Parasitol Int. 2014 May 27. pii: S1383-5769(14)00071-3. doi: 10.1016/j.parint.2014.05.005. [Epub ahead of print]

Role of glucocorticoids and Toxoplasma gondii infection on murine intestinal epithelial cells

Johnson SL¹, Gopal R², Enriquez A¹, Monroy FP³.

 

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 17kD, the presence of CORT during infection increased levels of 17kD 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.
Copyright © 2014. Published by Elsevier Ireland Ltd.

KEYWORDS:

Apicomplexa; GILZ; Glucocorticoids; Immunity; Immunosuppression; Parasite; Toxoplasma; siRNA

PMID:

24875937

[PubMed - as supplied by publisher]