NDLI: Neuraminidase reprograms lung tissue and potentiates lipopolysaccharide-induced acute lung injury in mice.

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Neuraminidase reprograms lung tissue and potentiates lipopolysaccharide-induced acute lung injury in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Blackwelder, William C. Nguyen, Chinh Goldblum, Simeon E. Feng, Chiguang Cross, Alan S. Zhang, Lei Vogel, Stefanie N.
Description	Author Affiliation: Feng C ( Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, MD 21201)
Abstract	We previously reported that removal of sialyl residues primed PBMCs to respond to bacterial LPS stimulation in vitro. Therefore, we speculated that prior desialylation can sensitize the host to generate an enhanced inflammatory response upon exposure to a TLR ligand, such as LPS, in a murine model of acute lung injury. Intratracheal instillation of neuraminidase (NA) 30 min prior to intratracheal administration of LPS increased polymorphonuclear leukocytes (PMNs) in the bronchoalveolar lavage fluid and the wet-to-dry lung weight ratio, a measure of pulmonary edema, compared with mice that received LPS alone. Administration of NA alone resulted in desialylation of bronchiolar and alveolar surfaces and induction of TNF- , IL-1ß, and chemokines in lung homogenates and bronchoalveolar lavage fluid; however, PMN recruitment in mice treated with NA alone did not differ from that of PBS-administered controls. NA pretreatment alone induced apoptosis and markedly enhanced LPS-induced endothelial apoptosis. Administration of recombinant Bcl-2, an antiapoptotic molecule, abolished the effect of NA treatment on LPS-induced PMN recruitment and pulmonary edema formation. We conclude that NA pretreatment potentiates LPS-induced lung injury through enhanced PMN recruitment, pulmonary edema formation, and endothelial and myeloid cell apoptosis. A similar 'reprogramming' of immune responses with desialylation may occur during respiratory infection with NA-expressing microbes and contribute to severe lung injury.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202673
Journal	The Journal of Immunology
Issue Number	9
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Acute Lung Injury Immunology Neuraminidase Metabolism Neutrophils Chemically Induced Animals Apoptosis Bronchoalveolar Lavage Fluid Cytology Disease Models, Animal Endothelial Cells Lipopolysaccharides Administration & Dosage Lung Mice Mice, Inbred C57bl Mice, Knockout Myeloid Cells N-acetylneuraminic Acid Proto-oncogene Proteins C-bcl-2 Pulmonary Edema Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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