2007
DOI: 10.1016/j.jsbmb.2006.12.058
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1,25(OH)2D3 inhibits in vitro and in vivo intracellular growth of apicomplexan parasite Toxoplasma gondii

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Cited by 25 publications
(20 citation statements)
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“…1,25(OH) 2 D 3 also induced NO synthesis and suppressed growth of Mycobacterium tuberculosis, another intracellular microorganism, in a human macrophage-link cell line [640]. These findings are consistent with the beneficial effects of pretreatment with 1,25(OH) 2 D 3 (0.5 µg/kg for 2 days) on various tissue pathological changes caused by peritoneal administration of oocysts in mice and histologically examined after seven days post inoculation [638]. It appeared that 1,25 (OH) 2 D 3 reduced tissue damage and parasite load in situ, and in particular the difference of the number of parasites per 1 mg of standardized tissue DNA was significant in the spleen (Table 41).…”
Section: T Gondiisupporting
confidence: 67%
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“…1,25(OH) 2 D 3 also induced NO synthesis and suppressed growth of Mycobacterium tuberculosis, another intracellular microorganism, in a human macrophage-link cell line [640]. These findings are consistent with the beneficial effects of pretreatment with 1,25(OH) 2 D 3 (0.5 µg/kg for 2 days) on various tissue pathological changes caused by peritoneal administration of oocysts in mice and histologically examined after seven days post inoculation [638]. It appeared that 1,25 (OH) 2 D 3 reduced tissue damage and parasite load in situ, and in particular the difference of the number of parasites per 1 mg of standardized tissue DNA was significant in the spleen (Table 41).…”
Section: T Gondiisupporting
confidence: 67%
“…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]. Ghaffarifar et al [639] demonstrated that in RPMI 1640 cell culture vitamin D 3 (1000 IU) similarly like IFN-γ (100 IU) significantly decreased proliferation of T. gondii (RH stran) tachyzoites per infected peritoneal macrophage of BALB/c mice as compared with control animals (Table 39).…”
Section: T Gondiisupporting
confidence: 66%
“…Treatment with vitamin D dose-dependently inhibits both in vivo and in vitro growth of T. gondii, possibly by limiting tachyzoite proliferation within the parasitophorous vacuole because of activity at a cellular level. 131 However, no difference occurred in the total number of infected cells regardless of the presence of vitamin D, perhaps refuting a role in cell invasion. Interestingly, vitamin D may be linked to increased mortality in mice infected with toxoplasmosis, presumably because of its downregulation of the Th1 cytokine response.…”
mentioning
confidence: 96%
“…Vitamin D may thus improve outcomes by reducing both local and systemic inflammatory actions as a result of modulating cytokine responses and decreasing TLR activation [808] . 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] .…”
Section: T Gondii Infectionmentioning
confidence: 99%
“…[809] ; with own modification). [810] ; with own modification). effects [820,821] and had both antiatherosclerotic [822] and atherogenic [823] properties.…”
Section: Vitamin D Actions In the Immune System Refsmentioning
confidence: 99%