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1.
Murine noroviruses (MNV) are currently the most prevalent viruses infecting mouse research colonies. Concurrent infection of research mice with these viruses can dramatically alter the experimental outcome in some research models, but not others. In this report, we investigated the effect of MNV1 and MNV4 on a murine model of intestinal inflammation and fibrosis induced by Salmonella typhimurium infection in C57BL/6 mice. Subsequent co-infection of these mice with MNV1 or MNV4 did not lead to major changes in histopathology, the inflammatory response, or the fibrotic response. Thus, MNV does not substantially alter all gastrointestinal research models, highlighting the importance of investigating potential alterations in the research outcome by MNV on an individual basis. We hypothesize that this is particularly important in cases of research models that use immunocompromised mice, which could be more sensitive to MNV infection-induced changes.  相似文献   

2.
Although a Yersinia pseudotuberculosis (Yptb) lung infection model has been developed to study Y. pestis pathogenesis, it is still necessary to establish a new animal model to mimic the pathophysiological features induced by Y. pestis infection. Here, we provide a new lung infection model using the Yptb strain, IP2777, which displayed rapid spread of bacteria to the liver, spleen, and blood. In addition, we examined whether TLR4 is involved in Yptb-induced pathogenesis in the lung infection model of mice we generated. Following lung infection of WT and TLR4-deficient mice with the Yptb strain IP2777, the survival rate, bacterial colonization, histopathology, and level of cytokines and chemokines in the lung, spleen, liver, and blood were analyzed. TLR4-deficient mice had a lower survival rate than WT mice in response to Yptb lung infection. Although the bacterial colonization and pathology of the lung were comparable between WT and TLR4-deficient mice, those of the spleen and liver were more severe in TLR4-deficient mice. In addition, the levels of TNF-α and CXCL2 in the liver and IL-6 and CXCL2 in the blood were higher in TLR4-deficient mice than in WT mice. Our results demonstrate that TLR4 is necessary for optimal host protection against Yptb lung infection and TLR4-deficient mice may serve as a better genetic model of Yptb infection for mimicking Y. pestis infection.  相似文献   

3.
Currently, murine noroviruses (MNV) are the most prevalent viral pathogens identified in laboratory animal facilities. While several reports exist concerning the prevalence of MNV in North American research facilities, very few reports are available for other parts of the world, including Korea. This study evaluated the prevalence of MNV infection in 745 murine sera collected from 15 animal facilities in Korea by enzyme linked immunosorbent assay (ELISA). Positive cases were subcategorized by murine strain/genetics, housing environments and animal sources. In summary, 6.6% of inbred/outbred mice purchased from commercial vendors were seropositive, 9.6% of in-house colonies were seropositive and 27.0% of genetically modified mice (GMM) were seropositive. Partial gene amplification of fecal isolates from infected animals showed that they were homologous (100%) with MNV-4.  相似文献   

4.
Dourine, caused by infection with Trypanosoma equiperdum, is one of the trypanosomiasis in equids. The clinical course of dourine is long-term, ranging from 1–2 months to several years. Since the pathogenesis of dourine has not yet been elucidated, experimental studies using mouse infection models are needed. Although mice are not susceptible to most T. equiperdum strains, some strains can infect mice. Even in such strains, infected mice develop rapidly transient parasitemia and die within 2–8 days. Therefore, mice experimentally infected with these T. equiperdum strains are not suitable for mouse infection models to analysis the pathogenesis of dourine. A sequential method of isolating parasites from dourine-affected horses and adapting them to in vitro cultures using soft agarose media was recently developed. Various T. equiperdum strains adapted to in vitro conditions have been established using this technique. We used one of these strains, the T. equiperdum IVM-t2 strain. In the present study, T. equiperdum IVM-t2 strain inoculated mice developed periodic parasitemia during the experimental period of 60 days. Histopathologically, vaginitis and dermatitis were observed. These findings were comparable to those of dourine-affected horses. Therefore, mice infected with T. equiperdum IVM-t2 strain may be a valuable tool for pathological, immunological, and parasitological in vivo research, and will contribute to investigations on the mechanisms underlying the disease process and the host-parasite relationship.  相似文献   

5.
Heme oxygenase-1 (HO-1) is an enzyme that catabolizes free heme, which induces an intense inflammatory response. The expression of HO-1 is induced by different stimuli, triggering an anti-inflammatory response during biological stress. It was previously verified that HO-1 is able to induce indoleamine 2,3-dioxygenase (IDO), an enzyme that is induced by IFN-γ in Toxoplasma gondii infection. To verify the role of HO-1 during in vivo T. gondii infection, BALB/c and C57BL/6 mice were infected with the ME49 strain and treated with zinc protoporphyrin IX (ZnPPIX) or hemin, which inhibit or induce HO-1 activity, respectively. The results show that T. gondii infection induced high levels of HO-1 expression in the lung of BALB/c and C57BL6 mice. The animals treated with ZnPPIX presented higher parasitism in the lungs of both lineages of mice, whereas hemin treatment decreased the parasite replication in this organ and in the small intestine of infected C57BL/6 mice. Furthermore, C57BL/6 mice infected with T. gondii and treated with hemin showed higher levels of IDO expression in the lungs and small intestine than uninfected mice. In conclusion, our data suggest that HO-1 activity is involved in the control of T. gondii in the lungs of both mouse lineages, whereas the hemin, a HO-1 inducer, seems to be involved in the control of parasitism in the small intestine of C57BL/6 mice.  相似文献   

6.
Human granulocytic anaplasmosis (HGA), an emerging disease of public health concern in many areas of the world, is caused by Anaplasma phagocytophilum. Small animal models of A phagocytophilum in laboratory mice have been developed and used to study the pathogenesis of HGA. In this study, we characterized the pathologic changes in acute infection of C3H/HeJ mice experimentally infected with the NY18 isolate of A phagocytophilum. Although no clinical signs were noted, acute infection was associated with gross splenomegaly, microscopic inflammatory lesions in the lung and liver, hyperplastic lesions on the spleen, and clinical pathology abnormalities including neutropenia and monocytosis. This study emphasizes the use of well-defined animal models as a valuable tool for the study of A phagocytophilum infections.  相似文献   

7.
Haemorrhagic septicaemia (HS) is an endemic disease of bovines, occuring in most tropical regions of Asia and Africa. In the present study, the suitability of using mice to study pathogenesis of HS was assessed using mortality, mean death time and bacterial multiplication in vital organs after infection with live P multocida. Mice were infected with 105, 103 and 101?cfu of P. multocida B:2 via intranasal and subcutaneous routes along with control groups. Bacterial multiplication in lung, liver and spleen of mice were determined at 24 h interval after intranasal and subcutaneous challenge. More than 80 % of challenged mice died within 48 h of inoculation, irrespective of the dose and route of inoculation. A heavy bacterial load (up to 108?cfu) was observed in lung, liver and spleen of mice titrated at 24 h and following death of mice. Results of the present study indicate that even ten bacteria are enough to cause mortality in mice and the organism multiplies rapidly in respiratory epithelium and disseminated to other vital organs viz liver and spleen suggesting the important role of mouse model in investigating the pathogenesis and challenge studies during vaccine development.  相似文献   

8.
The acute phase protein response is a well-described generalized early host response to tissue injury, inflammation and infection, observed as pronounced changes in the concentrations of a number of circulating serum proteins. The biological function of this response and its interplay with other parts of innate host defence reactions remain somewhat elusive. In order to gain new insight into this early host defence response in the context of bacterial infection we studied gene expression changes in peripheral lymphoid tissues as compared to hepatic expression changes, 14–18 h after lung infection in pigs. The lung infection was established with the pig specific respiratory pathogen Actinobacillus pleuropneumoniae. Quantitative real-time PCR based expression analysis were performed on samples from liver, tracheobronchial lymph node, tonsils, spleen and on blood leukocytes, supplemented with measurements of interleukin-6 and selected acute phase proteins in serum. C-reactive protein and serum amyloid A were clearly induced 14–18 h after infection. Extrahepatic expression of acute phase proteins was found to be dramatically altered as a result of the lung infection with an extrahepatic acute phase protein response occurring concomitantly with the hepatic response. This suggests that the acute phase protein response is a more disseminated systemic response than previously thought. The current study provides to our knowledge the first example of porcine extrahepatic expression and regulation of C-reactive protein, haptoglobin, fibrinogen, pig major acute phase protein, and transferrin in peripheral lymphoid tissues.  相似文献   

9.
目的研究感染性猪蛔虫卵经灌胃感染小白鼠的合适感染量。方法将小白鼠分成5组,每组感染剂量分别为3 000,3 500,4 000,4 500,5 000个猪蛔虫卵。经感染后的小白鼠饲养数日,剖杀,取样压片镜检,计数。结果低剂量组A和B感染较低,C组适中,3组都未出现死亡,而高剂量组E和F出现小鼠死亡。结论小白鼠经灌胃感染猪蛔虫卵的合适感染量为每只4 000个。  相似文献   

10.
本研究旨在了解TLR4信号转导在铜绿假单胞菌感染所致急性肺损伤的发病机理中的作用.通过使用Tlr4基因突变致正常TLR4信号转导缺失的C3H/HeJ小鼠,评估TLR4信号转导在调节铜绿假单胞菌引起的急性肺损伤中的作用.选用6～8周龄、雄性、TLR4缺陷型(C3H/HeJ)和SPF级野生型(C3H/HeN)的小鼠各21只...  相似文献   

11.
Toxocariasis is considered a neglected disease despite the importance of Toxocara spp. infections for human health and is little recognized as a significant problem by public health institutions in developing countries. Epidemiological studies suggest that infection with Toxocara cati contributes to the development of allergic asthma.In the present study, we investigated the effect of T. cati infection on experimental allergic airway inflammation using murine model. BALB/c mice were infected by oral administration with 500 embryonated T. cati eggs followed by ovalbumin (OVA) sensitization and challenge to induce allergic airway inflammation. Infection with T. cati in combination with OVA treatment leads to exacerbation of pulmonary inflammation, eosinophilia, airway hyperresponsiveness, OVA specific IgE. Cytokines measurement in bronchoalveolar lavage indicated that the levels of IL-4 and IL-5 in BAL fluid significantly increased after T. cati infected, OVA treated or a combination of both. Increased level of IL-5 was measured in the lungs of T. cati-infected or OVA-treated mice compared with controls. Moreover, combining infection and OVA treatment significantly increase the level of these cytokines.A direct association between T. cati infection and asthma was found in murine model. Although a wide range of helminth species have been demonstrated to modulate allergic responses, most notably the intestinal nematode T. cati, increases airway hyperresponsiveness, lung histopathology, eosinophil recruitment, and Th2 cytokines in alum-sensitized models of airway allergy.  相似文献   

12.
Gut-lung axis injury is a common finding in patients with respiratory diseases as well as in animal model of influenza virus infection. Influenza virus damages the intestinal microecology while affecting the lungs. Rifaximin, a non-absorbable derivative of rifamycin, is an effective antibiotic that acts by inhibiting bacterial RNA synthesis. This study aimed to determine whether rifaximin-perturbation of the intestinal microbiome leads to protective effects against influenza infection, via the gut-lung axis. Our results showed that influenza virus infection caused inflammation of and damage to the lungs. The expression of tight junction proteins in the lung and colon of H1N1 infected mice decreased significantly, attesting that the barrier structure of the lung and colon was damaged. Due to this perturbation in the gut-lung axis, the intestinal microbiota became imbalanced as Escherichia coli bacteria replicated opportunistically, causing intestinal injury. When influenza infection was treated with rifamixin, qPCR results from the gut showed significant increases in Lactobacillus and Bifidobacterium populations, while Escherichia coli populations markedly decreased. Furthermore, pathology sections and western blotting results illustrated that rifaximin treatment strengthened the physical barriers of the lung-gut axis through increased expression of tight junction protein in the colon and lungs. These results indicated that rifaximin ameliorated lung and intestine injury induced by influenza virus infection. The mechanisms identified were the regulation of gut flora balance and intestinal and lung permeability, which might be related to the regulation of the gut-lung axis. Rifaximin might be useful as a co-treatment drug for the prevention of influenza virus infection.  相似文献   

13.
The outer membrane proteins (OMPs) of Brucella (B.) abortus have been extensively studied, but their immunogenicity and protective ability against B. abortus infection are still unclear. In the present study, B. abortus Omp28, a group 3 antigen, was amplified by PCR and cloned into a maltose fusion protein expression system. Recombinant Omp28 (rOmp28) was expressed in Escherichia coli and was then purified. Immunogenicity of rOmp28 was confirmed by Western blot analysis with Brucella-positive mouse serum. Furthermore, humoral- or cell-mediated immune responses measured by the production of IgG1 or IgG2a in rOmp28-immunized mice and the ability of rOmp28 immunization to protect against B. abortus infection were evaluated in a mouse model. In the immunogenicity analysis, the mean titers of IgG1 and IgG2a produced by rOmp28-immunized mice were 20-fold higher than those of PBS-treated mice throughout the entire experimental period. Furthermore, spleen proliferation and bacterial burden in the spleen of rOmp28-immunized mice were approximately 1.5-fold lower than those of PBS-treated mice when challenged with virulent B. abortus. These findings suggest that rOmp28 from B. abortus is a good candidate for manufacturing an effective subunit vaccine against B. abortus infection in animals.  相似文献   

14.
BackgroundMouse hepatitis virus (MHV) A59 is a highly infectious pathogen and starts in the respiratory tract and progresses to systemic infection in laboratory mice. The complement system is an important part of the host immune response to viral infection. It is not clear the role of the classical complement pathway in MHV infection.ObjectivesThe purpose of this study was to determine the importance of the classical pathway in coronavirus pathogenesis by comparing C1qa KO mice and wild-type mice.MethodsWe generated a C1qa KO mouse using CRISPR/Cas9 technology and compared the susceptibility to MHV A59 infection between C1qa KO and wild-type mice. Histopathological and immunohistochemical changes, viral loads, and chemokine expressions in both mice were measured.ResultsMHV A59-infected C1qa KO mice showed severe histopathological changes, such as hepatocellular necrosis and interstitial pneumonia, compared to MHV A59-infected wild-type mice. Virus copy numbers in the olfactory bulb, liver, and lungs of C1qa KO mice were significantly higher than those of wild-type mice. The increase in viral copy numbers in C1qa KO mice was consistent with the histopathologic changes in organs. These results indicate that C1qa deficiency enhances susceptibility to MHV A59 systemic infection in mice. In addition, this enhanced susceptibility effect is associated with dramatic elevations in spleen IFN-γ, MIP-1 α, and MCP-1 in C1qa KO mice.ConclusionsThese data suggest that C1qa deficiency enhances susceptibility to MHV A59 systemic infection, and activation of the classical complement pathway may be important for protecting the host against MHV A59 infection.  相似文献   

15.
Monoclonal antibodies were produced against orf virus-specified cell surface proteins in an attempt to develop reagents capable of differentiating between members of the Parapoxviridae. Two immunization protocols were used to induce an anti-orf response in BALB/c mice, one of which resulted in virus replication in the recipient. The monoclonal antibodies produced were tested for crossreactivity with bovine papular stomatitis virus (BPS) and milker's node virus (MNV) by indirect immunofluorescence assay (IFA) and immunoblotting. The results indicate that significant antigenic overlap exists between isolates of orf, MNV and BPS, even at the level of specificity provided by monoclonal antibodies. One monoclonal antibody reacted strongly in IFA with orf virus isolates, very weakly with MNV, and not at all with BPS. On immunoblots this same antibody recognized a 40-43 kDa protein in orf virus-infected cells, and also a 45-48 kDa protein in cells infected with MNV or BPS virus. The data suggest that it may be possible to define parapoxvirus strains on the basis of small variations in specific virus-directed cell surface proteins.  相似文献   

16.
A suitable balance in the production of Th1/Th2-type cytokines has a crucial role in the control of microbial infections. We investigated cytokine production patterns and effects during Neospora caninum infection, based on two mouse models and an in vitro system. In the acute infection of N. caninum, BALB/c-background IFN-gamma-deficient mice that were sensitive to the N. caninum infection showed high levels of IL-10 production, whereas significant levels of interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) production were observed in resistant wild type mice. BALB/c mice vaccinated with recombinant vaccinia virus expressing N. caninum surface protein NcSRS2 resisted parasite spread throughout the body, low levels of IFN-gamma production and high levels of IL-4 production were observed compared to unvaccinated animals. The treatment of N. caninum-infected cells with IFN-gamma or IL-10 decreased the host-cell viability in an in vitro system using mouse macrophage J774A.1 cells. On the other hand, IL-4, but not IL-10 administration, increased the viability of N. caninum-infected and IFN-gamma-treated cells. In the light of the balance of Th1/Th2-type cytokine production, an IFN-gamma/IL-4 balance may have a crucial role for the control of cellular responses against the parasite invasion.  相似文献   

17.
To better understanding Brucella abortus infection, serum metabolites of B. abortus-infected and -uninfected mice were analyzed and twenty-one metabolites were tentatively identified at 3 and 14 days post-infection (d.p.i.). Level of most lysophosphatidylcholines (LPCs) was found to increase in infected mice at 3 d.p.i., while it was decreased at 14 d.p.i. as compared to uninfected mice. In contrast, acylcarnitines were initially reduced at 3 d.p.i then elevated after two-weeks of infection, while hydroxysanthine was increased at 14 d.p.i. in infected mice. Our findings suggest that the significant changes in LPCs and other identified metabolites may serve as potential biomarkers in acute phase of B. abortus infection.  相似文献   

18.
为探讨中药复方宫炎净注射液对小鼠急性炎症的抗炎作用,试验通过二甲苯致小鼠耳廓肿胀、蛋清致小鼠足趾肿胀、冰醋酸致小鼠腹腔毛细血管通透性及棉球致肉芽肿4个急性炎症模型来研究其抗炎作用。结果表明,中药复方宫炎净注射液能显著减少小鼠的耳廓肿胀率和降低小鼠腹腔毛细血管通透性（P＜0.05）;显著抑制棉球肉芽组织的生长和足趾肿胀率（P＜0.05）;其中以中药复方宫炎净注射液高剂量组效果最为显著,且与西药对照组相比无显著差异（P＞0.05）。因此,中药复方宫炎净注射液抗炎作用显著。  相似文献   

19.
为了研究银杏内酯A对非特异性肺损伤小鼠的保护作用,采用脂多糖（LPS）滴鼻法建立了小鼠急性肺损伤（ALI）模型。于造模前1h给予银杏内酯A（50,100mg/kg）,在LPS滴入后18h检测支气管肺泡灌洗液（BALF）中的细胞因子TNF-α、IL-6、IL-1β水平,观察肺部组织学的病理变化。结果表明：银杏内酯A可以显著抑制肺组织中炎性细胞的浸润,抑制肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）和白细胞介素1β（IL-1β）炎性细胞因子的产生。由此得出结论,银杏内酯A对LPS诱导的小鼠ALI具有一定的保护作用。  相似文献   

20.
Lymphoma is the third most common cancer diagnosed in children, and T-cell lymphoma has the worst prognosis based on clinical observations. To date, a lymphoma model with uniform penetrance has not yet been developed. In this study, we generated a p53 deficient mouse model by targeting embryonic stem cells derived from a C57BL/6J mouse strain. Homozygous p53 deficient mice exhibited a higher rate of spontaneous tumorigenesis, with a high spontaneous occurrence rate (93.3%) of malignant lymphoma. Because tumor models with high phenotypic consistency are currently needed, we generated a lymphoma model by a single intraperitoneal injection of 37.5 or 75 mg/kg N-methyl-N-nitrosourea to p53 deficient mice. Lymphoma and retinal degeneration occurred in 100% of p53+/− mice administered with higher concentrations of N-methyl-N-nitrosourea, a much greater response than those of previously reported models. The main anatomic sites of lymphoma were the thymus, spleen, bone marrow, and lymph nodes. Both induced and spontaneous lymphomas in the thymus and spleen stained positive for CD3 antigen, and flow cytometry detected positive CD4 and/or CD8 cells. Based on our observations and previous data, we hypothesize that mice with a B6 background are prone to lymphomagenesis.  相似文献   

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