Imhof BA Zimmerli C Gliki G Ducrest-Gay D Juillard P Hammel P Adams R Aurrand-Lions M 2007 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. https://sonar.ch/global/documents/245114 eng info:eu-repo/semantics/altIdentifier/doi/10.1002/path.2163 info:eu-repo/semantics/altIdentifier/pmid/17455169 The Journal of pathology. - 2007 Animals Bronchi Cell Adhesion Molecules Disease Susceptibility Endothelial Cells Esophageal Achalasia Esophagus Granulocytes Homeostasis Immunoglobulins Immunohistochemistry Leukocyte Count Lung Membrane Proteins Mice Mice, Mutant Strains Muscle, Smooth Neutrophils Peritonitis Pneumonia Receptors, CXCR4 Pulmonary dysfunction and impaired granulocyte homeostasis result in poor survival of Jam-C-deficient mice. http://purl.org/coar/resource_type/c_6501