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Assays for the Specific Growth Rate and Cell-binding Ability of Rotavirus
Published on: January 28, 2019
The epithelial cell response to rotavirus infection
E E Rollo1, K P Kumar, N C Reich
1Department of Medicine, Northport Veterans Affairs Medical Center, NY 11768, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|October 8, 1999
Summary
Rotavirus infection activates key immune pathways in intestinal cells, triggering chemokine production. This response is primarily mediated by intestinal epithelial cells, especially in young animals.
Area of Science:
- Immunology
- Virology
- Gastroenterology
Background:
- Rotavirus is a leading cause of severe infant gastroenteritis worldwide.
- The role of intestinal epithelial cells in the host response to rotavirus is not well understood.
Purpose of the Study:
- To investigate the innate immune response of intestinal epithelial cells to rotavirus infection.
- To identify the specific immune signaling pathways and cellular components involved.
Main Methods:
- Infection of HT-29 intestinal epithelial cells with rotavirus.
- Analysis of NF-kappaB, STAT1, and ISGF3 activation.
- Measurement of chemokine and cytokine mRNA expression.
- Infection of mice with different rotavirus strains.
- Assessment of chemokine responses in genetically modified mice and young vs. adult mice.
Main Results:
- Rotavirus infection rapidly activated NF-kappaB, STAT1, and ISGF3 in HT-29 cells.
- Both infectious rotavirus and virus-like particles induced NF-kappaB activation.
- Rotavirus infection upregulated mRNA for chemokines, IFNs, and GM-CSF in cells and mice.
- Chemokine induction occurred in young mice (<15 days) but not older mice.
- Macrophage inflammatory protein-1beta expression was localized to intestinal epithelial cells.
Conclusions:
- Intestinal epithelial cells are active participants in the host response to rotavirus.
- Rotavirus-induced chemokine production is largely independent of mast cells and lymphocytes.
- Age is a critical factor in the chemokine response to rotavirus infection.
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