Echinococcus granulosus: host lymphocyte transformation by parasite antigens.

Lymphocyte transformation, measured by in vitro tritiated thymidine incorporation, and indirect hemagglutination tests were carried out on hydatid patients and normal individuals using sheep and human hydatid fluid or scolex antigens. The hydatid patients showed statistically significant lymphocyte transformation with human and sheep hydatid fluid or scolex antigens when compared to normal individuals. The indirect hemagglutination tests resulted in high titers of antibody with sheep or human hydatid fluid antigens, while very low titers were obtained with scolex antigens. Unlike in the indirect hemagglutination test, the source of the antigen, scolex or fluid, was not of consequence in the lymphocyte transformation test. Furthermore, there was no correlation between the results of the serologic and lymphocyte transformation tests, since some patients with very high lymphocyte stimulation indices produced low indirect hemagglutination titers and vice versa. Similar results were obtained from rabbits which were immunized with sheep hydatid fluid or scolex extracts. The skin tests were of the immediate type of hypersensitivity reactions. Delayed skin reactions did not occur in spite of the presence of sensitized lymphocytes in the blood of the immunized rabbits.     

Trypanosoma musculi infections in complement-deficient mice

Strains of mice (CFW, C57B1/10Sn, B10.D2/nSn, and B10.D2/oSn) were infected with Trypanosoma musculi (Trypanosoma duttoni). The complement-deficient B10.D2/oSn mice showed typical parasitemias similar to those presented by the strains possessing hemolytic complement activity. Peak parasitemias occurred 12 days postinoculation. The highest parasitemias were measured in CFW mice (657 ± 82 T. musculi/30 hi-power fields), while infections in C56BL/10Sn (528 ±44 T. musculi/30 h.p.f.), B10.D2/oSn (502 ± 20 T. musculi/30 h.p.f.) and B10.D2/nSn (512 ± 35 T. musculi/30 h.p.f.) were less severe and quantitatively comparable. The percentages of dividing forms were similar during infections in each of the strains. While parasites were detected in peripheral blood until Day 22 of infection in three of 10 C57BL/10Sn mice, none could be found at this time in blood films of CFW, B10.D2/nSn or B10.D2/oSn mice. Giemsa stained kidney imprints indicated the presence of parasites in animals of each of the strains after 33 days, when trypanosomes could no longer be detected in the peripheral blood of the mice. The minor variations in the parasitemias appeared related to the mouse strain. Complement dependent, antibody mediated immune cytolysis was not indicated as a mechanism for the elimination of T. musculi by the infected mouse.     

Ablastin: Control of Trypanosoma musculi infections in mice

Trypanosoma musculi infections in CBA mice consist of a phase of increasing parasitemia during which dividing forms of the parasite are present in the blood, followed by a period when only nondividing trypomastigotes are seen. A second crisis terminates the blood infection and leaves the host immune, but small numbers of trypanosomes, including multiplicative forms, persist in the kidneys for many months. Studies were made involving infections in T-lymphocyte deprived mice, the effects of passive transfer of serum and cells, measurement of DNA synthesis by the parasite, serological responses, and in vitro effects of serum on the trypanosomes. These indicated that the initial check on the increase in blood parasitemia is due in part to two humoral factors. One of these has a trypanocidal effect (this is thought to be an IgM antibody) while the other, which may be an IgG antibody, is the ablastin that inhibits further reproduction by the parasite. Both trypanocidal and ablastic effects were demonstrable in the serum of immune mice yet the parasite was still able to survive and multiply in the kidneys.     

Trypanosoma cruzi: Immunoperoxidase antibody test for serologic diagnosis

An indirect antiglobulin immunoperoxidase test was developed for the serological diagnosis of American Trypanosomiasis. Purified rabbit antihuman IgG was labeled with the enzyme and the conjugate so obtained was characterized according to its immune and enzymatic activities, with the help of such parameters as the authors have recently described. For a maximal sensitivity in the tests, high antibody levels and a high-labeling ratio were chosen, as well as dilutions of conjugate ensuring maximal reactivity. Positive tests were found in all 90 serum samples from patients with Chagas' disease and titers did not differ significantly from those observed in immunofluorescence tests done in parallel. The specificity of both tests was also similar, as indicated by the results found for serum samples from 60 patients with other diseases, parasitic or not, showing high levels of antibodies against other infective agents or autoantibodies, and in 15 normals.     

Trichinella spiralis: anaphylactic antibody formation and susceptibility in strains of inbred mice.

The anaphylactic antibody response of various strains of inbred mice of different H-2 specificities was investigated using the passive cutaneous anaphylactic technique (PCA) for the detection of the antibody response. Neither IgC₁ nor reaginic antibody were detected in serum samples obtained at the end of the first week of infection with Trichinella spiralis. Subsequently, all animals had detectable IgG₁ antibodies, although in some strains the titers were very low. Reaginic antibody was detected in relatively high titers in C57L, A, and DBA/1 mice. Two other strains were very poor responders (SJL and AKR). In most strains, reagin and IgG₁ remained detectable for 14 wk or longer. The pattern of response of all strains was very reproducible, indicating genetic control of the anaphylactic antibody production to the infection. In F₁ hybrids obtained from crosses between good and poor anaphylactic antibody responders, intermediate levels of both antibody classes were detected.Adult worm recovery rates were established at various points during the intestinal phase of infection, and no correlation between worm numbers and reaginic antibody titers in the various strains of mice could be demonstrated. There were noticeable differences in larval yields obtained after muscle digestion of mice belonging to the different inbred strains. In fact, we generally observed an inverse relationship between the number of larvae recovered from a given strain and their reaginic antibody titer.The intravenous injection of newborn larvae (NBL), obtained upon in vitro incubation of adult worms, produced detectable antibodies only in mice of the DBA/1 strain. These antibodies were consistently of low titer and became detectable only after the administration of two additional injections of NBL. This contrasted with the results observed after “per os” infection of DBA/1 mice, where high titers of these antibodies were always obtained, in spite of comparable ratios of muscle larval yield.     

Eimeria acervulina,E. brunetti,E. maxima, and E. necatrix: Low doses of oocysts to immunize young chickens

Resistance to reinfection varied with the species of Eimeria and with the number of oocysts in the inoculum. Chickens immunized with doses of 20,000 and 80,000 oocysts of E. acervulina, 312 and 1250 oocysts of E. brunetti or E. necatrix, or 1250 and 5000 oocysts of E. maxima at 2 and 4 weeks of age, respectively, were almost completely immune to a challenge dose at 6 weeks of age. Resistance was slightly less in chickens immunized with 1250 and 5000 oocysts of E. acervulina or 312 and 1250 oocysts of E. maxima. Birds given three immunizing infections of 1250, 5000, and 20,000 oocysts of E. maxima were completely immune 8 weeks after the last dose. Resistance was slightly less in birds immunized with similar doses of E. brunetti or E. necatrix. Doses of 20,000, 80,000, and 320,000 oocysts appeared necessary to confer a high level of immunity to E. acervulina. More than three low doses of oocysts appear necessary to induce a complete and enduring immunity against a high challenge for E. acervulina, E. brunetti, and E. necatrix. Higher immunizing doses would not be satisfactory due to the pathogenic effects of the coccidia after the initial infection.     

Dysregulation of metallothionein and zinc aggravates periodontal diseases

BackgroundPeriodontitis (PD) is a multifaceted inflammatory disease connected to bacterial infection that results in the destruction of tooth supporting structures and eventually tooth loss. Given their involvement in infection and inflammation, both metallothionein (MT) and zinc (Zn) might play vital roles in the development and progression of PD. More specifically, both MT and Zn are heavily involved in regulating immune functions, controlling bacterial infection, balancing inflammatory responses, and reducing oxidative stress, all of which are associated with the pathogenesis of PD.ObjectiveThis review paper will explore the physiological functions of MT and Zn and hypothesise how dysregulation could negatively affect periodontal health, leading to PD.FindingsBacterial lipopolysaccharide (LPS) derived from periodontal pathogens, namely P. gingivalis initiates the acute phase response, thus upregulating the expression of MT which leads to the subsequent deficiency of Zn, a hallmark of periodontal disease. This deficiency leads to ineffective NETosis, increases the permeability of the gingival epithelium, and disrupts the humoral immune response, collectively contributing to PD. In addition, the presence of LPS in Zn deficient conditions favours M1 macrophage polarisation and maturation of dendritic cells, and also inhibits the anti-inflammatory activity of regulatory T cells. Collectively, these observations could theoretically give rise to the chronic inflammation seen in PD.ConclusionA disrupted MT and Zn homeostasis is expected to exert an adverse impact on periodontal health and contribute to the development and progression of PD.     

慢性氨氮胁迫对台湾泥鳅幼鱼生长、免疫及组织结构的影响

以平均体质量为(2.00±0.56) g的台湾泥鳅(Paramisgurnus dabryanus ssp. Taiwan)幼鱼为研究对象, 探究氨氮胁迫浓度为0、3.5、6.0、10.4和18.0 mg/L时台湾泥鳅幼鱼生长性能、免疫酶活性及组织结构的变化。经过56d的氨氮胁迫试验结果显示: 台湾泥鳅终末体质量(W_F)、增重率(WGR)和特定生长率(SGR)随氨氮浓度的升高而逐渐降低, 各组之间存活率无显著差异。10.4和18.0 mg/L处理组肝脏超氧化物歧化酶(SOD)、碱性磷酸酶(ALP)和鳃Na+K+-ATP酶活性均显著低于对照组(P<0.05); 18.0 mg/L处理组肝脏溶菌酶(LZM)活性显著低于对照组(P<0.05), 而丙二醛(MDA)含量显著高于对照组(P<0.05)。组织切片结果显示, 氨氮处理组幼鱼均存在不同程度的鳃组织损伤, 表现为鳃小片短小、上皮细胞水肿、细胞空泡化、上皮细胞坏死和脱落; 肝组织则表现为肝血窦扩张、细胞轮廓模糊、细胞水样变性、细胞核偏移和细胞核溶解; 且两种组织中其病变区域随着氨氮浓度升高而增大。上述结果表明, 氨氮胁迫对台湾泥鳅幼鱼的生长和免疫酶活性具有显著的抑制作用, 并对其鳃和肝组织造成损伤。     

Genomes of 12 fig wasps provide insights into the adaptation of pollinators to fig syconia

Figs and fig pollinators are one of the few classic textbook examples of obligate pollination mutualism. The specific dependence of fig pollinators on the relatively safe living environment with sufficient food sources in the enclosed fig syconia implies that they are vulnerable to habitat changes. However, there is still no extensive genomic evidence to reveal the evolutionary footprint of this long-term mutually beneficial symbiosis in fig pollinators. In fig syconia, there are also non-pollinator species. The non-pollinator species differ in their evolutionary and life histories from pollinators. We conducted comparative analyses on 11 newly sequenced fig wasp genomes and one previously published genome. The pollinators colonized the figs approximately 66.9 million years ago, consistent with the origin of host figs. Compared with nonpollinators, many more genes in pollinators were subject to relaxed selection. Seven genes were absent in pollinators in response to environmental stress and immune activation. Pollinators had more streamlined gene repertoires in the innate immune system, chemosensory toolbox, and detoxification system. Our results provide genomic evidence for the differentiation between pollinators and nonpollinators. The data suggest that owing to the long-term adaptation to the fig, some genes related to functions no longer required are absent in pollinators.