Immune responses of poultry to Newcastle disease virus

Newcastle disease (ND) remains a constant threat to poultry producers worldwide, in spite of the availability and global employment of ND vaccinations since the 1950s. Strains of Newcastle disease virus (NDV) belong to the order Mononegavirales, family Paramyxoviridae, and genus Avulavirus, are contained in one serotype and are also known as avian paramyxovirus serotype-1 (APMV-1). They are pleomorphic in shape and are single-stranded, non-segmented, negative sense RNA viruses. The virus has been reported to infect most orders of birds and thus has a wide host range. Isolates are characterized by virulence in chickens and the presence of basic amino acids at the fusion protein cleavage site. Low virulent NDV typically produce subclinical disease with some morbidity, whereas virulent isolates can result in rapid, high mortality of birds. Virulent NDV are listed pathogens that require immediate notification to the Office of International Epizootics and outbreaks typically result in trade embargos. Protection against NDV is through the use of vaccines generated with low virulent NDV strains. Immunity is derived from neutralizing antibodies formed against the viral hemagglutinin and fusion glycoproteins, which are responsible for attachment and spread of the virus. However, new techniques and technologies have also allowed for more in depth analysis of the innate and cell-mediated immunity of poultry to NDV. Gene profiling experiments have led to the discovery of novel host genes modulated immediately after infection. Differences in virus virulence alter host gene response patterns have been demonstrated. Furthermore, the timing and contributions of cell-mediated immune responses appear to decrease disease and transmission potential. In view of recent reports of vaccine failure from many countries on the ability of classical NDV vaccines to stop spread of disease, renewed interest in a more complete understanding of the global immune response of poultry to NDV will be critical to developing new control strategies and intervention programs for the future.     

Attachment style and immunity: A 1-year longitudinal study

Previous cross-sectional studies suggested an association between attachment-related avoidance and altered immune function. We aimed at testing this hypothesis with longitudinal data. A random sample of 65 female nurses provided a blood sample and completed measures of perceived stress, social support, alexithymia, and attachment style. Immune assays included lymphocyte proliferative response (LPR) to Phytohemagglutinin and NK cell cytotoxicity (NKCC). State measures (perceived stress and support) and immune measures were collected again after 4, 8, and 12 months. Linear mixed effects models were used to examine the relationship between attachment and immunity. While low to moderate levels of attachment-related avoidance were not associated with NKCC, there was a significant negative association (beta −.35; p = .005) between high levels of avoidance and NKCC. No association was observed between NKCC and attachment-related anxiety, and between LPR and both attachment dimensions. While our findings should be interpreted with caution due to study limitations such as the relatively small sample size and the inclusion of only female participants, they corroborate the notion that attachment is linked to physiology and health.     

靶向纳米级免疫偶联物诱导检查点抑制剂抗体治疗颅内胶质瘤的可行性实验研究

目的 探讨靶向纳米级免疫偶联物(Nanoscale immunoconjugates,NCI)诱导检查点抑制剂抗体治疗颅内胶质瘤的可行性。方法 无特定病原体级(Specific pathogen free,SPF)级、雌性大鼠168只,随机分为磷酸缓冲盐溶液(Phosphate buffer saline,PBS)组(24只),游离组(72只)及NIC组(72只); 所有大鼠均进行颅内胶质瘤细胞植入,构建颅内胶质瘤大鼠模型; PBS组不进行治疗; 游离组给予T淋巴细胞相关抗原4(Cytotoxic T lymphocyte associated antigen-4,a-CTLA-4)和程序性细胞死亡1(Anti programmed cell death protein-1,a-PD-1)及两者联合注射,每种各24只; NCI组给予纳米级免疫偶联物诱导检查点抑制剂抗体[分别为聚苹果酸/ T淋巴细胞相关抗原4(Polymalic malic acid/ Cytotoxic T lymphocyte associated antigen-4,P/a-CTLA-4)、聚苹果酸/程序性细胞死亡1(Polymalic malic acid/Anti programmed cell death protein-1,P/a-PD-1)及两盒联合注射]注射,每种各24只; 使用荧光素标记法观察不同组大鼠药物血脑屏障穿透效率,比较不同治疗方式大鼠治疗后CD3+T细胞(CD3+Pan T Cells,CD3+)、CD4+,CD8+、调节性T细胞(Regulatory T cells,Treg)、巨噬细胞(MΦ)、自然杀伤细胞(Natural killer cell,NK)细胞、自然杀伤T细胞(Natural killer T cell,NKT)细胞、干扰素γ(Interferon-γ,IFNγ)水平及大鼠CD4+,CD8+增殖活跃程度、生存期。结果 荧光实验显示,NIC组各治疗方式大鼠脑部荧光面积均显著高于游离组及PBS组; NCI各组CD3+、CD4+、CD8+、Treg、CD4+ki67、CD8+ki67、MΦ、M1MΦ、M2MΦ、NK细胞、NKT细胞、IFNγ每孔计数及总体生存期显著高于游离组及PBS组(P<0.05)。结论 NCI诱导检查点抑制剂抗体能促进药物透过血脑屏障,刺激大脑驻留的免疫系统,促使CD8+ T细胞增殖并触发多种免疫细胞因子的释放,增加M1型巨噬细胞的产生,从而协调针对GBM的免疫反应,提高颅内胶质瘤大鼠存活时间。     

Prophylactic Dose of Neem (Azadirachta indica) Leaf Preparation Restricting Murine Tumor Growth is Nontoxic,Hematostimulatory and Immunostimulatory

Significant restriction of growth of Ehrlich's carcinoma was observed following prophylactic treatment on Swiss albino mice with neem leaf preparation (NLP-1 unit) once weekly for four weeks. Toxic effects of this particular dose (1 unit), along with 0.5 unit and 2 units of NLP doses, were evaluated on different murine physiological systems. One hundred percent of mice could tolerate 4 injections of 0.5 and 1 unit NLP doses. Body weight, different organ-body weight ratios and physical behavior of treated mice remained completely unchanged during treatment with different NLP doses. All of these NLP doses were observed to stimulate hematological systems as evidenced by the increase in total count of RBC, WBC and platelets and hemoglobin percentage. As histological changes as well as elevation in serum alkaline phosphatase, SGOT, SGPT were not observed in mice treated with three different doses of NLP, the nonhepatotoxic nature of NLP was proved. The level of serum urea remained unaltered and normal architecture of the cortical and medullary parts of the kidney were also preserved after NLP treatment. Increased antibody production against B16 melanoma antigen was detected in mice immunized with 0.5 unit and 1 unit of NLP. Number of splenic T lymphocytes (CD4+ and CD8+) and NK cells were also observed to be increased in mice injected with 0.5 unit and 1 unit of NLP. However, NLP dose of 2 units could not exhibit such immunostimulatory changes; NLP mediated immunostimulation was correlated well with the growth restriction of murine carcinoma. In other words, tumor growth restriction was observed only when mice were injected with immunostimulatory doses of NLP (0.5 unit and 1 unit).     

Do Fish Thrombocytes Play an Immunological Role? Their Cytoenzymatic Profiles and Function During an Accidental Piscine Candidiasis in Aquarium

Fish (F) thrombocytes (THRs) from healthy trouts were studied in terms of cytoenzyme expression. FTHRs were positive to acid periodic of shiff (PAS) and acid phosphatase (ac. phos.) without tartaric acid (? TA) stainings, as well to alkaline phosphatase. However, when compared with autologous macrophages (MØs), they were negative to naphthol cloroacetate esterase (AS-D), α-naphthyl acetate esterase (Anae), peroxidase (perox) and control ac. phos. with tartaric acid (+ TA) stainings, thus indicating a lack of typical lysosomial enzymes. This evidence supports the notion that FTHRs are not true digesting cells. Quite interestingly, trouts and human MØs were positive for PAS, AS-D, Anae, and perox stainings, thus confirming that cellular cytochemistries are maintained across evolution as their phagocytic functions. Additionally, blood films from trouts, accidentally infected with Candida albicans in aquarium, were morphologically analyzed. Actually, FTHRs interact with erythrocytes, potentiating the formation of rosettes around a central MØ. Polymorph nuclear cells and lymphocytes are present in these cellular aggregates, thus suggesting that FTHRs may represent a link between innate and adaptive immunity.     

Household illness is the strongest predictor of upper respiratory tract symptom risk in elite rugby union players

ObjectivesTo identify periods of increased risk for upper respiratory tract symptom (URTS) episodes, and examine whether biomarkers and/or self-reported lifestyle and wellness data can predict URTS risk in elite rugby union players.DesignProspective, longitudinal and repeated-measures study.MethodsSalivary secretory immunoglobulin A (SIgA), salivary cortisol, URTS, internal training load and self-reported lifestyle and wellness data including household illness, stress, mood, fatigue, muscle soreness and sleep quality were repeatedly measured in elite Southern hemisphere rugby union players (n = 28) throughout a season. Univariate frailty model analysis, which included 495 observations, was used to determine predictors of URTS risk.ResultsSurprisingly, the highest incidence of URTS occurred after rest weeks, namely the Christmas break and bye weeks (i.e., no scheduled trainings or matches); whereas URTS risk was reduced during weeks involving international travel (Hazard ratio (HR): 0.43, p < 0.001)). Household illness was the strongest predictor of URTS risk; players were almost three-fold more at risk for an URTS episode when illness in the household was present (HR: 2.90, p = 0.002). A non-significant, but potentially important trend for an inverse association between SIgA concentration and URTS incidence was also observed (HR: 0.99, p = 0.070).ConclusionsRest weeks were identified as periods of increased risk for URTS; while international travel did not appear to increase players risk for URTS. Incidence of household illness and SIgA concentration independently predicted URTS risk, with household illness being the strongest predictor. These findings can assist practitioners monitoring and management of athletes to potentially reduce URTS risk.     

Personality pathways to mortality: Interleukin-6 links conscientiousness to mortality risk

Personality is associated consistently with mortality hazards, but the physiological pathways are not yet clear. Immune system dysregulation may be one such pathway due to its role in age-related morbidity and mortality. In this preregistered study, we tested whether interleukin-6 (IL-6) and C-reactive protein (CRP) mediated the associations between personality traits and mortality hazards. The sample included 957 participants (M ± SD = 58.65 ± 11.51 years; range = 35–86 years) from the Midlife in the United States Survey that had 14 years of follow-up. Higher conscientiousness was associated with lower mortality hazards, with each one standard deviation higher conscientiousness associated with a 35% lower mortality risk. IL-6, but not CRP, partially mediated this association, with IL-6 accounting for 18% of this association in the fully adjusted model. While there was initial evidence that the biomarkers mediated both neuroticism and agreeableness and mortality risk, the indirect effects were not significant when controlling for the sociodemographic variables. Taken together, higher conscientiousness may lead to a longer life partially as a result of lower IL-6. This work highlights the importance of biological pathways that link personality to future mortality risk.     

Can exercise-related improvements in immunity influence cancer prevention and prognosis in the elderly?

Cancer incidence increases with advancing age. Over 60% of new cancers and 70% of cancer deaths occur in individuals aged 65 years or older. One factor that may contribute to this is immunosenescence – a canopy term that is used to describe age-related declines in the normal functioning of the immune system. There are multiple age-related deficits in both the innate and adaptive systems that may play a role in the increased incidence of cancer. These include decreased NK-cell function, impaired antigen uptake and presentation by monocytes and dendritic cells, an increase in ‘inflammaging’, a decline in the number of naïve T-cells able to respond to evolving tumor cells, and an increase in functionally exhausted senescent cells. There is consensus that habitual physical exercise can offer protection against certain types of cancer; however the evidence linking immunological mechanisms, exercise, and reduced cancer risk remain tentative. Multiple studies published over the last two decades suggest that exercise can mitigate the deleterious effects of age on immune function, thus increasing anti-cancer immunity. The potential ameliorative effect of exercise on these mechanisms include evidence that physical activity is able to stimulate greater NK-cell activity, enhance antigen-presentation, reduce inflammation, and prevent senescent cell accumulation in the elderly. Here we discuss the role played by the immune system in preventing and controlling cancer and how aging may retard these anti-cancer mechanisms. We also propose a pathway by which exercise-induced alterations in immunosenescence may decrease the incidence of cancer and help improve prognosis in cancer patients.