1,25-Dihydroxyvitamin D3 induces splenocyte apoptosis and enhances BALB/c mice sensitivity to toxoplasmosis

Rajapakse, Rohan; Mousli, Marc; Pfaff, Alexander W.; Uring‐Lambert, B.; Marcellin, Luc; Bronner, Christian; Jeanblanc, Michaël; Villard, Odile; Letscher-Bru, Valérie; Klein, Jean‐Paul; Candolfi, Ermanno

doi:10.1016/j.jsbmb.2005.03.002

Cited by 28 publications

(26 citation statements)

References 23 publications

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“…Surprisingly, no increase in parasite load was observed in the organs, which suggested an inhibitory effect of 1,25(OH) 2 D 3 at a cellular level [636], like previously it was reported for Plasmodium faciparum [637]. Further studies showed that treatment with vitamin D dose-dependently inhibited both in vivo and in vitro growth of T. gondii intracellularly, possibly by limiting tachyzoite proliferation within the parasitophorous vacuole because of activity at the cellular level [627,638].…”

Section: T Gondiisupporting

confidence: 67%

“…In acute toxoplasmosis, 1,25(OH) 2 D 3 reduced survival rate of infected mice compared to untreated animals, and significantly decreased serum IFN-γ and IL-12p40 concentrations indicating inhibition of T H 1-type cytokines, as well as reduced CD4 + T lymphocyte and splenocyte counts, thus enhancing host sensitivity to T. gondii infection [636]. Surprisingly, no increase in parasite load was observed in the organs, which suggested an inhibitory effect of 1,25(OH) 2 D 3 at a cellular level [636], like previously it was reported for Plasmodium faciparum [637].…”

Section: T Gondiimentioning

confidence: 98%

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T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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Section: T Gondiisupporting

confidence: 67%

Section: T Gondiimentioning

confidence: 98%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

View full text Add to dashboard Cite

show abstract

“…Interestingly, vitamin D may be linked to increased mortality in mice infected with toxoplasmosis, presumably because of its downregulation of the Th1 cytokine response. 132 This finding suggests a delicate balance in overall immune response against this organism, and further studies would need to be done to establish the role of vitamin D among other variables in determining outcomes.…”

mentioning

confidence: 99%

Antimicrobial implications of vitamin D

Youssef

Miller

Elabbassi

et al. 2011

Dermato-Endocrinology

171

128

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“…Finally, it must emphasized that vitamin D significantly decreased in vitro proliferation of T. gondii tachyzoites in macrophages (Table 31), increased NO generation in these cells (Table 32) [809] , and diminished various tissue pathology in animals infected with the parasite (Table 33), possibly by acting on tachyzoites in parasitophorous vacuole [810] . Of note, vitamin D may however also be linked to the increased susceptibility and mortality of mice infected with the pathogen, probably because of its downregulation of the T H 1 type cytokine response [811] . In summary, experimental and clinical data provide vast evidence that vitamin D have important beneficial impact on immunity, as well as on T. gondii infection, and therefore it should find a solid place in various treatment regimens directed against both atherosclerosis and the pathogen.…”

Section: T Gondii Infectionmentioning

confidence: 99%

Possible Pivotal Role of Latent Chronic T. gondii Infection in the Pathogenesis of Atherosclerosis

Prandota

2017

Journal of Cardiology and Therapy

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1,25-Dihydroxyvitamin D3 induces splenocyte apoptosis and enhances BALB/c mice sensitivity to toxoplasmosis

Cited by 28 publications

References 23 publications

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Antimicrobial implications of vitamin D

Possible Pivotal Role of Latent Chronic T. gondii Infection in the Pathogenesis of Atherosclerosis

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