Proatherogenic lung and oral pathogens induce an inflammatory response in human and mouse mast cells. Export

@article{citeulike:2443178, abstract = {Objective- A broad variety of microbes are present in atherosclerotic plaques and chronic bacterial infection increases the risk of atherosclerosis by mechanisms that have remained vague. One possible mechanism is that bacteria or bacterial products activate plaque mast cells that are known to participate in the pathogenesis of atherosclerosis. Methods and Results- Here we show by real-time PCR analysis and ELISA that Chlamydia pneumoniae (Cpn) and a periodontal pathogen, Aggregatibacter actinomycetemcomitans (Aa), both induce a time and concentration-dependent expression and secretion of interleukin 8 (IL-8), tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) by cultured human peripheral blood-derived mast cells, but not anti-inflammatory molecules, such as IL-10 or transforming growth factor beta1 (TGF-beta1). The IL-8 and MCP-1 responses were immediate, whereas the onset of TNF-a secretion was delayed. The Cpn-mediated proinflammatory effect was attenuated when the bacteria were inactivated by UV-treatment. Human monocyte-derived macrophages that were preinfected with Cpn also induced a significant proinflammatory response in human mast cells, both in cocultures and when preconditioned media from Cpn-infected macrophages were used. Intranasal and intravenous administration of live Cpn and Aa, respectively, induced an accumulation of activated mast cells in the aortic sinus of apolipoprotein E-deficient mice, however, with varying responses in the systemic levels of LPS and TNF-alpha. Conclusions- Proatherogenic Cpn and Aa induce a proinflammatory response in cultured human connective tissue-type mast cells and activation of mouse aortic mast cells in vivo.}, address = {Wihuri Research Institute, Kalliolinnantie 4, FI-00140 Helsinki, Finland.}, author = {Oksaharju, Anna and Lappalainen, Jani and Tuomainen, Anita M M. and Pussinen, Pirkko J J. and Puolakkainen, Mirja and Kovanen, Petri T T. and Lindstedt, Ken A A.}, citeulike-article-id = {2443178}, citeulike-linkout-0 = {http://dx.doi.org/10.1111/j.1582-4934.2008.00285.x}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/18298659}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=18298659}, day = {24}, doi = {10.1111/j.1582-4934.2008.00285.x}, issn = {1582-1838}, journal = {J Cell Mol Med}, month = {February}, posted-at = {2008-02-28 11:57:29}, priority = {2}, title = {Proatherogenic lung and oral pathogens induce an inflammatory response in human and mouse mast cells.}, url = {http://dx.doi.org/10.1111/j.1582-4934.2008.00285.x}, year = {2008} }

TY - JOUR ID - citeulike:2443178 L3 - citeulike-article-id:2443178 N2 - Objective- A broad variety of microbes are present in atherosclerotic plaques and chronic bacterial infection increases the risk of atherosclerosis by mechanisms that have remained vague. One possible mechanism is that bacteria or bacterial products activate plaque mast cells that are known to participate in the pathogenesis of atherosclerosis. Methods and Results- Here we show by real-time PCR analysis and ELISA that Chlamydia pneumoniae (Cpn) and a periodontal pathogen, Aggregatibacter actinomycetemcomitans (Aa), both induce a time and concentration-dependent expression and secretion of interleukin 8 (IL-8), tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein-1 (MCP-1) by cultured human peripheral blood-derived mast cells, but not anti-inflammatory molecules, such as IL-10 or transforming growth factor beta1 (TGF-beta1). The IL-8 and MCP-1 responses were immediate, whereas the onset of TNF-a secretion was delayed. The Cpn-mediated proinflammatory effect was attenuated when the bacteria were inactivated by UV-treatment. Human monocyte-derived macrophages that were preinfected with Cpn also induced a significant proinflammatory response in human mast cells, both in cocultures and when preconditioned media from Cpn-infected macrophages were used. Intranasal and intravenous administration of live Cpn and Aa, respectively, induced an accumulation of activated mast cells in the aortic sinus of apolipoprotein E-deficient mice, however, with varying responses in the systemic levels of LPS and TNF-alpha. Conclusions- Proatherogenic Cpn and Aa induce a proinflammatory response in cultured human connective tissue-type mast cells and activation of mouse aortic mast cells in vivo. JF - J Cell Mol Med SN - 1582-1838 AD - Wihuri Research Institute, Kalliolinnantie 4, FI-00140 Helsinki, Finland. TI - Proatherogenic lung and oral pathogens induce an inflammatory response in human and mouse mast cells. AU - Oksaharju, Anna AU - Lappalainen, Jani AU - Tuomainen, Anita M AU - Pussinen, Pirkko J AU - Puolakkainen, Mirja AU - Kovanen, Petri T AU - Lindstedt, Ken A PY - 2008/02/24/ UR - http://dx.doi.org/10.1111/j.1582-4934.2008.00285.x ER -