Effects of iNOS inhibitor on IFN-γ production and apoptosis of splenocytes in genetically different strains of mice infected with Toxoplasma gondii

Kang, Ki-Man; Lee, Gye-Sung; Lee, Jae-Ho; Choi, In-Wook; Shin, Dong–Min; Lee, Young-Ha

doi:10.3347/kjp.2004.42.4.175

Cited by 13 publications

(11 citation statements)

References 19 publications

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“…The partial protection from apoptosis by the NO inhibitor is in contrast to a study by Kang et al. who showed that the number of apoptotic cells in T. gondii ‐infected C57BL/6 mice was not affected by AG treatment (35). However, they investigated cultured splenocytes from C57BL/6 mice orally infected with cysts of Me49 strain and in the present study we obtained peritoneal cells freshly isolated from C57BL/6 mice infected i.p.…”

Section: Discussioncontrasting

confidence: 83%

Toxoplasma gondii infection induces apoptosis in noninfected macrophages: role of nitric oxide and other soluble factors

Nishikawa

Kawase

Vielemeyer

et al. 2007

Parasite Immunology

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Apoptosis has been found to help in the defence against pathogens. Infection with the obligate intracellular parasite Toxoplasma gondii is known to trigger host-cell apoptosis. When using a T. gondii-infected macrophage cell line, J774A.1, treatment with IFN-gamma significantly enhanced apoptosis in noninfected bystander cells while parasitized cells became relatively resistant. Infection and IFN-gamma treatment activated the expression of inducible nitric oxide synthase (iNOS), and the production of nitric oxide (NO) and treatment of cells with an iNOS inhibitor, N(G)-monomethlyl-L-arginine acetate (L-NMMA) reduced the apoptosis frequency. However, the reversal was only partial suggesting that not only NO, but also other, as of yet, unknown factors are induced. Finally, we studied the effect in vivo by infecting mice with either a virulent or an avirulent strain. Challenge with the virulent strain lead to a higher parasite burden, induced host-cell apoptosis in peritoneal cells, and produced higher levels of IFN-gamma and NO. Moreover, treatment of mice with a NO synthase inhibitor, aminoguanidine, partially inhibited the host-cell apoptosis induced by the parasite infection. Altogether, our findings indicate that apoptosis in bystander host cells is due to the secretion of NO and other soluble factors released by parasite-infected cells.

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Section: Discussioncontrasting

confidence: 83%

Toxoplasma gondii infection induces apoptosis in noninfected macrophages: role of nitric oxide and other soluble factors

Nishikawa

Kawase

Vielemeyer

et al. 2007

Parasite Immunology

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“…NO is the product of arginine metabolism and one of the most effective O2-free toxins. There are also previous studies reporting an increase in the NO level in parasitic diseases [1,12]. It can be stated that the NO level increases as a defensive mechanism to protect the patient against the harmful effects of the parasite.…”

mentioning

confidence: 84%

“…It is reported that about one-third of the world population is infected with T. gondii, and the disease has asymptomatic progress in 90% of the patients with sound immune systems [1,2]. Toxoplasmosis can cause serious pathologies including hepatitis, pneumonia, blindness, and severe neurological disorders.…”

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confidence: 99%

Malondialdehyde, Glutathione, and Nitric Oxide Levels in Toxoplasma gondii Seropositive Patients

et al. 2008

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Abstract:The aim of this study was to investigate the difference in the serum malondialdehyde (MDA), glutathione (GSH), and nitric oxide (NO) levels between normal and T. gondii-infected patients. To this end, MDA, GSH, and NO levels in the sera of 37 seropositive patients and 40 participants in the control group were evaluated. In Toxoplasma ELISA, IgG results of the patient group were 1,013.0 ± ± 543.8 in optical density (mean ± ± SD). A statistically significant difference was found between patients and the control group in terms of MDA, GSH, and NO levels. A decrease in GSH activity was detected, while MDA and NO levels increased significantly. Consequently, it is suggested that the use of antioxidant vitamins in addition to a parasite treatment shall prove useful. The high infection vs control ratio of MDA and NO levels probably suggests the occurrence as a mechanism of tissue damage in cases of chronic toxoplasmosis. Moreover, it is recommended that the patient levels of MDA, GSH, and NO should be evaluated in toxoplasmosis.

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“…Recombinant protein derived from the putative genomic sequence of T. gondii, is able to produce nitrites [70]. In addition, NO modulates IFN-γ production in T. gondii-infected mice, and that NO is involved in mediating a protective response in toxoplasmosis susceptible, but not resistant, mice strain during acute infection [71].…”

Section: Toxoplasma Spmentioning

confidence: 99%

Involvement of nitric oxide and its up/down stream molecules in the immunity against parasitic infections

Nahrevanian

2009

Braz J Infect Dis

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Nitric oxide (NO) is a potent mediator with diverse roles in regulating cellular functions and signaling pathways. The NO synthase (NOS) enzyme family consists of three major isoforms, which convey variety of messages between cells, including signals for vasorelaxation, neurotransmission and cytotoxicity. This family of enzymes are generally classified as neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Increased levels of NO are induced from iNOS during infection; while eNOS and nNOS may be produced at the baseline in normal conditions. An association of some key cytokines appears to be essential for NOS gene regulation in the immunity of infections. Accumulating evidence indicates that parasitic diseases are commonly associated with elevated production of NO. NO plays a role in the immunoregulation and it is implicated in the host non-specific defence in a variety of infections. Nevertheless, the functional role of NO and NOS isoforms in the immune responses of host against the majority of parasites is still highly controversial. In the present review, the role of parasitic infections will be discussed in the controversy related to the NO production and iNOS gene expression in different parasites and a variety of experimental models.

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Effects of iNOS inhibitor on IFN-γ production and apoptosis of splenocytes in genetically different strains of mice infected with Toxoplasma gondii

Cited by 13 publications

References 19 publications

Toxoplasma gondii infection induces apoptosis in noninfected macrophages: role of nitric oxide and other soluble factors

Toxoplasma gondii infection induces apoptosis in noninfected macrophages: role of nitric oxide and other soluble factors

Malondialdehyde, Glutathione, and Nitric Oxide Levels in Toxoplasma gondii Seropositive Patients

Involvement of nitric oxide and its up/down stream molecules in the immunity against parasitic infections

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