Abstract
Trichuris muris is an intestinal nematode that invades the colonic epithelium triggering a mucosal inflammation. Vitamin A and its active metabolite retinoic acid are strongly linked with the modulation of gut immune responses. Here, we describe the temporal changes in the expression of aldehyde dehydrogenase (ALDH) enzymes, responsible for converting dietary-absorbed vitamin A into the immuno-modulatory retinoic acid in lamina propria leucocytes post-infection. We show that ALDH enzymes are expressed by both colonic macrophages and dendritic cells. Further, during an on-going T. muris infection, ALDH expression is repressed from uninfected levels and only recovers to normal levels following expulsion of the parasite. These results suggest that local regulation of cellular levels of retinoic acid is an important component of infection-driven inflammation.
Highlights
Trichuris trichiura is a nematode parasite that causes significant morbidity to more than 100 million people worldwide [1]
Our results suggest that retinoic acid production is down-regulated during an inflammatory insult to the gut, and that a threshold level of inflammation exists, which is needed to drive the decrease in the percentage of aldehyde dehydrogenase (ALDH)+ macrophages and dendritic cells (DCs) in the gut
To establish whether the production of retinoic acid changes over the course of an acute and/or chronic T. muris infection, the ALDEFLUOR assay was used to measure the expression of aldehyde dehydrogenases (ALDH) in large intestinal macrophages and dendritic cells (DCs)
Summary
Trichuris trichiura is a nematode parasite that causes significant morbidity to more than 100 million people worldwide [1]. The mouse analogue of this parasite, Trichuris muris, is used to model and dissect the immune responses that occur during the human infection [2]. Studies using T. muris have shown that the type of immune response that develops to the infection. Deficiency in vitamin A colocalizes geographically with nematode infections [7], and studies have shown that re-infection of children in Mexico with Ascaris lumbricoides is reduced with vitamin A supplementation [8]. The active metabolite of vitamin A, has been shown to be a key mediator of immune responses in the intestinal mucosa. Given that people harbouring parasitic worms are often vitamin A deficient and are supplemented with this vitamin, it is critical to understand the relationship between vitamin A and intestinal nematodes
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