Veterinary immunology and immunopathology · 2017
Dietary cinnamaldehyde enhances acquisition of specific antibodies following helminth infection in pigs.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Williams Andrew R, Hansen Tina V A, Krych Lukasz, Ahmad Hajar Fauzan Bin, Nielsen Dennis S, Skovgaard Kerstin, Thamsborg Stig M
Аннотация
Dietary phytonutrients such as cinnamaldehyde (CA) may contribute to immune function during pathogen infections, and CA has been reported to have positive effects on gut health when used as feed additive for livestock. Here, we investigated whether CA could enhance antibody production and specific immune responses during infection with an enteric pathogen. We examined the effect of dietary CA on plasma antibody levels in parasite-naïve pigs, and subsequently acquisition of humoral immune responses during infection with the parasitic nematode Ascaris suum. Parasite-naïve pigs fed diets supplemented with CA had higher levels of total IgA and IgG in plasma, and A. suum-infected pigs fed CA had higher levels of parasite-specific IgM and IgA in plasma 14days post-infection. Moreover, dietary CA increased expression of genes encoding the B-cell marker CD19, sodium/glucose co-transporter1 (SCA5L1) and glucose transporter 2 (SLC2A2) in the jejunal mucosa of A.suum-infected pigs. Dietary CA induced only limited changes in the composition of the prokaryotic gut microbiota of A. suum-infected pigs, and in vitro experiments showed that CA did not directly induce proliferation or increase secretion of IgG and IgA from lymphocytes. Our results demonstrate that dietary CA can significantly enhance acquisition of specific immune responses in pigs. The underlying mechanism remains obscure, but apparently does not derive simply from direct contact between CA and host lymphocytes and appears to be independent of the gut microbiota.