title: Modulation of lipopolysaccharide receptor expression by lactate dehydrogenase-elevating virus.
abstract: Lactate dehydrogenase-elevating virus (LDV) exacerbates mouse susceptibility to endotoxin shock through enhanced tumour necrosis factor (TNF) production by macrophages exposed to lipopolysaccharide (LPS). However, the in vivo enhancement of TNF production in response to LPS induced by the virus largely exceeds that found in vitro with cells derived from infected animals. Infection was followed by a moderate increase of Toll-like receptor (TLR)-4/MD2, but not of membrane CD14 expression on peritoneal macrophages. Peritoneal macrophages from LDV-infected mice unresponsive to type I interferons (IFNs) did not show enhanced expression of TLR-4/MD2 nor of CD14, and did not produce more TNF in response to LPS than cells from infected normal counterparts, although the in vivo response of these animals to LPS was strongly enhanced. In contrast, the virus triggered a sharp increase of soluble CD14 and of LPS-binding protein serum levels in normal mice. However, production of these LPS soluble receptors was similar in LDV-infected type I IFN-receptor deficient mice and in their normal counterparts. Moreover, serum of LDV-infected mice that contained these soluble receptors had little effect if any on cell response to LPS. These results suggest that enhanced response of LDV-infected mice to LPS results mostly from mechanisms independent of LPS receptor expression.
authors.affiliation: The Unit of Experimental Medicine, de Duve Institute, Université Catholique de Louvain, 1200 Bruxelles, Belgium.
authors.forename: Dan
authors.initials: D
authors.lastname: Su
authors.affiliation: The Unit of Experimental Medicine, de Duve Institute, Université Catholique de Louvain, 1200 Bruxelles, Belgium.
authors.forename: Thao
authors.initials: T
authors.lastname: Le-Thi-Phuong
authors.affiliation: The Unit of Experimental Medicine, de Duve Institute, Université Catholique de Louvain, 1200 Bruxelles, Belgium.
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Coutelier
mesh_terms: D000209:Acute-Phase Proteins / Q000235:genetics / Q000276:immunology; D000818:Animals; D018174:Arterivirus Infections / Q000235:genetics / Q000276:immunology / Q000662:veterinary* / Q000821:virology; D002352:Carrier Proteins / Q000235:genetics / Q000276:immunology; D002478:Cells, Cultured; D015536:Down-Regulation; D005260:Female; D007772:Lactate dehydrogenase-elevating virus / Q000276:immunology / Q000502:physiology*; D018950:Lipopolysaccharide Receptors / Q000235:genetics* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000276:immunology; D051218:Lymphocyte Antigen 96 / Q000235:genetics / Q000276:immunology; D017737:Macrophages, Peritoneal / Q000276:immunology / Q000821:virology; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D012376:Rodent Diseases / Q000235:genetics* / Q000276:immunology / Q000821:virology*; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D002352:Carrier Proteins; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D051218:Lymphocyte Antigen 96; D008562:Membrane Glycoproteins; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D000099231:Lipopolysaccharide-Binding Protein; C411728:Ly96 protein, mouse