaxis, Chitinase-3-Like Protein 1, Complement Activation, Complement C3, Female, Glycoproteins, Inflammation, Killer Cells, Natural, Lectins, Lipocalin-2, Lipocalins, Mice, Mice, Inbred BALB C, Mucus, Oncogene Proteins, Pulmonary Surfactant-Associated Protein D, Respiratory Hypersensitivity, Respiratory Mucosa, beta-N-Acetylhexosaminidases