Regulation of toll-like receptors in intestinal epithelial cells by stress and Toxoplasma gondii infection

R. Gopal, D. Birdsell, Fernando P Monroy

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Intestinal epithelial cells (IECs) form a barrier between invading microorganisms and the underlying host tissues. IECs express toll-like receptors (TLRs) that recognize specific molecular signatures on microbes, which activate intracellular signalling pathways leading to production of proinflammatory cytokines and chemokines. Stress hormones play an important role in modulation of proinflammatory cytokines and down-regulation of immune responses. Here we demonstrated that expression levels of TLR-2, TLR-4, TLR-9 and TLR-11 were significantly increased in mouse IECs following infection with Toxoplasma gondii on day 8 postinfection. In contrast, expression of TLRs was significantly decreased in infected mice subjected to cold water stress (CWS + INF). Expression of TLR-9 and TLR-11 in the mouse MODE-K cell line was significantly increased after infection. Expression of TLR-9 and TLR-11 in cells exposed to norepinephrine (NE) and parasites was significantly decreased when compared to cells exposed to parasites only. A significant increase was observed in SIGIRR, a negative regulator of TLRs in the CWS + INF group when compared to the INF group. Stress components were able to decrease expression levels of TLRs in IECs, decrease parasite load, and increase expression of a negative regulator thereby ameliorating intestinal inflammatory responses commonly observed during per oral T. gondii infection in C57BL/6 mice.

Original languageEnglish (US)
Pages (from-to)563-576
Number of pages14
JournalParasite Immunology
Volume30
Issue number11-12
DOIs
StatePublished - Nov 2008

Fingerprint

Toll-Like Receptors
Toxoplasmosis
Epithelial Cells
Toll-Like Receptor 9
Parasites
Parasite Load
Cytokines
Toll-Like Receptor 2
Toll-Like Receptor 4
Inbred C57BL Mouse
Dehydration
Chemokines
Norepinephrine
Down-Regulation
Hormones
Cell Line
Infection

Keywords

  • Innate immunity
  • Intestinal epithelial cells
  • Stress hormones
  • Toll-like receptors
  • Toxoplasma gondii

ASJC Scopus subject areas

  • Parasitology
  • Immunology

Cite this

Regulation of toll-like receptors in intestinal epithelial cells by stress and Toxoplasma gondii infection. / Gopal, R.; Birdsell, D.; Monroy, Fernando P.

In: Parasite Immunology, Vol. 30, No. 11-12, 11.2008, p. 563-576.

Research output: Contribution to journalArticle

@article{946cc3558d9a4a2abd1453b806a85da8,
title = "Regulation of toll-like receptors in intestinal epithelial cells by stress and Toxoplasma gondii infection",
abstract = "Intestinal epithelial cells (IECs) form a barrier between invading microorganisms and the underlying host tissues. IECs express toll-like receptors (TLRs) that recognize specific molecular signatures on microbes, which activate intracellular signalling pathways leading to production of proinflammatory cytokines and chemokines. Stress hormones play an important role in modulation of proinflammatory cytokines and down-regulation of immune responses. Here we demonstrated that expression levels of TLR-2, TLR-4, TLR-9 and TLR-11 were significantly increased in mouse IECs following infection with Toxoplasma gondii on day 8 postinfection. In contrast, expression of TLRs was significantly decreased in infected mice subjected to cold water stress (CWS + INF). Expression of TLR-9 and TLR-11 in the mouse MODE-K cell line was significantly increased after infection. Expression of TLR-9 and TLR-11 in cells exposed to norepinephrine (NE) and parasites was significantly decreased when compared to cells exposed to parasites only. A significant increase was observed in SIGIRR, a negative regulator of TLRs in the CWS + INF group when compared to the INF group. Stress components were able to decrease expression levels of TLRs in IECs, decrease parasite load, and increase expression of a negative regulator thereby ameliorating intestinal inflammatory responses commonly observed during per oral T. gondii infection in C57BL/6 mice.",
keywords = "Innate immunity, Intestinal epithelial cells, Stress hormones, Toll-like receptors, Toxoplasma gondii",
author = "R. Gopal and D. Birdsell and Monroy, {Fernando P}",
year = "2008",
month = "11",
doi = "10.1111/j.1365-3024.2008.01055.x",
language = "English (US)",
volume = "30",
pages = "563--576",
journal = "Parasite Immunology",
issn = "0141-9838",
publisher = "Wiley-Blackwell",
number = "11-12",

}

TY - JOUR

T1 - Regulation of toll-like receptors in intestinal epithelial cells by stress and Toxoplasma gondii infection

AU - Gopal, R.

AU - Birdsell, D.

AU - Monroy, Fernando P

PY - 2008/11

Y1 - 2008/11

N2 - Intestinal epithelial cells (IECs) form a barrier between invading microorganisms and the underlying host tissues. IECs express toll-like receptors (TLRs) that recognize specific molecular signatures on microbes, which activate intracellular signalling pathways leading to production of proinflammatory cytokines and chemokines. Stress hormones play an important role in modulation of proinflammatory cytokines and down-regulation of immune responses. Here we demonstrated that expression levels of TLR-2, TLR-4, TLR-9 and TLR-11 were significantly increased in mouse IECs following infection with Toxoplasma gondii on day 8 postinfection. In contrast, expression of TLRs was significantly decreased in infected mice subjected to cold water stress (CWS + INF). Expression of TLR-9 and TLR-11 in the mouse MODE-K cell line was significantly increased after infection. Expression of TLR-9 and TLR-11 in cells exposed to norepinephrine (NE) and parasites was significantly decreased when compared to cells exposed to parasites only. A significant increase was observed in SIGIRR, a negative regulator of TLRs in the CWS + INF group when compared to the INF group. Stress components were able to decrease expression levels of TLRs in IECs, decrease parasite load, and increase expression of a negative regulator thereby ameliorating intestinal inflammatory responses commonly observed during per oral T. gondii infection in C57BL/6 mice.

AB - Intestinal epithelial cells (IECs) form a barrier between invading microorganisms and the underlying host tissues. IECs express toll-like receptors (TLRs) that recognize specific molecular signatures on microbes, which activate intracellular signalling pathways leading to production of proinflammatory cytokines and chemokines. Stress hormones play an important role in modulation of proinflammatory cytokines and down-regulation of immune responses. Here we demonstrated that expression levels of TLR-2, TLR-4, TLR-9 and TLR-11 were significantly increased in mouse IECs following infection with Toxoplasma gondii on day 8 postinfection. In contrast, expression of TLRs was significantly decreased in infected mice subjected to cold water stress (CWS + INF). Expression of TLR-9 and TLR-11 in the mouse MODE-K cell line was significantly increased after infection. Expression of TLR-9 and TLR-11 in cells exposed to norepinephrine (NE) and parasites was significantly decreased when compared to cells exposed to parasites only. A significant increase was observed in SIGIRR, a negative regulator of TLRs in the CWS + INF group when compared to the INF group. Stress components were able to decrease expression levels of TLRs in IECs, decrease parasite load, and increase expression of a negative regulator thereby ameliorating intestinal inflammatory responses commonly observed during per oral T. gondii infection in C57BL/6 mice.

KW - Innate immunity

KW - Intestinal epithelial cells

KW - Stress hormones

KW - Toll-like receptors

KW - Toxoplasma gondii

UR - http://www.scopus.com/inward/record.url?scp=55349137780&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=55349137780&partnerID=8YFLogxK

U2 - 10.1111/j.1365-3024.2008.01055.x

DO - 10.1111/j.1365-3024.2008.01055.x

M3 - Article

C2 - 19067837

AN - SCOPUS:55349137780

VL - 30

SP - 563

EP - 576

JO - Parasite Immunology

JF - Parasite Immunology

SN - 0141-9838

IS - 11-12

ER -