Observation of TNF-α, IL-10 and HB-EGF gene expression by peripheral blood CD14+ mononuclear cells: a case of guttate psoriatic patient
DOI:
https://doi.org/10.15419/bmrat.v4i11.378Keywords:
CD14, guttate psoriasis, HB-EGF, IL-10, LPS, TNF-α, medicineAbstract
Introduction: Guttate is a type of psoriasis in which patients are sensitive to Streptococcus pneumoniae throughout innate immune responses. During the inflammation, tumour necrosis factor alpha (TNF-α), a well-known pro-inflammatory cytokine, is expressed; meanwhile interleukin 10 (IL-10) and heparin-binding EGF-like growth factor (HB-EGF), which are capable of inhibiting transcription of the TNF-α gene, are also prominent. Furthermore, HB-EGF only impacts fibroblasts and keratinocytes which promote psoriatic lesions. In this study, we looked for differences of TNF-α, IL-10 and HB-EGF expression between a psoriatic patient and a non-psoriatic relative.
Methods: To achieve our target, peripheral blood mononuclear cells (PBMCs) expressing LPS receptors or CD14 (CD14+ cells) derived from a guttate patient, and the donor’s father (without psoriatic symptoms), were activated for 7 days by a lysate of Streptococcus pneumoniae for 24 hours before being harvested.
Results: Results showed detectable mRNAs of TNF-α, IL-10 and HB-EGF from isolated CD14+ cells of guttate patient were more intensive expression than the non-psoriatic one at 24 hours after engaging the bacterial components. In addition, transcription of HB-EGF gene from the guttate patient was maintained over 168 hours, while its mRNA level from the non-psoriatic volunteer was only expressed within 24 hours.
Conclusion: Finally, in initial results of inflammatory effects between strains, the Streptococcal lysate was seen to have stronger immune responses than the Staphylococcal lysate on the immune cells of the guttate psoriasis.
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</ol>
<li class="show">Anderson, K., Petersson, S., Wong, J., Shubbar, E., Lokko, N., Carlström, M., & Enerbäck, C. (2010). Elevation of serum epidermal growth factor and interleukin 1 receptor antagonist in active psoriasis vulgaris. <em>British Journal of Dermatology</em>, 163(5), 1085–1089. <a href="https://doi.org/10.1111/j.1365-2133.2010.09990.x">https://doi.org/10.1111/j.1365-2133.2010.09990.x</a></li>
<li class="show">Arias-Santiago, S., Espiñeira-Carmona, M. J., & Aneiros-Fernández, J. (2013). The Koebner phenomenon: Psoriasis in tattoos. <em>Canadian Medical Association Journal</em>, 185(7), 585–585. <a href="https://doi.org/10.1503/cmaj.111299">https://doi.org/10.1503/cmaj.111299</a></li>
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<li class="show">Bhardwaj, R. S., Schwarz, A., Becher, E., Mahnke, K., Aragane, Y., Schwarz, T., & Luger, T. A. (1996). Pro-opiomelanocortin-derived peptides induce IL-10 production in human monocytes. <em>Journal of Immunology (Baltimore, Md.: 1950)</em>, 156, 2517–2521.</li>
<li class="show">Byrne, A., & Reen, D. J. (2002). Lipopolysaccharide induces rapid production of IL-10 by monocytes in the presence of apoptotic neutrophils.<em> Journal of Immunology (Baltimore, Md.: 1950)</em>, 168(4), 1968–1977. <a href="https://doi.org/10.4049/jimmunol.168.4.1968">https://doi.org/10.4049/jimmunol.168.4.1968</a></li>
<li class="show">Chiricozzi, A., Guttman-Yassky, E., Suárez-Farinas, M., Nograles, K. E., Tian, S., Cardinale, I., . . . Krueger, J. G. (2011). Integrative responses to IL-17 and TNF-α in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis. <em>The Journal of Investigative Dermatology</em>, 131(3), 677–687. <a href="https://doi.org/10.1038/jid.2010.340">https://doi.org/10.1038/jid.2010.340</a></li>
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<li class="show">Evans, H. G., Gullick, N. J., Kelly, S., Pitzalis, C., Lord, G. M., Kirkham, B. W., & Taams, L. S. (2009). In vivo activated monocytes from the site of inflammation in humans specifically promote Th17 responses. <em>Proceedings of the National Academy of Sciences of the United States of America</em>, 106(15), 6232–6237. <a href="https://doi.org/10.1073/pnas.0808144106">https://doi.org/10.1073/pnas.0808144106</a></li>
<li class="show">Evans, P., Ovaa, H., Hamon, M., Kilshaw, P., Hamm, S., Bauer, S., . . . Smith, T. (2004). Zinc-finger protein A20, a regulator of inflammation and cell survival, has de-ubiquitinating activity. <em>The Biochemical Journal</em>, 378(3), 727–734. <a href="https://doi.org/10.1042/bj20031377">https://doi.org/10.1042/bj20031377</a></li>
<li class="show">Gervin, K., Vigeland, M. D., Mattingsdal, M., Hammero, M., Nygard, H., Olsen, A. O., . . . Lyle, R. (2012). DNA methylation and gene expression changes in monozygotic twins discordant for psoriasis: Identification of epigenetically dysregulated genes. <em>PLOS Genetics</em>, 8(1), e1002454. <a href="https://doi.org/10.1371/journal.pgen.1002454">https://doi.org/10.1371/journal.pgen.1002454</a></li>
<li class="show">Gratchev, A., Kzhyshkowska, J., Kannookadan, S., Ochsenreiter, M., Popova, A., Yu, X., . . . Gooi, L. (2008). Activation of a TGF-β-specific multistep gene expression program in mature macrophages requires glucocorticoid-mediated surface expression of TGF-β receptor II. <em>Journal of Immunology</em> (Baltimore, Md.: 1950), 180(10), 6553–6565. <a href="https://doi.org/10.4049/jimmunol.180.10.6553">https://doi.org/10.4049/jimmunol.180.10.6553</a></li>
<li class="show">Gudjonsson, J., Thorarinsson, A., Sigurgeirsson, B., Kristinsson, K., & Valdimarsson, H. (2003). Streptococcal throat infections and exacerbation of chronic plaque psoriasis: A prospective study. <em>British Journal of Dermatology</em>, 149(3), 530–534. <a href="https://doi.org/10.1046/j.1365-2133.2003.05552.x">https://doi.org/10.1046/j.1365-2133.2003.05552.x</a></li>
<li class="show">Haider, A. S., Lowes, M. A., Suárez-Fariñas, M., Zaba, L. C., Cardinale, I., Khatcherian, A., . . . Krueger, J. G. (2008). Identification of cellular pathways of “type 1,” Th17 T cells, and TNF-and inducible nitric oxide synthase-producing dendritic cells in autoimmune inflammation through pharmacogenomic study of cyclosporine A in psoriasis. <em>Journal of Immunology</em> (Baltimore, Md.: 1950), 180(3), 1913–1920. <a href="https://doi.org/10.4049/jimmunol.180.3.1913">https://doi.org/10.4049/jimmunol.180.3.1913</a></li>
<li class="show">Inoue, M., Arikawa, T., Chen, Y.-H., Moriwaki, Y., Price, M., Brown, M., . . . Shinohara, M. L. (2014). T cells down-regulate macrophage TNF production by IRAK1-mediated IL-10 expression and control innate hyperinflammation. <em>Proceedings of the National Academy of Sciences of the United States of America</em>, 111(14), 5295–5300. <a href="https://doi.org/10.1073/pnas.1321427111 ">https://doi.org/10.1073/pnas.1321427111 </a></li>
<li class="show">Johnson, G. R., Kannan, B., Shoyab, M., & Stromberg, K. (1993). Amphiregulin induces tyrosine phosphorylation of the epidermal growth factor receptor and p185erbB2. Evidence that amphiregulin acts exclusively through the epidermal growth factor receptor at the surface of human epithelial cells. <em>The Journal of Biological Chemistry</em>, 268, 2924–2931.</li>
<li class="show">Johnston, A., Gudjonsson, J., Sigmundsdottir, H., Love, T., & Valdimarsson, H. (2004). Peripheral blood T cell responses to keratin peptides that share sequences with streptococcal M proteins are largely restricted to skin‐homing CD8+ T cells. <em>Clinical and Experimental Immunology</em>, 138(1), 83–93. <a href="https://doi.org/10.1111/j.1365-2249.2004.00600.x ">https://doi.org/10.1111/j.1365-2249.2004.00600.x </a></li>
<li class="show">Jordan, C. T., Cao, L., Roberson, E. D., Duan, S., Helms, C. A., Nair, R. P., . . . Hayashi, G. (2012). Rare and common variants in CARD14, encoding an epidermal regulator of NF-kappaB, in psoriasis. <em>American Journal of Human Genetics</em>, 90(5), 796–808. <a href="https://doi.org/10.1016/j.ajhg.2012.03.013 ">https://doi.org/10.1016/j.ajhg.2012.03.013 </a></li>
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2017-11-25
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Copyright The Author(s) 2017. This article is published with open access by BioMedPress. This article is distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0) which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
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Observation of TNF-α, IL-10 and HB-EGF gene expression by peripheral blood CD14+ mononuclear cells: a case of guttate psoriatic patient. (2017). Biomedical Research and Therapy, 4(11), 1733-1748. https://doi.org/10.15419/bmrat.v4i11.378
