Analysis of the mucosal immune responses induced by single and trickle infections with the bovine abomasal nematode Ostertagia ostertagi. (April 2014)

• Record Type: Journal Article
• Authors: Mihi, B.; van, F.; Vancoppernolle, S.; Rinaldi, M.; Chiers, K.; van den, W.; Goddeeris, B. M.; Vercruysse, J.; Claerebout, E.; Geldhof, P.
• Is Part Of: Parasite immunology. Volume 36:Number 4(2014:Apr.)
• Page Start: 150
• Page End: 156
• Publication Date: 2014-04
• Subjects: Veterinary parasitology -- Immunological aspects -- Periodicals; Host-parasite relationships -- Immunological aspects -- Periodicals; 571.96
• DOI: 10.1111/pim.12094
• Languages: English
• ISSNs: 0141-9838

Abstract

<abstract abstract-type="main" id="pim12094-abs-0001"> <title>Summary</title> <p>The purpose of this study was to provide more information on the kinetics of the immunological changes occurring in the abomasal mucosa after single and trickle infections with the bovine parasite <italic>Ostertagia ostertagi</italic>. The time course analysis of gene expression revealed that the major changes coincided with the emergence of adult worms from the gastric glands. These changes consisted of a simultaneous upregulation of Th1‐ and Th2‐type cytokines. In addition, a single <italic>O. ostertagi</italic> infection elicited an upregulation of the epithelial‐derived cytokine <italic>IL33</italic>, while <italic>TSLP</italic> expression levels were not impacted. Apart from the massive increase in inflammatory cytokines <italic>IL6</italic>, <italic> IL17</italic> and <italic>IL21</italic>, <italic> O. ostertagi</italic> infection also elicited an upregulation of the immunosuppressors <italic>TGFB</italic>, <italic> IL10</italic> and <italic>ARG1, </italic> as well as NK and γδ‐T cell markers. Furthermore, the cytotoxic factors granulysin, perforin and granzyme B were upregulated following an <italic>O. ostertagi</italic> infection. Analysis of cytokine transcript levels in animals receiving trickle infections for 60 days showed a similar trend as observed following a single infection except for <italic>IL33</italic>, <italic> IL6</italic>, <italic> GATA‐3</italic>, <italic> TBX21</italic> and <italic>NCR1</italic>, which were no longer upregulated after trickle infections. Finally, the long trickle infections were associated with mucosal eosinophilia and mastocytosis.</p> </abstract>