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Fasciola hepatica products can alter the response of bovine immune cells to Mycobacterium avium subsp. paratuberculosis
Author(s) -
NaranjoLucena Amalia,
GarcíaCampos Andrés,
GarzaCuartero Laura,
Britton Louise,
Blanco Alfonso,
Zintl Annetta,
Mulcahy Grace
Publication year - 2020
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12779
Subject(s) - hepatica , fasciola hepatica , biology , immune system , immunology , mycobacterium avium subspecies paratuberculosis , paratuberculosis , cd14 , peripheral blood mononuclear cell , antigen , mycobacterium , in vitro , helminths , bacteria , genetics , biochemistry
Abstract Background Fasciola hepatica causes economically important disease in livestock worldwide. The relevance of this parasitic infection extends beyond its direct consequences due to its immunoregulatory properties. Objectives Given the importance of the T helper 1 (Th1) immune response in controlling infections with Mycobacterium avium subspecies paratuberculosis (MAP) in cattle, we aimed to establish the immunological consequences that co‐infection with F. hepatica might have on the course of Johne’s disease (JD). Methods This study compared the in vitro response of bovine immune cells to infection with MAP or exposure to MAP antigens following F. hepatica infection or stimulation with F. hepatica products. Results We found a decreased proliferation of peripheral blood mononuclear cells (PBMCs) after infection with F. hepatica . This reduction was inversely correlated with fluke burden. Pre‐stimulation with F. hepatica molecules produced a significant reduction of ileocaecal lymph node leucocyte proliferation in response to MAP antigens. Additionally, F. hepatica products reduced expression of the CD14 receptor by macrophages and increased levels of apoptosis and bacterial (MAP) uptake. Conclusions Overall, F. hepatica infection had little impact on the in vitro response of immune cells to MAP, whereas in vitro co‐stimulation with F. hepatica molecules had a measurable effect. Whether this is likely to affect JD progression during in vivo chronic conditions remains unclear.