Abstract
BackgroudEnteromyxum leei is a myxozoan parasite that produces a slow-progressing intestinal disease. This parasite invades the paracellular space of the intestinal epithelium and progresses from the posterior to the anterior intestine. The aim of the present study was to gain insights into fish T cell responses in the gilthead sea bream-E. leei infection model using a PCR-array with 30 signature molecules for different leukocyte responses in head kidney, spleen, anterior and posterior intestine.ResultsThe PCR-array results suggest that E. leei induced migration of T cells from head kidney to intestines where TH1, CTL and TH17 profiles were activated and kept in balance by the upregulation of regulatory cytokines. These results were partially validated by the use of cross-reacting antibodies and BrdU immunostaining to monitor proliferation. Zap70 immunostaining supported the increased number of T cells in the anterior intestine detected by gene expression, but double staining with BrdU did not show active proliferation of this cell type at a local level, supporting the migration from lymphohaematopoietic tissues to the site of infection. Global analyses of the expression profiles revealed a clear separation between infected and exposed, but non-infected fish, more evident in the target organ. Exposed, non-infected animals showed an intermediate phenotype closer to the control fish.ConclusionsThese results evidence a clear modulation of the T cell response of gilthead sea bream upon E. leei infection. The effects occurred both at local and systemic levels, but the response was stronger and more specific at the site of infection, the intestine. Altogether, this research poses a promising basis to understand the response against this important parasite and establish effective preventive or palliative measures.
Highlights
Gilthead sea bream (Sparus aurata), a marine teleost species, is the main farmed fish in the Mediterranean [1]
The recipient fish (RCPT) group showed significantly lower weight, size and condition factor than the CTRL group, evidencing the typical infection signs induced by this parasite [4] (Table 1)
The current results suggest that the increase in Helper T cell (TH) cells induced by the parasitic infection in gilthead sea bream anterior intestine is due to activation of TH1 and TH17 profiles
Summary
Gilthead sea bream (Sparus aurata), a marine teleost species, is the main farmed fish in the Mediterranean [1]. Recruitment of mast cells and depletion of acidophilic granulocytes have been described in infected gilthead sea bream intestine [8]. Interleukin gene expression profiles elicited by E. leei infections were characterized by an early pro-inflammatory profile that later switched to an anti-inflammatory pattern in infected posterior intestinal segments [9]. This parasite regulates the immune response, mainly at a local level (intestine), and systemically. The progression pattern of the disease, where the parasite is only present at the anterior intestine at later infection stages, indicates that different responses are taking place at the different intestinal segments. This study constitutes the first step for understanding the T cell response of gilthead sea bream upon infection with E. leei
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