NDLI: Pulmonary chemoreflex responses are potentiated by tumor necrosis factor-alpha in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lin, Ruei-Lung Lin, Yu-Jung Geer, Marcus J. Kryscio, Richard Lee, Lu-Yuan
Description	Country affiliation: United States Author Affiliation: Lin RL ( Department of Physiology, University of Kentucky, Lexington, Kentucky 40536-0298, USA.)
Abstract	Inhalation of tumor necrosis factor-alpha (TNF- ), a proinflammatory cytokine, induces airway hyperresponsiveness, and the underlying mechanism is not fully understood. Hypersensitivity of vagal bronchopulmonary C-fiber afferents is known to contribute to the airway hyperresponsiveness during an airway inflammatory reaction. Because activation of these afferents can elicit pulmonary chemoreflexes, this study was designed to determine if a pretreatment with TNF- induced airway inflammation and enhanced the pulmonary chemoreflex sensitivity in anesthetized mice; and if so, whether the effect was mediated through activation of either or both of the TNF receptors, p55 and p75. Our results showed that TNF- instilled into the lung caused an increased sensitivity of pulmonary chemoreflex responses to various chemical stimulants of the vagal bronchopulmonary C-fiber afferents. The increased sensitivity was found 24 h later, persisted at 48 h, and then gradually declined after several days. The TNF- -induced airway hypersensitivity was accompanied by airway inflammation as shown by a striking elevation of the levels of eosinophils and neutrophils, several potent bronchoactive inflammatory mediators, and proinflammatory cytokines in the bronchoalveolar lavage fluid. Furthermore, the increase in pulmonary chemoreflex response caused by TNF- was partially abrogated in both p55-null and p75-null mice, but completely abolished in p55/p75-null mice. In conclusion, TNF- pretreatment induced airway inflammation and a sustained elevation of pulmonary chemoreflex sensitivity, which was mediated through an activation of both types of TNF receptors.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
DOI	10.1152/japplphysiol.01301.2012
Journal	Journal of Applied Physiology
Issue Number	11
Volume Number	114
Language	English
Publisher	American Physiological Society
Publisher Date	2013-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Physiology Chemoreceptor Cells Immunology Lung Pneumonia Chemically Induced Receptors, Tumor Necrosis Factor Tumor Necrosis Factor-alpha Administration, Inhalation Animals Radiation Effects Drug Effects Mice Mice, Inbred C57bl Mice, Knockout Administration & Dosage Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Research Support, U.s. Gov't, Non-p.h.s.
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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