Cytokine and goblet cell gene expression in equine cyathostomin infection and larvicidal anthelmintic therapy

Aims The role of the immune response to cyathostomin infections in horses remains unknown. Intestinal goblet cell hyperplasia has previously been noted as a component in cyathostomin infection; however, the function is unclear. The goal of this study was to evaluate the local and systemic gene expre...

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Veröffentlicht in:Parasite immunology 2020-06, Vol.42 (6), p.e12709-n/a
Hauptverfasser: Steuer, Ashley E., Stewart, John C., Barker, Virginia D., Adams, Amanda A., Nielsen, Martin K.
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Sprache:eng
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Zusammenfassung:Aims The role of the immune response to cyathostomin infections in horses remains unknown. Intestinal goblet cell hyperplasia has previously been noted as a component in cyathostomin infection; however, the function is unclear. The goal of this study was to evaluate the local and systemic gene expression to cyathostomin infections following larvicidal treatment and explore their relation to goblet cells. Methods and Results Thirty‐six ponies with naturally acquired cyathostomin infections were randomly allocated into three groups: fenbendazole‐treated (10 mg/kg PO 5 days), moxidectin‐treated (0.4 mg/kg PO once) and untreated control. Whole blood from all horses was collected weekly, and tissue samples from the large intestine collected during necropsy at 2 and 5 weeks post‐treatment (WPT). Gene expression of interleukin (IL)‐4, IL‐5, IL‐6, IL‐10, IL‐13, IL‐17A, IL‐22, IFN‐γ, resistin‐like molecule beta (RELM‐β), Mucin 2 (MUC2) and tumour necrosis factor (TNF)‐α was measured using qRT‐PCR. There were statistically significant linear correlations between luminal worm burdens and MUC2 (r = −.2358) and RELM‐β (r = −.2261). Conclusion This suggests an active role of immune system post‐treatment in parasite expulsion, specifically in goblet cells, and that the organs respond differently to treatment and the larvae themselves. This may have implications in the disease process and treatment.
ISSN:0141-9838
1365-3024
DOI:10.1111/pim.12709