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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
10
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pubmed:dateCreated |
2002-5-7
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pubmed:abstractText |
TNF-alpha is a cytokine associated with inflammatory diseases, including asthma. Increased levels of TNF-alpha were found in the bronchoalveolar lavage fluid of mice undergoing a dinitrofluorobenzene (DNFB)-induced non-IgE-mediated pulmonary hypersensitivity reaction. We report in this work that TNF-alpha increases the susceptibility of sensory neurons to dinitrobenzene sulfonic acid (DNS) and capsaicin, leading to a tracheal vascular hyperpermeability response in DNFB-sensitized and DNS-challenged mice. mAb against TNF-alpha or the TNFR1 inhibited this hyperpermeability response in DNFB-sensitized and DNS-challenged mice. Furthermore, the hyperpermeability response after DNS challenge was abolished in DNFB-sensitized mast cell-deficient WBB6F(1)-W/W(V) mice. These animals showed a remarked decrease of TNF-alpha bronchoalveolar lavage fluid levels after a single DNS challenge. The hyperpermeability response after DNS challenge was regained in mast cell-deficient mice after mast cell reconstitution. These findings indicate a prominent role for TNF-alpha and its TNFR1 in the DNFB-induced tracheal hyperpermeability response. We propose that a priming effect of mast cell-derived TNF-alpha on the sensory neurons could be the mechanism of action of TNF-alpha in the vascular hyperpermeability response in tracheas of mice undergoing a pulmonary hypersensitivity reaction.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Benzenesulfonates,
http://linkedlifedata.com/resource/pubmed/chemical/Capsaicin,
http://linkedlifedata.com/resource/pubmed/chemical/Dinitrofluorobenzene,
http://linkedlifedata.com/resource/pubmed/chemical/Haptens,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/dinitrobenzenesulfonic acid
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
168
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5297-302
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:11994487-Administration, Topical,
pubmed-meshheading:11994487-Animals,
pubmed-meshheading:11994487-Antibodies, Monoclonal,
pubmed-meshheading:11994487-Antigens, CD,
pubmed-meshheading:11994487-Benzenesulfonates,
pubmed-meshheading:11994487-Bronchoalveolar Lavage Fluid,
pubmed-meshheading:11994487-Capillary Permeability,
pubmed-meshheading:11994487-Capsaicin,
pubmed-meshheading:11994487-Dinitrofluorobenzene,
pubmed-meshheading:11994487-Haptens,
pubmed-meshheading:11994487-Immunization, Secondary,
pubmed-meshheading:11994487-Injections, Intravenous,
pubmed-meshheading:11994487-Male,
pubmed-meshheading:11994487-Mast Cells,
pubmed-meshheading:11994487-Mice,
pubmed-meshheading:11994487-Mice, Inbred BALB C,
pubmed-meshheading:11994487-Mice, Mutant Strains,
pubmed-meshheading:11994487-Nerve Endings,
pubmed-meshheading:11994487-Neurons, Afferent,
pubmed-meshheading:11994487-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:11994487-Receptors, Tumor Necrosis Factor, Type I,
pubmed-meshheading:11994487-Receptors, Tumor Necrosis Factor, Type II,
pubmed-meshheading:11994487-Respiratory Hypersensitivity,
pubmed-meshheading:11994487-Trachea,
pubmed-meshheading:11994487-Tumor Necrosis Factor-alpha
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pubmed:year |
2002
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pubmed:articleTitle |
Mast cell-derived TNF-alpha primes sensory nerve endings in a pulmonary hypersensitivity reaction.
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pubmed:affiliation |
Department of Pharmacology and Pathophysiology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, 3508 TB Utrecht, The Netherlands. A.H.vanHouwelingen@pharm.uu.nl
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pubmed:publicationType |
Journal Article
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