title: Expression of caveolin-1 and podocalyxin in rat lungs challenged with 2-kDa macrophage-activating lipopeptide and Flt3L.
abstract: Caveolin-1 is one of the important regulators of vascular permeability in inflamed lungs. Podocalyxin is a CD34 protein expressed on vascular endothelium and has a role in podocyte development in the kidney. Few data are available on the expression of caveolin-1 and podocalyxin in lungs challenged with Toll-like receptor 2 (TLR2) agonists such as mycoplasma-derived macrophage activating lipopeptide or with immune modulators such as Fms-like tyrosine kinase receptor-3 ligand (Flt3L), which expands dendritic cell populations in the lung. Because of the significance of pathogen-derived molecules that act through TLR2 and of the role of immune modulators in lung physiology, we examine the immunohistochemical expression of caveolin-1 and podocalyxin in lungs from rats challenged with a 2-kDa macrophage-activating lipopeptide (MALP-2) and Flt3L. Normal rat lungs expressed caveolin-1 in alveolar septa, vascular endothelium and airway epithelium, especially along the lateral borders of epithelial cells but not in alveolar macrophages. MALP-2 and Flt3L decreased and increased, respectively, the expression of caveolin-1. Caveolin-1 expression seemed to increase in microvessels in bronchiole-associated lymphoid tissue (BALT) in Flt3L-challenged lungs but not in normal or MALP-2-treated lungs. Podocalyxin was absent in the epithelium and alveolar macrophages but was present in the vasculature of control, Flt3L- and MALP-2-treated rats. Compared with control and MALP-2-treated rats, Flt3L-treated lungs showed greater expression of podocalyxin in BALT vasculature and at the interface of monocytes and the endothelium. These immunohistochemical data describing the altered expression of caveolin-1 and podocalyxin in lungs treated with MALP-2 or Flt3L encourage further mechanistic studies on the role of podocalyxin and caveolin-1 in lung inflammation.
authors.affiliation: Institute of Anatomy and Cell Biology, Saarland University, Homburg, Saar, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Tschernig
authors.forename: R
authors.initials: R
authors.lastname: Pabst
authors.forename: M
authors.initials: M
authors.lastname: Kasper
authors.forename: Mustafa
authors.initials: M
authors.lastname: El-Hadi
authors.forename: B
authors.initials: B
authors.lastname: Singh
mesh_terms: D000818:Animals; D051242:Caveolin 1 / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D055666:Lipopeptides / Q000494:pharmacology*; D008168:Lung / Q000098:blood supply / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins / Q000494:pharmacology*; D008970:Molecular Weight; D051381:Rats; D011917:Rats, Inbred Lew; D012795:Sialoglycoproteins / Q000378:metabolism*; D013194:Staining and Labeling
chemical_list: D051242:Caveolin 1; D055666:Lipopeptides; D008565:Membrane Proteins; D012795:Sialoglycoproteins; C084881:flt3 ligand protein; C001643:podocalyxin; C106335:macrophage stimulatory lipopeptide 2