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In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
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Published on: October 19, 2018

TLR4 mediates MAPK-STAT3 axis activation in bladder epithelial cells.

Huang Ying1, Liu Da, Shi Yu-xiu

  • 1Department of Ultrasound, Shengjing Hospital of China Medical University, 110004, Shenyang, China, huangying712@163.com.

Inflammation
|April 25, 2013
PubMed
Summary

Toll-like receptor 4 (TLR4) activation in bladder epithelial cells (BECs) triggers interleukin-10 (IL-10) production through mitogen-activated protein (MAP) kinase pathways. This study reveals a crucial crosstalk between MAP kinase and STAT3 signaling in response to lipopolysaccharide (LPS).

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Toll-like receptor 4 (TLR4) is crucial in immune responses, but its role in bladder epithelial cells (BECs) and associated signaling pathways remains unclear.
  • The interplay between mitogen-activated protein (MAP) kinase and signal transducer and activator of transcription (STAT)3 pathways in TLR4-mediated signaling in BECs has not been previously elucidated.

Purpose of the Study:

  • To investigate TLR4-mediated signal transduction in BECs, focusing on the crosstalk between MAPK and STAT3 pathways.
  • To analyze the inflammatory cytokine response, specifically IL-10, induced by TLR4 activation in BECs.
  • To examine the relevance of this crosstalk in inflammatory conditions like cystitis glandularis (CG).

Main Methods:

  • Utilized human bladder cancer T24 cell line for in vitro studies.
  • Assessed TLR4, p38, ERK, JNK, and STAT3 expression using RT-PCR, quantitative PCR, and Western blotting.
  • Measured IL-10 secretion via ELISA and analyzed signaling pathway activation through Western blotting.
  • Investigated in vivo models of rat bladder infection and human CG patient tissues.

Main Results:

  • TLR4 expression was significantly upregulated by lipopolysaccharide (LPS) in T24 cells.
  • LPS stimulation led to dose- and time-dependent phosphorylation of MAPK and STAT3 pathways, and increased IL-10 secretion.
  • Inhibition of p38 and JNK pathways attenuated LPS-induced IL-10 production and STAT3 expression.
  • Elevated IL-10 mRNA levels were observed in inflamed tissues from rats and CG patients.

Conclusions:

  • TLR4 activation in BECs induces IL-10 expression mediated by p38 and JNK activation.
  • STAT3 activation is upregulated in conjunction with MAPK pathway activation.
  • A critical reciprocal crosstalk between MAPK and STAT3 signaling pathways is successively activated by LPS in BECs, contributing to inflammation.