A high corticosterone/DHEA-s ratio in young rats infected with Trypanosoma cruzi is associated with increased susceptibility

Pérez, Ana Rosa; Bertoya, Aymará Ana; Revelli, Silvia; García, Fernando

doi:10.1590/s0074-02762011000400006

Cited by 10 publications

(9 citation statements)

References 33 publications

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“…Another study [13] reported that when T.evansi was inoculated into albino rats, the parasite appeared in the blood on the 5th day, the density of trypanosomes in the blood reached its peak on the 6th day, and all animals succumbed to infection between the 6th and 8th day of inoculation. The susceptibility of small rodents such as mice and rats correlated with the immunosuppression that was associated with an elevation of hormone levels such as corticosterone (CT) and corticosterone dehydroepiandrosterone-sulfate (CT/DHEA-s) as described previously [14] in mice and rats infected with T. cruzi.…”

Section: Discussionmentioning

confidence: 85%

A comparative study on susceptibility, course of parasitemia, and pattern of infection with Trypanosoma evansi between different laboratory animals

Sadek

2020

Journal of Taibah University for Science

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This study investigated the susceptibility of eight different animal species (rat, mice, guinea pigs, hamsters, rabbits, sheep, goats, and chicken) experimentally infected with Trypanosoma evansi isolated from camels. In all laboratory animals, the number of trypanosomes was standardized according to the weight of the animal, and daily examination of the blood was conducted to assess the presence of trypanosomes to determine the prepatent period and the peak of parasitemia. Results suggested that mice and rats were the most susceptible laboratory animals to infection, whereas hamsters and guinea pigs displayed a certain degree of tolerance to infection. Rabbits exhibited a chronic course of infection, but the level of parasitemia was very low. In sheep and goats, trypanosomes were detectable only by subpassage to rats and mice, whereas all the chickens remained uninfected even with increasing doses of infection.

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Section: Discussionmentioning

confidence: 85%

A comparative study on susceptibility, course of parasitemia, and pattern of infection with Trypanosoma evansi between different laboratory animals

Sadek

2020

Journal of Taibah University for Science

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“…However, chronic chagasic patients with different degrees of myocarditis presented a marked reduction in DHEA-s levels. Interestingly, although the alterations in the levels of DHEA in animals are not seen in patients with Chagas disease, both animals and patients presented an increase in GC/DHEA-s ratio, which is important for the development of an anti-inflammatory milieu ( 66 , 67 ).…”

Section: Systemic Hormonal Imbalance In Chagas Diseasementioning

confidence: 97%

“…Besides GC and pituitary hormones, some gonadal steroid hormones, including dehydroepiandrosterone-sulfate (DHEA-s) and testosterone, can be altered in human or experimental Chagas disease ( 66 , 67 ). Animals infected with T. cruzi presented a reduction in serum testosterone levels in the acute phase of infection.…”

Section: Systemic Hormonal Imbalance In Chagas Diseasementioning

confidence: 99%

“…However, histological analyses in testes, seminal vesicles, and epididymis did not reveal any differences between control and infected animals ( 68 ). In addition, T. cruzi- infected animals showed an increase in circulating levels of estradiol ( 67 ). Regarding DHEA-s levels, rats infected with T. cruzi did not alter the DHEA-s systemic levels.…”

Section: Systemic Hormonal Imbalance In Chagas Diseasementioning

confidence: 99%

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Role of Hormonal Circuitry Upon T Cell Development in Chagas Disease: Possible Implications on T Cell Dysfunctions

et al. 2018

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T cell response plays an essential role in the host resistance to infection by the protozoan parasite Trypanosoma cruzi, the causative agent of Chagas disease. This infection is often associated with multiple manifestations of T cell dysfunction, both during the acute and the chronic phases of disease. Additionally, the normal development of T cells is affected. As seen in animal models of Chagas disease, there is a strong thymic atrophy due to massive death of CD4+CD8+ double-positive cells by apoptosis and an abnormal escape of immature and potentially autoreactive thymocytes from the organ. Furthermore, an increase in the release of corticosterone triggered by T. cruzi-driven systemic inflammation is strongly associated with the alterations seen in the thymus of infected animals. Moreover, changes in the levels of other hormones, including growth hormone, prolactin, and testosterone are also able to contribute to the disruption of thymic homeostasis secondary to T. cruzi infection. In this review, we discuss the role of hormonal circuits involved in the normal T cell development and trafficking, as well as their role on the thymic alterations likely related to the peripheral T cell disturbances largely reported in both chagasic patients and animal models of Chagas disease.

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“…Additionally, the activation of HPA axis leads to secretion of other adrenal steroids, such as dehydroepiandrosterone (DHEA). In this regard, the increased vulnerability of T. cruzi infected young animals was associated with a high corticosterone/DHEA-sulfate ratio as compared to the adult counterparts (Pérez et al, 2011 ). Similarly, patients with severe chronic chagasic myocarditis also revealed a disruption in the activation of HPA axis as characterized by decreased concentrations of DHEA-sulfate and unbalanced cortisol/DHEA-sulfate ratio in comparison to asymptomatic or healthy individuals (Pérez et al, 2011 ).…”

Section: The Immune-endocrine Imbalance Is a Key Determinant Of Parasmentioning

confidence: 99%

Evasion and Immuno-Endocrine Regulation in Parasite Infection: Two Sides of the Same Coin in Chagas Disease?

et al. 2016

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Chagas disease is a serious illness caused by the protozoan parasite Trypanosoma cruzi. Nearly 30% of chronically infected people develop cardiac, digestive, or mixed alterations, suggesting a broad range of host-parasite interactions that finally impact upon chronic disease outcome. The ability of T. cruzi to persist and cause pathology seems to depend on diverse factors like T. cruzi strains, the infective load and the route of infection, presence of virulence factors, the parasite capacity to avoid protective immune response, the strength and type of host defense mechanisms and the genetic background of the host. The host-parasite interaction is subject to a constant neuro-endocrine regulation that is thought to influence the adaptive immune system, and as the infection proceeds it can lead to a broad range of outcomes, ranging from pathogen elimination to its continued persistence in the host. In this context, T. cruzi evasion strategies and host defense mechanisms can be envisioned as two sides of the same coin, influencing parasite persistence and different outcomes observed in Chagas disease. Understanding how T. cruzi evade host's innate and adaptive immune response will provide important clues to better dissect mechanisms underlying the pathophysiology of Chagas disease.

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A high corticosterone/DHEA-s ratio in young rats infected with Trypanosoma cruzi is associated with increased susceptibility

Cited by 10 publications

References 33 publications

A comparative study on susceptibility, course of parasitemia, and pattern of infection with Trypanosoma evansi between different laboratory animals

A comparative study on susceptibility, course of parasitemia, and pattern of infection with Trypanosoma evansi between different laboratory animals

Role of Hormonal Circuitry Upon T Cell Development in Chagas Disease: Possible Implications on T Cell Dysfunctions

Evasion and Immuno-Endocrine Regulation in Parasite Infection: Two Sides of the Same Coin in Chagas Disease?

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