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Lipopolysaccharide and hypoxia significantly alters interleukin-8 and macrophage chemoattractant protein-1 production by human fibroblasts but not fibrosis related factors

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Autor
Eleftheriadis, T.; Liakopoulos, V.; Lawson, B.; Antoniadi, G.; Stefanidis, I.; Galaktidou, G.
Fecha
2011
Materia
fibroblast
hypoxia
infection
fibrosis
chemokines
lipopolysaccharide
cobalt chloride
monocyte chemoattractant protein-1
interlukin-8
NF-KAPPA-B
NEUTROPHIL CHEMOTACTIC FACTOR
SYNOVIAL FIBROBLASTS
INDUCIBLE FACTOR-1
MATRIX-METALLOPROTEINASE
IMMUNE-RESPONSES
INNATE
IMMUNITY
EXPRESSION
RECEPTOR
BETA
Medicine, General & Internal
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Resumen
Besides extracellular matrix production, fibroblasts are able to produce various cytokines. Their ubiquitous position makes fibroblasts appropriate cells for sensing various noxious stimuli and for attracting immune cells in the affected area. In the present study the effect of lipopolysaccharide (LPS) and cobalt chloride (CoCl(2)) on the above fibroblasts functions were evaluated in primary human skin fibroblasts cultures. Collagen, matrix metalloproteinase-1, tissue inhibitor of metalloproteinases-1, transforming growth factor-beta 1, interleukin-8 (IL-8) and macrophage chemoattractant protein-1 (MCP-1) were measured in fibroblasts culture supernatants. Fibroblasts proliferation and viability were assessed as well. Hypoxia inducible factor-1 alpha and the phosphorylated p65 portion of NF-kappa B were assessed in fibroblasts protein extracts. LPS and CoCl(2) had a minor effect on fibrosis related factors in human primary fibroblasts, possibly due to the absence of interplay with other cell types in the used experimental system. On the contrary both LPS and CoCl(2) increased significantly IL-8. LPS also increased considerably MCP-1, but CoCl(2) decreased it. Thus LPS and CoCl(2) induce a sentinel, nevertheless not identical, phenotype in primary human fibroblasts. The last disparity could result in different body response to infectious or hypoxic noxious stimuli. Hippokratia 2011; 15 (3): 238-243
URI
http://hdl.handle.net/11615/27323
Colecciones
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]
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