27 research outputs found
Trypanosoma congolense Infections: Induced Nitric Oxide Inhibits Parasite Growth In Vivo
Wild-type (WT) C57BL/6 mice infected intraperitoneally with 5 × 106 Trypanosoma congolense survive for more than 30 days. C57BL/6 mice deficient in inducible nitric oxide synthase (iNOS−/−) and infected with 103 or 5 × 106 parasites do not control the parasitemia and survive for only 14 ± 7 or 6.8 ± 0.1 days, respectively. Bloodstream trypanosomes of iNOS−/− mice infected with 5 × 106 T. congolense had a significantly higher ratio of organisms in the S+G2+M phases of the cell cycle than trypanosomes in WT mice. We have reported that IgM anti-VSG-mediated phagocytosis of T. congolense by macrophages inhibits nitric oxide (NO) synthesis via CR3 (CD11b/CD18). Here, we show that during the first parasitemia, but not at later stages of infection, T. congolense-infected CD11b−/− mice produce more NO and have a significantly lower parasitemia than infected WT mice. We conclude that induced NO contributes to the control of parasitemia by inhibiting the growth of the trypanosomes
Intradermal Infections of Mice by Low Numbers of African Trypanosomes Are Controlled by Innate Resistance but Enhance Susceptibility to Reinfection
Antibodies are required to control blood-stage forms of African trypanosomes in humans and animals. Here, we report that intradermal infections by low numbers of African trypanosomes are controlled by innate resistance but prime the adaptive immune response to increase susceptibility to a subsequent challenge. Mice were found 100 times more resistant to intradermal infections by Trypanosoma congolense or Trypanosoma brucei than to intraperitoneal infections. B cell–deficient and RAG2−/− mice are as resistant as wild-type mice to intradermal infections, whereas inducible nitric oxide synthase (iNOS)−/− mice and wild-type mice treated with antibody to tumor necrosis factor (TNF) α are more susceptible. We conclude that primary intradermal infections with low numbers of parasites are controlled by innate defense mediated by induced nitric oxide (NO). CD1d−/− and major histocompatibility complex (MHC) class II−/− mice are more resistant than wild-type mice to primary intradermal infections. Trypanosome-specific spleen cells, as shown by cytokine production, are primed as early as 24 h after intradermal infection. Infecting mice intradermally with low numbers of parasites, or injecting them intradermally with a trypanosomal lysate, makes mice more susceptible to an intradermal challenge. We suggest that intradermal infections with low numbers of trypanosomes or injections with trypanosomal lysates prime the adaptive immune system to suppress protective immunity to an intradermal challenge
Effect of Fitness Qigong-Wuqinxi exercise on some physiological indexes of female college students
To know the reaction and adaption of human body after taking Fitness Qigong-Wuqinxi exercise and promote the popularity of Fitness Qigong-Wuqinxi exercise in universities,especially in female college students who do not major in sports,we observed their gas metabolism indexes and heart rates and contrast body shape and some physical quality indexes before and after the regular exercise for 16 weeks.The results showed that the indexes of waist,BMI,back force,grip force,and proneness when sitting improved obviously.Although height,weight,abdominal skinfold thickness,body fate percentage didn′t have significant change,the development trend is toward the direction of health.After exercise for 16 weeks,the three indexes of lung ventilation (VE、VO2、VCO2) showed wave shape.It is obvious that Fitness Qigong-Wuqinxi exercise can obviously improve the body shape,physical quality,and the function of heart and lung.Also,the wave feature of the indexes of lung ventilation can adjust the cardiopulmonary function,so Fitness Qigong-Wuqinxi exercise is a new safe and reliable fitness program
Trypanosoma congolense infections: antibody-mediated phagocytosis by Kupffer cells
Abstract: Immunohistochemical double-label tech-nique was used to detect trypanosomal antigen in macrophages. Immunoglobulin (Ig)M as well as IgG2a monoclonal antibodies (mAb) specific for the variant surface glycoprotein (VSG) mediated phagocytosis of Trypanosoma congolense variant antigenic type (VAT) TC13 by macrophages [bone marrow-derived macrophage cell line from BALB/c (BALB.BM)] in vitro. Administration of these IgM or IgG2a antibodies to BALB/c mice 30 min after injec-tion of 3 108 T. congolense mediated phagocytosis of trypanosomes by Kupffer cells of the liver within 1 h. Plasma levels of the monokines interleukin (IL)-1, IL-10, and IL-12p40 were significantly increased 6–48 h after phagocytosis. In BALB/c mice infected with 103 T. congolense, a small de-gree of phagocytosis of trypanosomes by Kupffer cells, mediated by actively synthesized antibodies, was detected as early as 5 days after infection. Phagocytosis of trypanosomes was dramatically en-hanced on day 6. Concomitantly, the Kupffer cells trippled in size. In BALB/c mice infected for 6 days, treatment with IgM or IgG2a mAb specific for T. congolense VSG led to clearance of VAT TC13 parasitemia but did not prevent death at the second parasitemia of a different VAT. We conclude that IgM as well as IgG antibody mediate phagocytosis of trypanosomes by Kupffer cells. J. Leukoc. Biol
Impaired Kupffer Cells in Highly Susceptible Mice Infected with Trypanosoma congolense
In highly susceptible BALB/c mice infected with Trypanosoma congolense, the total number of Kupffer cells in the liver remains constant; however, their mean size increases fivefold towards the terminal stage. About 25% of Kupffer cells undergo apoptosis. We suggest that development of an impairment of the macrophage system might be a major mechanism for inefficient elimination of trypanosomes
Experimental African Trypanosomiasis: A Subset of Pathogenic, IFN-γ-Producing, MHC Class II-Restricted CD4 +
Loving home village project : collective production of village songs
Moderator: LI Cuihuan (Green Ground Eco-Tech Centre (Beijing), China
Speakers: SUN Heng (Loving Home-Village Songs Project, Beijing, China) LÜ Li (Mukai Nur Township, Otog Banner, Ordos City, Inner Mongolia, China) PAN Guojian (No.4 High School, Pingnan County, Fujian Province, China) SHAO Qiulu (Postgraduate, Ningxia University, China) GUO Lingyan (Southwest University, China) FU Haihong (Chongqing Technology and Business University, China) PAN Jiaen (Southwest University, China) BU Wei (Chinese Academy of Social Sciences, China
The Long Noncoding RNA MEG3 Contributes to Cisplatin Resistance of Human Lung Adenocarcinoma.
Long noncoding RNAs (lncRNAs) have been identified as oncogenes or tumor suppressors that are involved in tumorigenesis and chemotherapy drug resistance. Maternally expressed gene 3 (MEG3) is an imprinted gene located at 14q32 that encodes an lncRNA, and decreased MEG3 expression plays an important role in multiple cancers. However, its biological role in the development of the chemoresistance phenotype of human lung adenocarcinoma (LAD) is unknown. This study aimed to observe the expression of MEG3 in LAD and to evaluate its biological role and clinical significance in the resistance of LAD cells to cisplatin. MEG3 expression was markedly decreased in cisplatin-resistant A549/DDP cells compared with parental A549 cells as shown by an lncRNA microarray. MEG3 overexpression in A549/DDP cells increased their chemosensitivity to cisplatin both in vitro and in vivo by inhibiting cell proliferation and inducing apoptosis. By contrast, MEG3 knockdown in A549 cells decreased the chemosensitivity. Moreover, MEG3 was decreased in cisplatin-insensitive LAD tissues while p53 protein levels were decreased and Bcl-xl protein levels increased. Furthermore, patients with lower levels of MEG3 expression showed worse responses to cisplatin-based chemotherapy. These findings demonstrate that MEG3 is significantly downregulated in LAD and partially regulates the cisplatin resistance of LAD cells through the control of p53 and Bcl-xl expression. Thus, MEG3 may represent a new marker of poor response to cisplatin and could be a potential therapeutic target for LAD chemotherapy