Role of glucocorticoids and Toxoplasma gondii infection on murine intestinal epithelial cells |
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| Institution: | 1. Department of Biological Sciences, Northern Arizona University, P.O. Box 5640, Flagstaff, AZ 86011, USA;2. Children''s Hospital of Pittsburgh, University of Pittsburgh Medical Center (UPMC), 4401 Penn Avenue, Pittsburgh, PA 15224, USA;1. Department of Pathology and Pathogen Biology, Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield AL9 7TA, United Kingdom;2. School of Marine and Tropical Biology, Discipline of Aquaculture, James Cook University, Cairns, Queensland 4878, Australia;3. School of Biological Sciences, The University of Queensland, St Lucia, Queensland 4072, Australia;4. Department of Veterinary Medicine, University of Cambridge, Madingley Rd, Cambridge CB3 0ES, United Kingdom;5. Centre for Biodiscovery and Molecular Development of Therapeutics, Australian Institute of Tropical Health and Medicine, James Cook University, Cairns, Queensland 4878, Australia;1. Laboratory of Pathology, School of Veterinary Medicine, Azabu University, 1-17-71 Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan;2. Laboratory of Parasitology, School of Veterinary Medicine, Azabu University, 1-17-71 Fuchinobe, Chuo-ku, Sagamihara, Kanagawa 252-5201, Japan;1. Department of Veterinary Pathology, São Paulo State University (Unesp), Jaboticabal, Brazil;2. Researcher from Brazilian Agricultural Research Corporation-EMBRAPA, Sergipe, Brazil;3. Laboratory of Animal Pharmacology and Toxicology, Camilo Castelo Branco University, Brazil |
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| Abstract: | Glucocorticoids (GCs) are stress hormones secreted in response to perceived psychological and or physiological stress. GCs have been shown to reduce tissue inflammation by down-regulating the production of inflammatory chemokines produced by epithelial cells. The protozoan parasite Toxoplasma gondii is known to increase cytokine, chemokine, and Toll-like receptors (TLRs) expression in parasite infected mouse intestinal epithelial cells (IECs). We sought to analyze the role of an anti-inflammatory protein, glucocorticoid-induced leucine zipper (GILZ) in MODE-K cells during infection with T. gondii. GILZ expression in MODE-K cells was assessed by PCR and immunoblotting after stimulation with GCs (corticosterone, CORT) or T. gondii infection. GILZ mRNA was constitutively expressed in MODE-K cells but not its protein product. While infection and pre-exposure to CORT decreased GILZ isoforms of 28 and 17 kD, the presence of CORT during infection increased levels of 17 kD isoform. Infected cells treated with CORT had decreased expression of chemokines (IP-10/CXCL10, MCP-1/CCL2, MIP-2/CXCL8) while their expression was increased when endogenous GILZ was removed by siRNA treatment. GILZ up-regulation during infection may serve as a mechanism to decrease epithelial cell responses and facilitate parasite replication. |
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