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Pulmonary dysfunction and impaired granulocyte homeostasis result in poor survival of Jam-C-deficient mice

Gliki, Georgia
Ducrest-Gay, Dominique
Juillard, P.
Adams, Ralf
Published in The Journal of Pathology. 2007, vol. 212, no. 2, p. 198-208
Abstract Jam-C(-/-) mice exhibit growth retardation and multilobular pneumonia concomitant with poor survival of the mice under conventional housing conditions. The deficient mice present a mega-oesophagus and have altered airway responsiveness. In addition, the number of circulating granulocytes is increased in Jam-C(-/-) mice as compared to control animals. These phenotypes probably reflect the different functions of JAM-C expressed by endothelial and mesenchymal cells. Indeed, the deregulation in the number of circulating granulocytes is caused by the lack of JAM-C expression on endothelial cells since rescuing endothelial expression of the protein in the Jam-C(-/-) mice is sufficient to restore homeostasis. More importantly, the rescue of vascular JAM-C expression is accompanied by better survival of deficient mice, suggesting that endothelial expression of JAM-C is mandatory for animal survival from opportunistic infections and fatal pneumonia.
Keywords AnimalsBronchi/immunologyCell Adhesion Molecules/analysis/ deficiency/immunologyDisease Susceptibility/immunologyEndothelial Cells/immunologyEsophageal Achalasia/immunology/physiopathologyEsophagus/immunology/physiopathologyGranulocytes/ immunologyHomeostasis/ immunologyImmunoglobulins/analysis/ deficiency/immunologyImmunohistochemistry/methodsLeukocyte CountLung/ immunology/physiopathologyMembrane Proteins/analysis/ deficiency/immunologyMiceMice, Mutant StrainsMuscle, Smooth/immunologyNeutrophils/immunologyPeritonitis/immunology/physiopathologyPneumonia/immunologyReceptors, CXCR4/analysis
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PMID: 17455169
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