Abstract
The interaction of the nervous, immune, and endocrine systems is crucial in maintaining homeostasis in vertebrates, and vital in mammals. The spleen is a key organ that regulates the neuroimmunoendocrine system. The Taenia crassiceps mouse system is an excellent experimental model to study the complex host–parasite relationship, particularly sex-associated susceptibility to infection. The present study aimed to determine the changes in neurotransmitters, cytokines, sex steroids, and sex-steroid receptors in the spleen of cysticercus-infected male and female mice and whole parasite counts. We found that parasite load was higher in females in comparison to male mice. The levels of the neurotransmitter epinephrine were significantly decreased in infected male animals. The expression of IL-2 and IL-4 in the spleen was markedly increased in infected mice; however, the expression of Interleukin (IL)-10 and interferon (IFN)-γ decreased. We also observed sex-associated differences between non-infected and infected mice. Interestingly, the data show that estradiol levels increased in infected males but decreased in females. Our studies provide evidence that infection leads to changes in neuroimmunoendocrine molecules in the spleen, and these changes are dimorphic and impact the establishment, growth, and reproduction of T. crassiceps. Our findings support the critical role of the neuroimmunoendocrine network in determining sex-associated susceptibility to the helminth parasite.
Highlights
Murine intraperitoneal cysticercosis is caused by the helminth cestode Taenia crassiceps
Few studies have investigated the effects of chronic infection on the neuroimmunoendocrine response in lymphoid organs [28]
The spleen is the largest secondary immune organ. It comprises two main compartments: (1) the red pulp, which filters the blood of foreign material and damaged erythrocytes, and (2) the white pulp, which initiates immune reactions to blood-borne antigens [31]. This is the first study to demonstrate a relationship between helminth infection and the neuroimmunoendocrinology of the spleen
Summary
Murine intraperitoneal cysticercosis is caused by the helminth cestode Taenia crassiceps. Intraperitoneal T. crassiceps cysticercosis of mice lends itself well to controlled and reproducible experimentation, generating substantial parasite loads in individual mice in a matter of a few weeks after infection [1,2] This experimental model allows for a good representation of other forms of cysticercosis because of the parasite’s extensive sharing of antigens with other taenias and cestodes, since T. crassiceps and T. solium have high genetic homology [3–6]. These characteristics have made murine cysticercosis a convenient instrument for testing vaccine candidates and new treatments against cysticercosis and evaluating the complex host-cysticercus interaction [7,8]. The absence of estrogens does not prevent the growth of the parasites in both genders, demonstrating that estradiol favors T. crassiceps development, it is not indispensable for rapid parasite growth [16]
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