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Perturbations in cytokine gene expression after inoculation of C57BL/6 mice with Pasteurella pneumotropica.

ABSTRACT: Pasteurella pneumotropica can cause inflammation and abscess formation in a variety of tissues. Most commonly, P. pneumotropica produces clinical disease in immunodeficient mice or those concurrently infected with other pathogens. Because clinical disease is infrequent in immunocompetent mice harboring P. pneumotropica, some scientists consider it an opportunistic pathogen with little clinical relevance to biomedical research. However, other infectious agents, including mouse parvoviruses, mouse rotavirus, and Helicobacter spp. alter physiologic or biologic responses without causing clinical signs of illness. We investigated the potential for P. pneumotropica to modulate the transcription of cytokine genes in immunocompetent mice. In C57BL/6 mice inoculated oronasally with a minimal colonizing dose of P. pneumotropica, modest but statistically significant elevations of IL1beta, TNFalpha, CCL3, CXCL1, and CXCL2 mRNA were detected in mandibular and superficial cervical lymph nodes at 7 d after inoculation, and upregulation of IL1beta mRNA was detected 28 d after inoculation. These perturbations were not present in C57/BL6 mice inoculated with heat killed-P. pneumotropica or the related bacterium Actinobacillus muris. Nasal mucosal cytokine transcription did not vary significantly in C57BL/6 mice given a high dose of P. pneumotropica. These data indicate that slight and transient experimental perturbations are possible in immunocompetent mice colonized with P. pneumotropica. Knowing the full health status of experimental mice is paramount to avoid unwanted experimental variables, especially when using exquisitely sensitive testing methodologies such as those for quantification of gene expression.

SUBMITTER: Patten CC

PROVIDER: S-EPMC2826080 | biostudies-literature | 2010 Feb

REPOSITORIES: biostudies-literature

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Perturbations in cytokine gene expression after inoculation of C57BL/6 mice with Pasteurella pneumotropica.

Patten Calvin C CC Myles Matthew H MH Franklin Craig L CL Livingston Robert S RS

Comparative medicine 20100201 1

Pasteurella pneumotropica can cause inflammation and abscess formation in a variety of tissues. Most commonly, P. pneumotropica produces clinical disease in immunodeficient mice or those concurrently infected with other pathogens. Because clinical disease is infrequent in immunocompetent mice harboring P. pneumotropica, some scientists consider it an opportunistic pathogen with little clinical relevance to biomedical research. However, other infectious agents, including mouse parvoviruses, mouse ...[more]

PMID: 20158944

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Project description:BACKGROUND:Mice are a natural host for Rodentibacter (R.) pneumotropicus. Despite specific monitoring, it is still one of the most important infectious agents in laboratory animals. The objective of this study was to determine the virulence of a prevalent pathotype of R. pneumotropicus and characterize the host response in a new animal model. RESULTS:Intranasal infection of C57BL/6 and BALB/c mice with a R. pneumotropicus strain (JF4Ni) bearing the genes of the three known repeats in toxin (RTX) toxins resulted in an unprecedented high mortality and morbidity above 50 and 80%, respectively. Morbidity was associated with severe weight loss as well as conjunctivitis and dyspnea. A main pathology was a catarrhal purulent to necrotic bronchopneumonia. Specific immune globuline (Ig) A was detected in tracheonasal lavages of most surviving mice which were still colonized by R. pneumotropicus. Furthermore, all surviving animals showed a distinct production of IgG antibodies. To differentiate T-helper cell (Th) 1 and Th2 immune responses we used subclasses of IgGs as indicators. Mean ratios of IgG2b to IgG1 were below 0.8 in sera drawn from both mice strains prior infection and from BALB/c mice post infection. In contrast, C57BL/6 mice had a mean IgG2b/IgG1 ratio of 1.6 post infection indicating a Th1 immune response in C57BL/6 versus a Th2 response in BALB/c mice associated with a tenfold higher bacterial load in the lung. In accordance with a Th1 response high antigen-specific IgG2c titers were detected in the majority of surviving C57BL/6 mice. CONCLUSIONS:R. pneumotropicus JF4Ni is a highly virulent strain causing severe pneumonia and septicemia after intranasal infection of C57BL/6 and BALB/c mice. Persisting infections in the two mice strains are associated with Th1 and Th2 immune responses, respectively, and differences in the bacterial burden of the lung. The described model is ideally suited for future vaccination studies using the natural host.

Project description:BACKGROUND:Alveolar echinococcosis (AE) is caused by the larval stage of Echinococcus multilocularis (E. multilocularis), and considered as public health issue. Parasite-host immune interaction is pivotal during infection. As a subset of innate lymphoid cells, NK cells are known to play an important role during virus, bacteria, intra/extracellular parasitic infections and tumor progression. However, the possible role of NK cells in E. multilocularis infection in both human and murine is little known. Herein, the functional alteration of hepatic NK cells and their related molecules in E. multilocularis infected mice were studied. METHODS:2000 protoscoleces (PSCs) were injected to C57BL/6 mice via the portal vein to establish secondary E. multilocularis infection. NK cells population and their related molecules (CD69, Ly49D, Ly49G2, Ly49H, Ly49I, NKG2A, NKG2D, granzyme B, IFN-?, TNF-?) were assessed by using fluorescence-activated cell sorter (FACS) techniques and qRT-PCR. NK cell depletion was performed for further understanding the possible function of NK cells during infection. RESULTS:The total frequencies of NK cells and NK-derived IFN-? production were significantly reduced at designated time points (2, 4, 12?weeks). The liver resident (CD49a+DX5-) NK cells are decreased at 4?weeks after inoculation and which is significantly lower than in control mice. Moreover, in vivo antibody-mediated NK cell depletion increased parasitic load and decreased peri-parasitic fibrosis. Expression of the inhibitory receptor NKG2A was negatively related to NK- derived IFN-? secretion. CONCLUSIONS:Our study showed down regulates of NK cells and upper regulates of NKG2A expression on NK cells during E. multilocularis infection. Reduction of NK cell frequencies and increased NKG2A might result in low cytotoxic activity through decreased IFN-? secretion in E. multilocularis infection. This result might be helpful to restore NK cell related immunity against E. multilocularis infection to treat alveolar echinococcosis.

Project description:[Pasteurella] pneumotropica biotypes Jawetz and Heyl and [Actinobacillus] muris are the most prevalent Pasteurellaceae species isolated from laboratory mouse. However, mechanisms contributing to their high prevalence such as the ability to form biofilms have not been studied yet. In the present investigation we analyze if these bacterial species can produce biofilms in vitro and investigate whether proteins, extracellular DNA and polysaccharides are involved in the biofilm formation and structure by inhibition and dispersal assays using proteinase K, DNase I and sodium periodate. Finally, the capacity of the biofilms to confer resistance to antibiotics is examined. We demonstrate that both [P.] pneumotropica biotypes but not [A.] muris are able to form robust biofilms in vitro, a phenotype which is widely spread among the field isolates. The biofilm inhibition and dispersal assays by proteinase and DNase lead to a strong inhibition in biofilm formation when added at the initiation of the biofilm formation and dispersed pre-formed [P.] pneumotropica biofilms, revealing thus that proteins and extracellular DNA are essential in biofilm formation and structure. Sodium periodate inhibited the bacterial growth when added at the beginning of the biofilm formation assay, making difficult the assessment of the role of β-1,6-linked polysaccharides in the biofilm formation, and had a biofilm stimulating effect when added on pre-established mature biofilms of [P.] pneumotropica biotype Heyl and a majority of [P.] pneumotropica biotype Jawetz strains, suggesting that the presence of β-1,6-linked polysaccharides on the bacterial surface might attenuate the biofilm production. Conversely, no effect or a decrease in the biofilm quantity was observed by biofilm dispersal using sodium periodate on further biotype Jawetz isolates, suggesting that polysaccharides might be incorporated in the biofilm structure. We additionally show that [P.] pneumotropica cells enclosed in biofilms were less sensitive to treatment with amoxicillin and enrofloxacin than planktonic bacteria. Taken together, these findings provide a first step in understanding of the biofilm mechanisms in [P.] pneumotropica, which might contribute to elucidation of colonization and pathogenesis mechanisms for these obligate inhabitants of the mouse mucosa.

Dataset Information

Perturbations in cytokine gene expression after inoculation of C57BL/6 mice with Pasteurella pneumotropica.

Publications

Perturbations in cytokine gene expression after inoculation of C57BL/6 mice with Pasteurella pneumotropica.

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