NDLI: Ablation of leptin receptor-mediated ERK activation impairs host defense against Gram-negative pneumonia.

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Ablation of leptin receptor-mediated ERK activation impairs host defense against Gram-negative pneumonia.

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Ablation of leptin receptor-mediated ERK activation impairs host defense against Gram-negative pneumonia.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Serezani, Carlos H. O'Brien, Edmund Mancuso, Peter Aronoff, David M. Goldberg, Jared Myers, Martin G. Goel, Deepti Peters-Golden, Marc
Description	Country affiliation: United States Author Affiliation: Mancuso P ( Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI 48109, USA. pmancuso@umich.edu)
Abstract	The adipocyte-derived hormone leptin plays an important role in regulation of energy homeostasis and the innate immune response against bacterial infections. Leptin's actions are mediated by signaling events initiated by phosphorylation of tyrosine residues on the long form of the leptin receptor. We recently reported that disruption of leptin receptor-mediated STAT3 activation augmented host defense against pneumococcal pneumonia. In this report, we assessed leptin receptor-mediated ERK activation, a pathway that was ablated in the l/l mouse through a mutation of the tyrosine 985 residue in the leptin receptor, to determine its role in host defense against bacterial pneumonia in vivo and in alveolar macrophage (AM) antibacterial functions in vitro. l/l mice exhibited increased mortality and impaired pulmonary bacterial clearance after intratracheal challenge with Klebsiella pneumoniae. The synthesis of cysteinyl-leukotrienes was reduced and that of PGE(2) enhanced in AMs in vitro and the lungs of l/l mice after infection with K. pneumoniae in vivo. We also observed reduced phagocytosis and killing of K. pneumoniae in AMs from l/l mice that was associated with reduced reactive oxygen intermediate production in vitro. cAMP, known to suppress phagocytosis, bactericidal capacity, and reactive oxygen intermediate production, was also increased 2-fold in AMs from l/l mice. Pharmacologic blockade of PGE(2) synthesis reduced cAMP levels and overcame the defective phagocytosis and killing of bacteria in AMs from l/l mice in vitro. These results demonstrate that leptin receptor-mediated ERK activation plays an essential role in host defense against bacterial pneumonia and in leukocyte antibacterial effector functions.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200465
Journal	The Journal of Immunology
Issue Number	2
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Extracellular Signal-regulated Map Kinases Antagonists & Inhibitors Metabolism Klebsiella Infections Immunology Map Kinase Signaling System Genetics Pneumonia, Bacterial Receptors, Leptin Physiology Amino Acid Substitution Animals Cells, Cultured Immunity, Innate Pathology Prevention & Control Klebsiella Pneumoniae Leucine Macrophages, Alveolar Enzymology Mice Mice, Inbred C57bl Mice, Transgenic Deficiency Tyrosine Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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