Affordable Access

deepdyve-link
Publisher Website

Increased Innate Lymphoid Cell 3 and IL-17 Production in Mouse Lamina Propria Stimulated with Giardia lamblia.

Authors
  • Lee, Hye-Yeon1
  • Park, Eun-Ah1
  • Lee, Kyung-Jo2
  • Lee, Kyu-Ho2
  • Park, Soon-Jung1
  • 1 Department of Environmental Medical Biology and Institute of Tropical Medicine, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul 03722, Korea. , (North Korea)
  • 2 Department of Life Science, Sogang University, Seoul 04107, Korea. , (North Korea)
Type
Published Article
Journal
The Korean journal of parasitology
Publication Date
Jun 01, 2019
Volume
57
Issue
3
Pages
225–232
Identifiers
DOI: 10.3347/kjp.2019.57.3.225
PMID: 31284344
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Innate lymphoid cells (ILCs) are key players during an immune response at the mucosal surfaces, such as lung, skin, and gastrointestinal tract. Giardia lamblia is an extracellular protozoan pathogen that inhabits the human small intestine. In this study, ILCs prepared from the lamina propria of mouse small intestine were incubated with G. lamblia trophozoites. Transcriptional changes in G. lamblia-exposed ILCs resulted in identification of activation of several immune pathways. Secretion of interleukin (IL)-17A, IL-17F, IL-1β, and interferon-γ was increased, whereas levels of IL-13, IL-5, and IL22, was maintained or reduced upon exposure to G. lamblia. Goup 3 ILC (ILC3) was found to be dominant amongst the ILCs, and increased significantly upon co-cultivation with G. lamblia trophozoites. Oral inoculation of G. lamblia trophozoites into mice resulted in their presence in the small intestine, of which, the highest number of parasites was detected at the 5 days-post infection. Increased ILC3 was observed amongst the ILC population at the 5 days-post infection. These findings indicate that ILC3 from the lamina propria secretes IL-17 in response to G. lamblia, leading to the intestinal pathology observed in giardiasis.

Report this publication

Statistics

Seen <100 times