Propionibacterium acnes stimulates pro-matrix metalloproteinase-2 expression through tumor necrosis factor-alpha in human dermal fibroblasts.
Jee-Young Choi,Mei Shan Piao,Jee-Bum Lee,Jong Seok Oh,In-Gyu Kim,Seung-Chul Lee
The Journal of investigative dermatology
128
2008
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Propionibacterium acnes (P. acnes) is a commensal microorganism found in sebum-rich skin and plays a role in acne inflammation by stimulating keratinocyte to produce a number of proinflammatory cytokines. However, the role of P. acnes in the dermis of acne lesions, where tissue remodeling after inflammation eventually takes place, is not known. In this study, we investigated whether P. acnes induces matrix metalloproteinase (MMP), a key enzyme involved in matrix remodeling in human dermal fibroblasts (hDF). We found that P. acnes increased expression of pro-matrix metalloproteinase (proMMP)-2 mRNA/protein in hDF, but not that of proMMP-9. Concomitantly, P. acnes induced tumor necrosis factor-alpha (TNF-alpha) mRNA/protein expression in hDF, which in turn increases both proMMP-2 mRNA and protein expression. P. acnes induced such changes through the activated NF-kappaB pathway. Doxycycline was found to inhibit the expression of proMMP-2 induced either by P. acnes or TNF-alpha. These results suggest that P. acnes stimulates hDF to produce TNF-alpha, which mediates the expression of proMMP-2 through the NF-kappaB pathway. The secretion of proMMP-2 from hDF upon P. acnes stimulation may contribute to the pathogenesis of tissue remodeling in acne skin. | 18049448
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Inflammatory cytokine levels are influenced by interactions between THP-1 monocytic, U-373 MG astrocytic, and SH-SY5Y neuronal cell lines of human origin.
Klegeris, A and McGeer, P L
Neurosci. Lett., 313: 41-4 (2001)
2001
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We measured the secretion of interleukin (IL)1beta, IL-6 and tumor necrosis factor-alpha (TNF-alpha) from human monocytic (THP-1), astrocytic (U-373 MG) and neuronal (SH-SY5Y) cell lines alone and in co-culture, with and without stimulation by a combination of lipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma) or amyloid beta peptide 1-40 (Abeta). LPS+IFN-gamma stimulation increased IL-1beta secretion 16-fold from THP-1 cells. It increased IL-6 secretion 23-fold from THP-1 cells and 2.5-fold from U-373 MG cells. It increased TNF-alpha secretion 3.4-fold from THP-1 cells, but did not influence its secretion from U-373 MG cells. It did not affect the secretion of any of the cytokines from SH-SY5Y cells. Abeta stimulation increased IL-6 secretion 2.3-fold from U-373 MG cells but did not influence secretion of IL-1beta or TNF-alpha. Abeta stimulation also failed to influence secretion of any of the cytokines from THP-1 or SH-SY5Y cells. When THP-1 and U-373 MG cells were cocultured, IL-1beta and IL-6 secretion, but not TNF-alpha secretion, were significantly reduced from the levels obtained in independent cultures, suggesting that a mutual suppressive action may occur between microglia and astrocytes. | 11684335
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