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Mastocytosis and intraepithelial lymphocytosis in the ileum and colon characterize chronic Toxoplasma gondii infection in mice.
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- Additional Information
- Source:
Publisher: Churchill Livingstone Country of Publication: Scotland NLM ID: 0214745 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1532-3072 (Electronic) Linking ISSN: 00408166 NLM ISO Abbreviation: Tissue Cell Subsets: MEDLINE
- Publication Information:
Publication: Edinburgh : Churchill Livingstone
Original Publication: Edinburgh, Oliver & Boyd.
- Subject Terms:
- Abstract:
Toxoplasma gondii is the causative agent of toxoplasmosis, a common zoonotic disease affecting vertebrates with high global incidence. For the parasite to disseminate throughout the body, it crosses the intestinal barrier, triggering inflammatory reactions. This study aimed to assess the tissue response in the ileum and colon of mice following chronic infection with T. gondii. Fourteen mice were divided into two groups: the infected group received 1000 T. gondii oocysts via gavage, and after 60 days, the mice were euthanized. The ileum and colon were collected and processed for histological analysis, inflammatory marker measurement and myenteric neuron analysis. Chronic infection resulted in a significant increase in intraepithelial lymphocytes and mast cells, as well as morphometric changes such as increased total intestinal wall thickness of the ileum, crypt depth, collagen fiber area, and a decrease in myeloperoxidase activity, without altering nitric oxide levels. While the number of myenteric neurons remained unchanged, there was an increase in vasoactive intestinal peptide expression. These results suggest persistence intestinal inflammatory stimuli in chronic T. gondii infection.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
- Contributed Indexing:
Keywords: Chronic infection; Immunoregulatory cell; Intestine; Mast cells; Toxoplasmosis
- Publication Date:
Date Created: 20240830 Date Completed: 20241208 Latest Revision: 20241208
- Publication Date:
20241210
- Accession Number:
10.1016/j.tice.2024.102533
- Accession Number:
39213782
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