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Rotavirus double-stranded RNA induces apoptosis and diminishes wound repair in rat intestinal epithelial cells
Akiko Sato1, Masahiro Iizuka, Osamu Nakagomi
1Department of Internal Medicine, Akita University School of Medicine, Akita, Japan.
Insights
Rotavirus double-stranded RNA (dsRNA) triggers toll-like receptor 3 (TLR3) in intestinal cells, causing apoptosis and hindering wound repair. This mechanism may contribute to rotavirus-induced enteritis.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Toll-like receptor 3 (TLR3) recognizes double-stranded RNA (dsRNA).
- Rotaviruses possess a dsRNA genome and infect intestinal epithelial cells (IEC).
- Rotavirus infection causes acute gastroenteritis in young children.
Purpose of the Study:
- To investigate the role of rotavirus dsRNA in intestinal epithelial cells (IEC).
- To clarify the pathophysiological function of rotavirus dsRNA in IEC.
Main Methods:
- Assessed TLR3 mRNA and protein expression in IEC cell lines (IEC-6, HT-29, Caco-2) using RT-PCR, Western blot, and immunohistochemistry.
- Evaluated cytokine mRNA induction and signal protein activation (ERK1/2 MAPK, IkappaB-alpha) in IEC after dsRNA stimulation.
- Assessed IEC-6 cell migration and apoptosis following dsRNA exposure.
Main Results:
- TLR3 mRNA and protein were detected in IEC, with potential upregulation by IFN-gamma.
- Rotavirus dsRNA stimulation induced cytokine mRNA and activated signal proteins.
- dsRNA exposure dose-dependently diminished epithelial wound repair and induced apoptosis, effects suppressed by anti-TLR3 antibody or caspase inhibitor.
Conclusions:
- Rotavirus dsRNA induces significant apoptosis and impairs wound repair in IEC via TLR3.
- These findings suggest a role for TLR3 in the pathogenesis of rotavirus-induced enteritis.
Background:
Recent studies have shown that toll-like receptor 3 (TLR3) recognizes double-stranded RNA (dsRNA). Rotaviruses, having a dsRNA genome, infect intestinal epithelial cells (IEC) and cause acute gastroenteritis in young children. The aim of the present study was to clarify the pathophysiological function of rotavirus dsRNA in IEC.
Methods:
Expression of TLR3 mRNA or protein in IEC cell lines (IEC-6, HT-29, Caco-2) was assessed by reverse transcription polymerase chain reaction (RT-PCR), Western blot analysis or immunohistochemistry. Induction of cytokines (TNF-alpha, interferon-beta, interleukin-6) mRNA and activation of signal proteins (ERK1/2 MAPK and IkappaB-alpha) in IEC after stimulation with rotavirus dsRNA were assessed by RT-PCR or Western blot analysis. IEC-6 cells were wounded and cell migration into wound areas after stimulation with rotavirus dsRNA (1-25 microg/mL) was assessed. Induction of apoptosis after stimulation with rotavirus dsRNA was also assessed.
Results:
Expression of TLR3 mRNA and TLR3 protein was detected in IEC. Expression of TLR3 mRNA in IEC-6 tended to be up-regulated by exposure to IFN-gamma. Induction of cytokine mRNA and activation of the signal proteins were detected after stimulation with rotavirus dsRNA. Apoptosis was induced and epithelial migration into the wound area was dose-dependently diminished (44.1-94.4%, P < 0.01) by exposure to rotavirus dsRNA. Diminishment of wound repair was suppressed by anti-TLR3 antibody or caspase inhibitor.
Conclusion:
Rotavirus dsRNA induces severe apoptosis and diminishes wound repair in IEC through TLR3, which might be involved in the pathogenesis of rotavirus-induced enteritis.
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