Exacerbation of murine respiratory mycoplasmosis in gnotobiotic F344/N rats by Sendai virus infection

Six- to eight-week-old gnotobiotic F344/N rats were inoculated intranasally with 10(5.0) colony-forming units of Mycoplasma pulmonis or were sham inoculated, then one week later were given 10(0.2) 50% tissue culture infective doses of Sendai virus or sterile medium. Groups of rats were killed immediately after virus inoculation and three, five, ten, and 20 days later. Lesions in nasal passages, middle ears, larynxes, tracheas, and lungs from half of the rats in each group were subjectively scored. Organs from the other rats were quantitatively cultured for M. pulmonis and for Sendai virus. Rats given Sendai virus alone had mild, patchy, necrotizing rhinitis, laryngitis, tracheitis, and bronchitis, but not bronchiolitis or interstitial pneumonia. M. pulmonis alone induced mild lesions of murine respiratory mycoplasmosis including mild to moderate suppurative rhinitis, otitis media, laryngitis, and tracheitis with submucosal lymphoid accumulation and epithelial hyperplasia, but not lung lesions. Rats given M. pulmonis and Sendai virus had severe lesions characteristic of advanced mycoplasmal disease throughout the respiratory tract, including suppurative bronchitis with extensive lymphoid accumulations and epithelial hyperplasia; some rats also had suppurative pneumonia and bronchiectasis. Larger numbers of M. pulmonis colony-forming units were in rats given Sendai virus, but there was no statistically significant difference in Sendai virus infectious units between rats also given M. pulmonis and those given virus only.     

Measles virus infection induces interleukin-8 release in human pulmonary epithelial cells

Measles virus (MV) infection primarily targets epithelial cells of the respiratory tract, which have the potential to synthesize a variety of cytokines. In this report, we studied the effect of MV infection on the production of interleukin (IL)-8 by the pulmonary epithelial cells. A549 cells, a lower airway epithelial cell line, produced IL-8 after MV inoculation in a dose- and time-dependent manner. The IL-8 production was little affected by UV-inactivation of MV and scarcely suppressed by cycloheximide treatment. These results indicated that MV particle binding to and/or incorporation into cells stimulated IL-8 expression in A549 cells.     

In vitro propagation of canine distemper virus: establishment of persistent infection in Vero cells

Primary cultures of bovine fibroblast (BF) and canine brain cells, persistently infected with virulent R252-canine distemper virus (CDV), were cocultured with African green monkey (Vero) cells. Transfer of persistent CDV from BF to Vero cells varied inversely with the in vitro passage level (age) of the CDV-infected BF cells. Successful transfer of CDV to Vero cells was signaled by the transient appearance of viral syncytia, rapid spread of viral antigen to all Vero cells in the culture, and by recovery of cell-free Vero-infectious virus in culture fluids. With time, viral cytopathic effects in Vero cells containing CDV disappeared, and the infected lines could not be distinguished from noninfected control Vero cells, except by immunoassay for viral antigen.     

病毒感染诱导细胞凋亡分子机制的研究进展

病毒感染与靶细胞凋亡之间存在着密切的关系,在病毒感染引起细胞凋亡过程中有许多基因和蛋白得到表达,并参与作用。另外,细胞因子和免疫细胞也直接或间接地参与该过程。试验表明,病毒感染诱导细胞凋亡与病毒复制增殖相关联。对细胞凋亡与病毒感染关系的进一步研究,为病毒感染性疾病的预防和诊治提供新的思路和手段。     

Pulmonary eosinophilia and granulomatous pulmonary arteritis induced in rats by intravenous Sephadex.

Airway eosinophilia has been proposed as a major pathogenetic event in bronchial asthma and airway hyperresponsiveness. Intravenous injection of Sephadex G200 in rats induces pulmonary and blood eosinophilia and alters pulmonary responsiveness to 5-hydroxytryptamine. To characterize the early pulmonary inflammatory responses following Sephadex administration, and to determine the timing of the onset of pulmonary eosinophilia relative to blood eosinophilia, Sprague-Dawley rats were injected intravenously with Sephadex G200 beads. Lungs and other tissues were examined by light and transmission electron microscopy at 4, 12, 24, 48, 72, and 96 hours after injection. Blood eosinophil counts were determined at 0, 24, and 96 hours after injection. Sephadex beads were trapped initially in small caliber muscular pulmonary arteries associated with terminal bronchioles and in intra-acinar locations. There was marked infiltration of eosinophils and macrophages around the beads and into arterial walls and edematous periarterial and peribronchiolar connective tissue as early as 4 hours after injection. Periarterial-peribronchiolar eosinophil aggregates peaked in density at 24 and 48 hours. Macrophages and multinucleated cells dominated the inflammatory cell responses in arteries immediately surrounding partially degraded Sephadex beads from 24 to 96 hours. Bone marrow eosinophilopoiesis and blood eosinophilia were not detected until 96 hours. We conclude that Sephadex induces pulmonary eosinophilia prior to blood eosinophilia and suggest that Sephadex may induce pulmonary release of one or more eosinophil chemotactic substance(s). This model may prove useful in the study of factors that influence eosinophil migration into the lung in various disease states.     

Establishment of persistent avian infectious bronchitis virus infection in antibody-free and antibody-positive chickens

Avian infectious bronchitis virus (IBV) causes a highly contagious and economically significant disease in chickens. Establishment of a carrier state in IBV infection and the potential for the persistent virus to undergo mutations and recombination in chicken tissues have important consequences for disease management. Nevertheless, whether chickens can maintain persistent IBV infection in the absence of reinfection from exogenous sources or the presence of antibody in the host can modulate virus persistence remains unclear. Indeed, whether or not IBV genome can undergo genetic changes during in vivo infection has not been demonstrated experimentally. In the present study, IBV shedding and tissue persistence were monitored in individual chickens maintained under strict isolation that precluded reinfection from exogenous sources. In the first of two experiments, intranasal exposure of 6-wk-old antibody-free chickens to IBV vaccine virus resulted in intermittent shedding of the virus from both trachea and cloaca of individual birds for up to 63 days. Also, the virus was recovered from the internal organs (spleen, gonad, kidney, lung, cecal tonsil, and cloacal bursa) of six of eight birds killed at various intervals between 27 and 163 days postinoculation (DPI). In the second experiment, IBV exposure of 1-day-old maternal antibody-positive chicks led to periodic virus shedding from the trachea and cloaca in all chickens until 77 days; however, internal organs (lungs and kidneys) of only one of seven birds (killed at 175 DPI) were virus positive, suggesting that presence of antibody at the time of infection protects internal organs from IBV infection. When the lung and kidney isolates of IBV from the latter experiment were compared with the parent-vaccine virus, no changes in their antigenicity, tissue tropism, or the nucleotide sequence of the S1 glycoprotein gene were observed. These findings indicate that, unlike the mammalian coronaviruses, propensity for frequent genetic change may not be inherent in the IBV genome.     

The involvement of mast cells and mast cell proteinases in the intestinal response to equine cyathostomin infection

Cyathostomins (Cyathostominae) are regarded as the most pathogenic equine nematode worldwide. These nematodes are difficult to control in equine populations due to emerging anthelmintic resistance and evasion of encysted larval cyathostomins to regular modern anthelmintics. Mast cells and their proteinases have been shown to play a role in the mammalian immune response to nematode infections. Involvement of mast cells and mast cell proteinases in the equine immune response to cyathostomin infection is proposed. A technique was established to perform immunohistochemical staining using polyclonal rabbit anti-equine mast cell proteinase-1 (eqMCP-1) and anti-equine tryptase on formalin-fixed large intestinal sections, from horses classified as cyathostomin positive and negative at the time of death based upon larval enumeration. Quantitative analysis of antibody labelled mast cells was used to detect mast cell proteinases in equine large intestinal sections positive and negative for cyathostomin larvae. This demonstrated an increase in equine tryptase labelled mucosal and submucosal mast cells in cyathostomin positive horses. This study has established an immunohistochemical technique to demonstrate mast cell proteinases in formalin-fixed large intestinal sections. This technique may be used to determine possible involvement of mast cells and their proteinases in the equine immune response to cyathostomin larvae. Further studies are required to define a specific role.     

Anaphylaxis and systemic inflammatory response syndrome induced by inadvertent intravenous administration of mare's milk in a neonatal foal

Objective – To describe the diagnostic procedures, therapeutic management and successful outcome of a case of anaphylaxis induced by the inadvertent intravenous (IV) administration of mare's milk to a neonatal foal. Case Summary – A 3‐day‐old Thoroughbred colt was presented for treatment of bilateral flexural limb deformities of the forelimbs. Because the foal was unable to ambulate initially, mare's milk was administered via nasoesophageal tube feedings during treatment of the musculoskeletal disorder. Anaphylaxis resulted after unintentional administration of a bolus of 150 mL of mare's milk through a jugular catheter. Aggressive therapy for anaphylaxis and careful monitoring resulted in the successful recovery of the foal after 9 days of intensive care. New or Unique Information Provided – This case is the first published report to describe the effects of accidental IV administration of mare's milk to a neonatal foal. Medical errors are commonly reported in pediatric medicine; the intent of this report is to raise awareness of medical errors and student education in equine medicine as well as describe the therapy and outcome of anaphylaxis induced by IV administration of mare's milk in a neonatal foal.     

Incidence of persistent viraemia and latent feline leukaemia virus infection in cats with lymphoma

In the past, feline leukaemia virus (FeLV) infection, and also latent FeLV infection, were commonly associated with lymphoma and leukaemia. In this study, the prevalence of FeLV provirus in tumour tissue and bone marrow in FeLV antigen-negative cats with these tumours was assessed. Seventy-seven diseased cats were surveyed (61 antigen-negative, 16 antigen-positive). Blood, bone marrow, and tumour samples were investigated by two polymerase chain reaction (PCR) assays detecting deoxyribonucleic acid (DNA) sequences of the long terminal repeats (LTR) and the envelope (env) region of the FeLV genome. Immunohistochemistry (IHC) was performed in bone marrow and tumour tissue. None of the antigen-negative cats with lymphoma was detectably infected with latent FeLV. The prevalence of FeLV viraemia in cats with lymphoma was 20.8%. This suggests that causes other than FeLV play a role in tumorigenesis, and that latent FeLV infection is unlikely to be responsible for most feline lymphomas and leukaemias.     

持续低产蛋率蛋鸭群主要病毒感染的检测与分析

为了明确持续低产蛋率开产蛋鸭群的主要病毒病感染情况,应用已建立的间接ELISA方法和血凝抑制试验对2013年1月至2015年10月采自福建、广东、广西、江西、浙江、江苏和安徽等7省(区)免疫过H5亚型和H9亚型禽流感灭活疫苗但未免疫禽1型副黏病毒病疫苗和禽坦布苏病毒病疫苗,表现为持续低产蛋率的29个开产蛋鸭群的4 737份血清样品进行抗体检测,同时采集蛋鸭卵巢组织进行RT-PCR检测。结果显示,29个开产蛋鸭群中,H5亚型禽流感、H9亚型禽流感、禽1型副黏病毒病和禽坦布苏病毒病抗体的群阳性率分别为100.0%,100.0%,10.3%和100.0%,群内阳性率分别为79.4%~100.0%,82.5%~100.0%,0.0%~13.1%和33.7%~100.0%;蛋鸭卵巢组织中H5亚型禽流感病毒、H9亚型禽流感病毒、禽1型副黏病毒和禽坦布苏病毒的阳性率依次为13.8%(4/29),0.0%(0/0),3.5%(1/29)和86.2%(25/29)。上述结果表明,我国以上7省(区)表现持续低产蛋率的开产蛋鸭群存在禽坦布苏病毒的严重感染,应引起养鸭生产者的高度重视。     

Acute phase response in porcine reproductive and respiratory syndrome virus infection

This study was focused on the changes observed in the serum concentration of haptoglobin (Hp), C-reactive protein (CRP), serum amyloid A (SAA) and Pig-major acute protein (Pig-MAP), during experimental porcine reproductive and respiratory syndrome virus (PRRSV) infection and in their relationship with the expression of interleukin 1β (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α). Hp and Pig-MAP serum levels were increased at 10 dpi, but CRP and SAA showed a delayed and highly variable increase. All three proinflammatory cytokines were poorly expressed, and only a mild increase in IL-1β was observed at 7 dpi. The increased expression of Hp coincided with the light enhancement observed in both IL-6 and TNF-α, and might be related with an increased expression of IL-10. The low expression of TNF-α might point to a possible mechanism of viral evasion of host-immune response. This issue and the delayed expression of CRP and SAA should be taken into account in future studies about modulation of the immune response by PRRSV infection.     

庆大霉素致原代大鼠肾小管上皮细胞凋亡的研究

为了探究庆大霉素致原代肾小管上皮细胞的凋亡作用,以0、1、2、4、8、16 mmol/L浓度的庆大霉素分别作用原代大鼠肾小管上皮细胞24 h,采用cck-8法检测细胞相对活力,hochest 33258染色法观察细胞核形态以及利用流式细胞术检测细胞凋亡率。结果表明,与对照组相比,随着庆大霉素浓度的增加,细胞活性呈显著或极显著下降(P0.05或P0.01),细胞凋亡率呈显著或极显著上升(P0.05或P0.01),hochest33258染色观察到细胞核出现固缩或碎裂(P0.01)。结果提示,庆大霉素能引起细胞发生凋亡和损伤,并且这可能与其肾毒性有密切的联系。     

Development and serial passage of persistent lymphocytosis associated with bovine leukemia virus infection in cattle

Two calves each were inoculated with 1.5 x 10(8) or 5 x 10(9) lymphocytes collected from each one cow which had persistent lymphocytosis (PL) and antibodies to bovine leukemia virus (BLV). A sudden increase in the number of peripheral blood lymphocytes (PBL) was observed 14 and 23 days, respectively, after inoculation and the maximum number reached 29,000 and 52,000/microliters 72 and 57 days after inoculation. Although the degree of PL decreased gradually in these cattle, it continued until 14 and 44 months after inoculation when one animal was sacrificed and the other died of lymphosarcoma. The PL was passaged in cattle by inoculation of a large number of PBL obtained from cattle at the stage of PL (PLL). The degree of PL was severer in cattle inoculated with a larger number of PLL. PL was not caused by inoculation of PBL obtained from either BLV-infected non-PL cattle or cattle free of BLV. The PL was also caused by inoculation of PLL into BLV-infected non-PL cattle. On the other hand, it was not observed after inoculation of a large amount of cell-free virus obtained from short-term cultures of PLL. Antibodies to BLV developed earlier and to higher levels in cattle inoculated with PLL than in those inoculated with cell-free virus. These facts show that infection with BLV was established more effectively by PLL than by cell-free virus, the infection may occur by lymphocyte to lymphocyte interaction and the actual number of infected BLV may have an important role in development of PL.     

Kinetin inhibits apoptosis of aging spleen cells induced by D-galactose in rats

Kinetin (Kn) is a cytokinin growth factor that exerts several anti-aging and antioxidant effects on cells and organs. To investigate the mechanism underlying apoptotic events in aging cells induced by D-galactose (D-gal), we examined the effect of Kn delivered via nuchal subcutaneous injection on D-gal-induced aging and apoptosis in rats. Our results showed that interleukin (IL)-2 levels and mitochondrial membrane potential (ΔΨm) were decreased by Kn in aging rats while IL-6 production and apoptosis increased. In addition, the expression of anti-apoptotic Bcl-2 was low while that of Bax was high in the aging group. After treated with Kn, compared with aging group, there showed obvious difference in Kn group with elevated IL-2, proliferation index, Bcl-2, ΔΨm and decreased IL-6 and Bax in splenic lymphocyte. Based on these results, we concluded that Kn can effectively protect the rat spleen from aging, apoptosis, and atrophy.