Abstract
The parasitic nematode Trichinella spiralis causes trichinellosis, a serious food-borne parasitic zoonosis worldwide. Infection with T. spiralis may also cause myocarditis. In the present study, we used mouse models to assess the impact of blockage of galectin-receptor interactions by α-lactose on cardiac immunopathology during acute T. spiralis experimental infection. Our data demonstrated that, after T. spiralis infection, blockage of galectin-receptor interactions resulted in cardiac dysfunction detected by transthoracic conventional echocardiography, and increased serum Gal-3 level, a biomarker of myocardial damage. In addition, there were increased eosinophil number in peripheral blood, and increased eosinophil infiltration in the heart and spleen tissues accompanied with increased mRNA levels of eosinophil granule proteins (including eosinophil cationic protein (ECP) and eosinophil peroxidase (EPO)) and IL-5 in these organs; increased cardiac fibrosis accompanied with increased Gal-3 and collagen 1 expressions in the hearts of mice with blockage of galectin-receptor interactions after T. spiralis infection. Correlation analysis showed that significant positive correlations existed between the mRNA levels of Gal-3 and ECP/EPO/eosinophil major basic protein/IL-5/CCL11/CCR3/α-SMA/collagen 1 in the hearts of both T. spiralis-infected mice and T. spiralis-infected mice with blockage of galectin-receptor interactions. Our data suggest that galectin-receptor interactions play a pivotal role during acute T. spiralis infection, and lack of galectin-receptor interactions upregulates Gal-3 which, in turn, leads to elevated heart eosinophil recruitment, exacerbated heart pathology and fibrosis, and heart functional damage.
Highlights
Trichinellosis is one of the most important foodborne parasitic zoonoses caused by nematodes of the genus Trichinella, which are worldwide distributed, including Europe, Southeast Asia, North and South America, and North Africa [1]
Inflammation and eosinophil infiltration were observed in the heart tissues of T. spiralis-infected mice; more severe inflammation and more eosinophil infiltration were observed in the heart tissues of T. spiralis-infected mice plus a-lactose treatment (Figure 1A)
The results suggest that a-SMA and collagen 1 may involve in the cardiac fibrosis caused by T. spiralis infection
Summary
Trichinellosis is one of the most important foodborne parasitic zoonoses caused by nematodes of the genus Trichinella, which are worldwide distributed, including Europe, Southeast Asia, North and South America, and North Africa [1]. Though T. spiralis causes muscle pain almost without life risk, myocarditis and neurological disorders is the most serious complication of human infestation. Galectin-Receptor Interactions Regulates Cardiac Pathology by T. spiralis, and myocarditis that may lead to death without treatment [7]. When T. spiralis parasitized in the host, it can induce host’s immune response and high numbers of eosinophils in the peripheral blood, which play an important role in defense against infestations. Eosinophilic myocarditis is a severe complication of trichinellosis that can lead to death due to rhythm disorders [9]. The pathological mechanisms of eosinophilic myocarditis caused by T. spiralis remains poorly understood
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