Immune characteristics of Plasmodium reinfections in mice following chloroquine cure of primary Plasmodium infections / 中国血吸虫病防治杂志

ObjectiveTo investigate the disease progression and immunoprotective characteristics in mice re-infected with homogeneous/heterogeneous Plasmodium strains following cure of Plasmodium infections with chloroquine at the peak of parasitemia. MethodsC57BL/6 mice were infected with the non-lethal P. yoelii 17XNL strain, and half of mice were given treatment with chloroquine at the peak of parasitemia (9 days post-infection), while the other mice were self-cured naturally. Then, all cured mice were re-infected with the equivalent lethal P. yoelii 17XL or P. berghei ANKA strain 90 days following primary Plasmodium infections. The parasitemia levels during primary infections and reinfections were measured by microscopic examinations of Giemsa-stained thin blood films, and the levels of the IgG antibody in sera and the percentages of memory T cell subsets in spleen cells were detected in mice using ELISA and flow cytometry before and after parasite reinfections, respectively. Results Following primary infections with the P. yoelii 17XNL strain, the serum IgG antibody levels were (5.047 ± 0.924) pg/mL in the selfcured mice and (4.429 ± 0.624) pg/mL in the chloroquine-treated mice, respectively (t = 0.437, P > 0.05), which were both significantly higher than that in the uninfected mice (1.624 pg/mL ± 0.280 pg/mL) (F = 22.522, P < 0.01). There was no significant difference in the serum IgG antibody level among self-cured and chloroquine-treated mice re-infected with the P. yoelii 17XL strain or the P. berghei ANKA strain (F = 0.542, P > 0.05); however, the serum IgG antibody levels were all significantly higher in selfcured and chloroquine-treated mice re-infected with the P. yoelii 17XLstrain[(15.487±1.173)pg/mLand(15.965±1.150)pg/mL] or the P. berghei ANKA strain [(14.644 ± 1.523) pg/mL and (15.185 ± 1.333) pg/mL] relative to primary infections (F = 67.383, P < 0.01). There was no significant difference in the proportion of CD4+ [(34.208 ± 2.106), (32.820 ± 1.930), (34.023 ± 2.289), (35.608 ± 1.779) pg/mL] or CD8+ T memory cells [(17.935 ± 2.092), (18.918 ± 2.823), (17.103 ± 1.627), (17.873 ± 1.425) pg/mL] in self-cured and chloroquine-treated mice with primary infections with the P. yoelii 17XNL strain followed by re-infections with the P. yoelii 17XL strain or the P. berghei ANKA strain (F = 0.944 and 0.390, both P > 0.05); however, the proportions of the CD4+ or CD8+ T memory cells were significantly greater in self-cured and chloroquine-treated mice with primary infections with the P. yoelii 17XNL strain followed by re-infections with the P. yoelii 17XL strain or the P. berghei ANKA strain than in mice with primary infections (F = 50.532 and 21.751, both P < 0.01). Conclusions The cure of murine Plasmodium infections with chloroquine does not affect the production of effective immune protections in mice during parasite re-infections. Following a primary infection, mice show a protection against re-infections with either homogeneous or heterogeneous Plasmodium strains, and a higher-level resistance to re-infections with homogeneous parasite strains is found than with heterogeneous strains.

[Inhibition of Toxoplasma gondii excretory - secretory antigens on growth of murine Lewis lung carcinoma].

OBJECTIVE: To investigate the effect of Toxoplasma gondii excretory-secretory antigens (ESA) on CD4+ CD25+ Foxp3+ T (Treg) cells in mice carrying Lewis lung carcinoma, and examine the inhibitory effect of T. gondii ESA on tumor growth. METHODS: C57BL/6 mice were randomly assigned into the PBS group (n = 14) and the Lewis group (n = 34). Mice in the Lewis group were subcutaneously injected with 2 × 105 Lewis lung carcinoma cells in the right axilla, while animals in the PBS group were injected with the same volume of sterile PBS. On day 7 post-injection (D7), mice in the PBS group were further divided into the PBS2 group and the PBS2 + ESA group, of 7 mice in each group, and mice in the Lewis group were further divided into the Lewis2 group and the Lewis2 + ESA group, of 17 mice in each group. Then, mice in the PBS2 + ESA group and the Lewis2 + ESA group were intraperitoneally injected with 100 µL of ESA. The mouse spleen coefficient was calculated in each group 7 days post-injection with ESA, and the changes of Treg cell counts and the long-term tumor growth were measured in tumor-bearing mice. RESULTS: The spleen coefficient was significantly greater in the PBS2 + ESA group and the Lewis2 + ESA group than in the PBS2 (0.66% ± 0.09% vs. 0.30% ± 0.02%, P < 0.05) and Lewis2 groups (0.69% ± 0.07% vs. 0.33% ± 0.03%, P < 0.05) 7 days post-treatment with ESA, respectively, and the percentage of splenic Treg cells in splenocytes was significantly lower in the PBS2 + ESA group and the Lewis2 + ESA group than in the PBS2 (1.28% ± 0.14% vs. 2.06% ± 0.07%, P < 0.05) and Lewis2 groups (1.58% ± 0.14% vs. 2.44% ± 0.23%, P < 0.05), respectively. T. gondii ESA treatment caused a delay in tumor growth, and the tumor size was significantly smaller in the Lewis2 + ESA group than in the Lewis2 group (P < 0.05). CONCLUSIONS: T. gondii ESA may reduce the proportion of splenic Treg cells in splenocytes and inhibit tumor growth in mice carrying Lewis lung carcinoma.

Inhibition of Toxoplasma gondii excretory - secretory antigens on growth of murine Lewis lung carcinoma / 中国血吸虫病防治杂志

Objective To investigate the effect of Toxoplasma gondii excretory-secretory antigens (ESA) on CD4+ CD25+ Foxp3+ T (Treg) cells in mice carrying Lewis lung carcinoma, and examine the inhibitory effect of T. gondii ESA on tumor growth. Methods C57BL/6 mice were randomly assigned into the PBS group (n = 14) and the Lewis group (n = 34). Mice in the Lewis group were subcutaneously injected with 2 × 105 Lewis lung carcinoma cells in the right axilla, while animals in the PBS group were injected with the same volume of sterile PBS. On day 7 post-injection (D7), mice in the PBS group were further divided into the PBS2 group and the PBS2 + ESA group, of 7 mice in each group, and mice in the Lewis group were further divided into the Lewis2 group and the Lewis2 + ESA group, of 17 mice in each group. Then, mice in the PBS2 + ESA group and the Lewis2 + ESA group were intraperitoneally injected with 100 μL of ESA. The mouse spleen coefficient was calculated in each group 7 days post-injection with ESA, and the changes of Treg cell counts and the long-term tumor growth were measured in tumor-bearing mice. Results The spleen coefficient was significantly greater in the PBS2 + ESA group and the Lewis2 + ESA group than in the PBS2 (0.66% ± 0.09% vs. 0.30% ± 0.02%, P < 0.05) and Lewis2 groups (0.69% ± 0.07% vs. 0.33% ± 0.03%, P < 0.05) 7 days post-treatment with ESA, respectively, and the percentage of splenic Treg cells in splenocytes was significantly lower in the PBS2 + ESA group and the Lewis2 + ESA group than in the PBS2 (1.28% ± 0.14% vs. 2.06% ± 0.07%, P < 0.05) and Lewis2 groups (1.58% ± 0.14% vs. 2.44% ± 0.23%, P < 0.05), respectively. T. gondii ESA treatment caused a delay in tumor growth, and the tumor size was significantly smaller in the Lewis2 + ESA group than in the Lewis2 group (P < 0.05). Conclusion T. gondii ESA may reduce the proportion of splenic Treg cells in splenocytes and inhibit tumor growth in mice carrying Lewis lung carcinoma.

Inhibition of Toxoplasma gondii excretory - secretory antigens on growth of murine Lewis lung carcinoma / 中国血吸虫病防治杂志

Objective To investigate the effect of Toxoplasma gondii excretory-secretory antigens (ESA) on CD4+ CD25+ Foxp3+ T (Treg) cells in mice carrying Lewis lung carcinoma, and examine the inhibitory effect of T. gondii ESA on tumor growth. Methods C57BL/6 mice were randomly assigned into the PBS group (n = 14) and the Lewis group (n = 34). Mice in the Lewis group were subcutaneously injected with 2 × 105 Lewis lung carcinoma cells in the right axilla, while animals in the PBS group were injected with the same volume of sterile PBS. On day 7 post-injection (D7), mice in the PBS group were further divided into the PBS2 group and the PBS2 + ESA group, of 7 mice in each group, and mice in the Lewis group were further divided into the Lewis2 group and the Lewis2 + ESA group, of 17 mice in each group. Then, mice in the PBS2 + ESA group and the Lewis2 + ESA group were intraperitoneally injected with 100 μL of ESA. The mouse spleen coefficient was calculated in each group 7 days post-injection with ESA, and the changes of Treg cell counts and the long-term tumor growth were measured in tumor-bearing mice. Results The spleen coefficient was significantly greater in the PBS2 + ESA group and the Lewis2 + ESA group than in the PBS2 (0.66% ± 0.09% vs. 0.30% ± 0.02%, P < 0.05) and Lewis2 groups (0.69% ± 0.07% vs. 0.33% ± 0.03%, P < 0.05) 7 days post-treatment with ESA, respectively, and the percentage of splenic Treg cells in splenocytes was significantly lower in the PBS2 + ESA group and the Lewis2 + ESA group than in the PBS2 (1.28% ± 0.14% vs. 2.06% ± 0.07%, P < 0.05) and Lewis2 groups (1.58% ± 0.14% vs. 2.44% ± 0.23%, P < 0.05), respectively. T. gondii ESA treatment caused a delay in tumor growth, and the tumor size was significantly smaller in the Lewis2 + ESA group than in the Lewis2 group (P < 0.05). Conclusion T. gondii ESA may reduce the proportion of splenic Treg cells in splenocytes and inhibit tumor growth in mice carrying Lewis lung carcinoma.

[Anti-tumor effect of Plasmodium yoelii infection on melanoma in mice].

OBJECTIVE: To explore the anti-tumor effect of 17XL strains of Plasmodium yoelii (P.y) infection on melanoma in mice. METHODS: B16F10 tumor cells were axillarilly injected into the right flank of 20 C57BL/6 mice to establish tumor-bearing mouse models. The next day, the mice were randomly divided into a P.y infection group and control group, 10 mice each group. Each mouse of the P.y infection group was intraperitoneally injected with 1×106 red blood cells including 20% P.y infection red blood cells, and each one of the control group were intraperitoneally injected with 1×106 normal red blood cells of C57BL/6 mice. The time of tumor formation of the mice in the two groups was observed and the tumor volumes were measured. RESULTS: The time of tumor formation in the P.y infection groupï¼» (11.30 ± 0.21) dï¼½was significantly later than that in the control group ï¼» (10.40 ± 0.22) dï¼½ (P < 0.05). From the tumors could be accurately measured to the study end point, both the tumors of mice in the two groups were growing, and the tumor volumes of mice in the P.y infection group were significantly less than those in the control group at each time point (all P < 0.05). The growth rate of tumors in the P.y infection group ï¼» (71.10 ± 6.29) mm3/dï¼½ was significantly slower than that in the control group ï¼» (302.80 ± 49.94) mm3/dï¼½ (P < 0.05), and the growth rates of tumors everyday in the P.y infection group were significantly slower than those in the control group (all P < 0.05). CONCLUSIONS: The P.y infection can delay the occurrence of tumor and inhibit the growth of melanoma.

[Experience and analysis of excellent works of human parasitology in national medical colleges and universities].

Teaching competition is an effective way for college and university teachers to improve their teaching skills. Based on the teaching practice and experience in medical parasitology, this paper discusses several key issues in teaching competition including topics, teaching designs and teaching methods. It provides references for the teachers in department of parasitology of universities and colleges to improve the quality of classroom teaching.

[Effect of exogenous nitric oxide on antioxidants from mice infected with Trichinella spiralis].

OBJECTIVE: To study the effect of exogenous nitric oxide donor sodium nitroprusside (SNP) on antioxidant enzymes activities and lipid peroxidation of mice infected with Trichinella spiralis. METHODS: BALB/c mice were infected with T. spiralis separated by the digestion method. Forty-two days post-infection, the peripheral blood and hepatic tissue from the infected or normal mice were collected. Then 4 groups were set：liver homogenate from infected mice + SNP (Group A), liver homogenate from normal mice + SNP (Group B), peripheral blood from infected mice + SNP (Group C), and peripheral blood from normal mice + SNP (Group D). The final concentrations of SNP in each group were set as 0 (blank control), 2, 5, 10 µmol/L and 30 µmol/L, respectively. After reacting with SNP at 37 ℃ for 30 min, the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activities, and malondialdehyde (MDA) concentration were examined and compared. RESULTS: The levels of SOD, CAT, GSH-Px and MDA concentration in the liver and the blood from the mice infected with T. spiralis were significantly higher than those of the normal ones (all P < 0.05). When reacted with 10 µmol/L and 30 µmol/L SNP, the SOD, GSH-Px, and CAT activities in Group A and B decreased significantly (all P < 0.05), while the liver MDA concentration reacted with 2-30 µmol/L SNP increased obviously (all P < 0.05). As reacted with 30 µmol/L SNP, the activities of blood SOD, GSH-Px, and CAT in Group C and D decreased, while the MDA concentration in blood still increased (all P < 0.01). When the SNP concentration was in the range of 2-30 µmol/L, there were a negative correlation between the SNP concentrations and SOD, GSH-Px, and CAT activities, as well as a positive correlation with the MDA concentration in the liver and blood from the mice infected with T. spiralis (all P < 0.05). CONCLUSIONS: T. spiralis infection could cause oxidative damage to mice, and increase SOD, GSH-Px, and CAT activities. Nitric oxide released from SNP can decrease antioxidase activities, and inhibit the antioxidant capacity of mice infected with T. spiralis.