Calomys callosus: An Experimental Animal Model Applied to Parasitic Diseases Investigations of Public Health Concern

Abstract

The appearance and spread of parasitic diseases around the world aroused the interest of the scientific community to discover new animal models for improving the quality and specificity of surveys. Calomys callosus is a rodent native to South America, an easy handling model, with satisfactory longevity and reproducibility. C. callosus is susceptible to toxoplasmosis and can be used as experimental model for the study the pathogenesis, treatment, vertical transmission, and ocular toxoplasmosis. C. callosus can also be used to study cutaneous and visceral leishmaniasis, as the animals present cutaneous lesions, as well as parasites in the organs. C. callosus has epidemiological importance in Chagas disease, and since it is a Trypanosoma cruzi natural host in which rodents show high parasitemia and lethality, they are also effective as a model of congenital transmission. In the study of schistosomiasis, Schistosoma mansoni was proven to be a C. callosus natural host; thus, this rodent is a great model for fibrosis, hepatic granulomatous reaction, and celloma associated with lymphomyeloid tissue (CALT) during S. mansoni infection. In this review, we summarize the leading studies of parasitic diseases that used C. callosus as a rodent experimental model, describing the main uses and characteristics that led them to be considered an effective model.

The trophoblast giant cells of cricetid rodents

“…A deeper knowledge of the biology of TGCs in cricetid rodents will contribute not only to clarify evolutionary aspects of maternal-fetal communication, but may increase our knowledge in different fields: 1) maternal tolerance and immunomodulation during trophoblast invasion and vascular remodelling; 2) how changes of gene copy number and their expression affect normal and abnormal cell differentiation, for which TGCs are an interesting model; 3) the distribution of histone variants such as H3.3, in the genome of TGCs; 4) the development of knockout models for genes of interest (including exclusive markers for specific TGC lineages), which could generate data regarding placental abnormalities; 5) since the placental trophoblasts are responsible for fetal protection, and infection of these cells is directly involved in the pathogenesis of several intracellular parasites, knowledge of TGC diversity in cricetids will be helpful for the establishment of effective laboratory models, as has been shown in Calomys callosus ( Costa et al, 2009 ; Rosa et al, 2022 ); and finally 6) exploration of specific TGC-lineages as models for cancer development and metastasis, especially using cell cultures and 3D models.…”

“…Primary TGCs Derived from mural trophectoderm and migrate to decidua Similar Phagocytic and may enlarge implantation chamber (Disse, (1906) Parietal TGCs Parietal yolk sac beneath Reichert's membrane; distinct layer between junctional zone and decidua; accumulation at placental margin Identical location in parietal yolk sac and between junctional zone and decidua Accumulation at margin described for several families of cricetids (Sansom, (1922); Pijnenborg, (1975); Favaron et al (2011) (Pijnenborg et al (1974), although uNK cells are more important (Croy et al (1996) Migratory TGCs Found in numerous locations including the uterine wall where they can survive postpartum Apart from early migration towards the spiral arteries, murine TGCs seem to wander less than in cricetids Prominent feature of cricetid placentation (Sansom, (1922); Ozdzenski and Mystkowka, (1976);Parkening, (1976); Copp and Clarke, (1988); Blankenship et al (1990); Ferro and Bevilacqua, (1994) Frontiers in Cell and Developmental Biology frontiersin.org aspects of maternal-fetal communication, but may increase our knowledge in different fields: 1) maternal tolerance and immunomodulation during trophoblast invasion and vascular remodelling; 2) how changes of gene copy number and their expression affect normal and abnormal cell differentiation, for which TGCs are an interesting model; 3) the distribution of histone variants such as H3.3, in the genome of TGCs; 4) the development of knockout models for genes of interest (including exclusive markers for specific TGC lineages), which could generate data regarding placental abnormalities; 5) since the placental trophoblasts are responsible for fetal protection, and infection of these cells is directly involved in the pathogenesis of several intracellular parasites, knowledge of TGC diversity in cricetids will be helpful for the establishment of effective laboratory models, as has been shown in Calomys callosus (Costa et al, 2009;Rosa et al, 2022); and finally 6) exploration of specific TGC-lineages as models for cancer development and metastasis, especially using cell cultures and 3D models.…”

Phylogenetic and biogeographical traits predict unrecognized hosts of zoonotic leishmaniasis

“…Host competence (i.e., the ability to become infected and infectious) has been demonstrated in the lab for four species: the Virginia oppossum, the large vesper mouse (Calomys callosus) , spix’s yellow toothed cavy (Galea spixii) , and the Mexican free-tailed bat (Tadarida brasiliensis) (Araujo Carreira et al, 2017; Barbosa et al, 2008; Berzunza-Cruz et al, 2015; Rosa et al, 2022). Our model suggests that these animals are also likely to be naturally infected in the wild; the large vesper mouse is one of the top predicted species for L. (Vianna) .…”

“…Host competence (i.e., the ability to become infected and infectious) has been demonstrated in the lab for four of the predicted species: the Virginia opossum (Didlephis virginiana), the large vesper mouse (Calomys callosus), spix's yellow toothed cavy (Galea spixii), and the Mexican free-tailed bat (Tadarida brasiliensis) (69,(73)(74)(75). Although host competence for these animals has been tested in the laboratory, infection/exposure has not been tested in the wild or animals have not tested positive in the wild (possibly due to minimal sampling of the species).…”

Neuroprotective Treatments for Digestive Forms of Chagas Disease in Experimental Models: A Systematic Review

“…The easy and practical handling, low cost, and need for low concentration of interventions in the new drug discovery phase are advantages that increase the incidence of using these experimental models in studies focused on CD [63]. With pathogenesis similar to that of CD in humans (immunological, pathological, and physiological), it is essential to consider that models such as mice and rats may not accurately reflect the progression and manifestations of CD, with dependence on the strain used in infection, concentration, route, and form of the protozoan used in inoculum and the genetic background of the experimental model [63][64][65]. As an example, depending on the strain, inoculum, and experimental model used, infection in the acute experimental phase can result in up to 100% mortality rate, while for humans, the rate is 5% [63,66].…”