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CUTTING EDGE |
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* Department of Pharmaceutical Sciences, School of Pharmacy, University of Maryland, Baltimore, MD 21201;
Lovelace Respiratory Research Institute, Albuquerque, NM 87108;
Department of Medicine, School of Medicine, University of Maryland, Baltimore, MD 21201;
Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Scottsdale, AZ 85259; and
¶ Department of Pathology and Laboratory Medicine, School of Medicine, Emory University, Atlanta, GA 30322
MUC1 (MUC1 in human and Muc1 in nonhumans) is a membrane-tethered mucin that interacts with Pseudomonas aeruginosa (PA) through flagellin. In this study, we compared PA pulmonary clearance and proinflammatory responses by Muc1–/– mice with Muc1+/+ littermates following intranasal instillation of PA or flagellin. Compared with Muc1+/+ mice, Muc1–/– mice showed increased PA clearance, greater airway recruitment of neutrophils, higher levels of TNF-
and KC in bronchoalveolar lavage fluid, higher levels of TNF- in media of flagellin-stimulated alveolar macrophages, and higher levels of KC in media of tracheal epithelial cells. Knockdown of MUC1 enhanced flagellin-induced IL-8 production by primary human bronchial epithelial cells. Expression of MUC1 in HEK293T cells attenuated TLR5-dependent IL-8 release in response to flagellin, which was completely ablated when its cytoplasmic tail was deleted. We conclude that MUC1/Muc1 suppresses pulmonary innate immunity and speculate its anti-inflammatory activity may play an important modulatory role during microbial infection.
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