title: Role of glucocorticoids and Toxoplasma gondii infection on murine intestinal epithelial cells.
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.
authors.affiliation: Department of Biological Sciences, Northern Arizona University, P.O. Box 5640, Flagstaff, AZ 86011, USA.
authors.forename: Stacy L
authors.initials: SL
authors.lastname: Johnson
authors.affiliation: Children's Hospital of Pittsburgh, University of Pittsburgh Medical Center (UPMC), 4401 Penn Avenue, Pittsburgh, PA 15224, USA.
authors.forename: Radha
authors.initials: R
authors.lastname: Gopal
authors.affiliation: Department of Biological Sciences, Northern Arizona University, P.O. Box 5640, Flagstaff, AZ 86011, USA.
authors.forename: Amber
authors.initials: A
authors.lastname: Enriquez
authors.affiliation: Department of Biological Sciences, Northern Arizona University, P.O. Box 5640, Flagstaff, AZ 86011, USA. Electronic address: Fernando.Monroy@nau.edu.
authors.forename: Fernando P
authors.initials: FP
authors.lastname: Monroy
mesh_terms: D000818:Animals; D002460:Cell Line; D004847:Epithelial Cells / Q000187:drug effects* / Q000469:parasitology*; D005938:Glucocorticoids / Q000494:pharmacology*; D007413:Intestinal Mucosa / Q000166:cytology*; D051379:Mice; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering; D014122:Toxoplasma; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: C498608:Dsip1 protein, mouse; D005938:Glucocorticoids; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D014157:Transcription Factors
keywords: GILZ; Glucocorticoids; Immunity; MODE-K; Toxoplasma; siRNA