Transient gestational hypothyroxinemia accelerates and enhances ulcerative colitis-like disorder in the male offspring

Introduction: Gestational hypothyroxinemia (HTX) is a condition that occurs frequently at the beginning of pregnancy, and it correlates with cognitive impairment, autism, and attentional deficit in the offspring. Evidence in animal models suggests that gestational HTX can increase the susceptibility of the offspring to develop strong inflammation in immune-mediated inflammatory diseases. Ulcerative colitis (UC) is a frequent inflammatory bowel disease with unknown causes. Therefore, the intensity of ulcerative colitis-like disorder (UCLD) and the cellular and molecular factors involved in proinflammatory or anti-inflammatory responses were analyzed in the offspring gestated in HTX (HTX-offspring) and compared with the offspring gestated in euthyroidism (Control-offspring). Methods: Gestational HTX was induced by the administration of 2-mercapto-1- methylimidazole in drinking water to pregnant mice during E10–E14. The HTXoffspring were induced with UCLD by the acute administration of dextran sodium sulfate (DSS). The score of UCLD symptomatology was registered every day, and colon histopathology, immune cells, and molecular factors involved in the inflammatory or anti-inflammatory response were analyzed on day 6 of DSS treatment. Results: The HTX-offspring displayed earlier UCLD pathological symptoms compared with the Control-offspring. After 6 days of DSS treatment, the HTXoffspring almost doubled the score of the Control-offspring. The histopathological analyses of the colon samples showed signs of inflammation

Notas

Indexación: Scopus

Palabras clave

gestational hypothyroxinemia, ulcerative colitis, colon inflammation, immune cells, autoimmunity, radical oxygen species

Citación

Frontiers in Endocrinology Volume14 2024

DOI

10.3389/fendo.2023.1269121

URI

https://repositorio.unab.cl/handle/ria/61302

Colecciones

Fac.CV - Artículos de Revista

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