CORYNEBACTERIAL PSEUDOTUBERCULOSIS IN MICE : II. ACTIVATION OF NATURAL AND EXPERIMENTAL LATENT INFECTIONS

Latent corynebactenai infection occurs naturally in many strains of mice. It can be evoked into the active disease, pseudotuberculosis, by a single injection of 10 mg of cortisone. The cortisone effect was tested in 21 colonies, representing 11 genetically different strains of mice. Animals of the C57B1/6, DBA/2, and RIII strains were shown to be latently infected with Corynebacterium kutscheri by the fact that they developed fatal pseudotuberculosis following cortisone treatment. Virulent C. kutscheri could not be isolated from homogenates of organs obtained from latently infected animals before cortisone administration; however, these homogenates yielded small translucent colonies of avirulent organisms. Recovery of these atypical colonies was facilitated by preincubating the organ homogenates before plating. The organisms constituting such colonies differed morphologically and immunologically from C. kutscheri, but had similar biochemical properties with the exception that they lacked urease and catalase activity. Mice treated with cortisone yielded both the avirulent bacteria and virulent C. kutscheri. The latter was the predominant organism present in the organs at the height of infection. Injection of avirulent organisms into Swiss Lynch mice, which are normally free of latent corynebacteria, occasionally established a latent infection which could be converted into corynebacterial pseudotuberculosis by cortisone. Cultures of fully virulent C. kutscheri were then obtained from the lesions. Latency was produced experimentally with a streptomycin-resistant strain of virulent C. kutscheri (CKsr) derived from the stock culture. When sublethal doses of CKsr were injected into NCS mice (Institut Pasteur colony), they induced a latent infection characterized by the presence of avirulent organisms possessing the streptomycin resistance marker. These were isolated in the form of small translucent colonies from the livers of the infected animals. Administration of cortisone to these animals subsequently evoked active infection from which virulent CKsr could be obtained. Injection of the avirulent streptomycin-resistant organisms into normal NCS mice established a latent infection which could be uniformly converted into corynebacterial pseudotuberculosis by cortisone. The virulent C. kutscheri obtained from the lesions bore the genetic marker of streptomycin resistance, thus being identical with CKsr. Except for streptomycin resistance, the avirulent organisms isolated from the experimentally induced latent infections were identical with those found in the naturally occurring latent infections. These results suggest that C. kutscheri can persist in vitro in an avirulent form which is resistant to the defense mechanisms of the host, and can thus establish a latent infection. Treatment of the animal with cortisone results in the conversion of the avirulent form into virulent C. kutscheri, and of the latent infection into active corynebacterial pseudotuberculosis. The findings are discussed with regard to their relevance to infection immunity, and to the conversion of latent infection into overt disease

Assessing wildlife habitats and natural resources in neighborhoods and urban environments (2013)

"Natural resources."New 9/13/Web

Managing oaks for acorn production to benefit wildlife in Missouri (2013)

Many landowners are interested in managing their woodlands and forests not only for potential income from sales of wood products but also for enhanced wildlife habitat. This publication provides information on techniques that can be used to help make informed decisions on the management of oaks on a property for increased mast production and other wildlife benefits.New 8/13/Web

Quantitative PCR for detection of the OT-1 transgene

BACKGROUND: Transgenic TCR mice are often used experimentally as a source of T cells of a defined specificity. One of the most widely used transgenic TCR models is the OT-1 transgenic mouse in which the CD8+ T cells express a TCR specific for the SIINFEKL peptide of ovalbumin presented on k(b). Although OT-1 CD8+ can be used in a variety of different experimental settings, we principally employ adoptive transfer and peptide-driven expansion of OT-1 cells in order to explore the distribution and fate of these antigen-specific OT-1 T cells. We set out to develop a quantitative PCR assay for OT-1 cells in order to assess the distribution of OT-1 CD8+ T cells in tissues that are either intrinsically difficult to dissociate for flow cytometric analysis or rendered incompatible with flow cytometric analysis through freezing or fixation. RESULTS: We show excellent correlation between flow cytometric assessment of OT-1 cells and OT-1 signal by qPCR assays in cell dilutions as well as in in vivo adoptive transfer experiments. We also demonstrate that qPCR can be performed from archival formalin-fixed paraffin-embedded tissue sections. In addition, the non-quantitative PCR using the OT-1-specific primers without the real-time probe is a valuable tool for OT-1 genotyping, obviating the need for peripheral blood collection and subsequent flow cytometric analysis. CONCLUSION: An OT-1 specific qPCR assay has been developed to quantify adoptively transferred OT-1 cells. OT-1 qPCR to determine cell signal is a valuable adjunct to the standard flow cytometric analysis of OT-1 cell number, particularly in experimental settings where tissue disaggregation is not desirable or in tissues which are not readily disassociate

Microwave Components with MEMS Switches

RF MEMS switches with metal-metal contacts are being developed for microwave applications where broadband, high linearity performance is required. These switches provide less than 0.2 dB insertion loss through 40 GHz. This paper describes the integration of these switches into selected microwave components such as reconfigurable antenna elements, tunable filters, switched delay lines, and SPDT switches. Microwave and millimeter wave measured results from these circuits are presented

COMPARATIVE EFFECTS OF CORTICOSTEROIDS ON HOST RESISTANCE TO INFECTION IN RELATION TO CHEMICAL STRUCTURE

In a comparative study concerning the effect of corticosteroids on host resistance to infections, five compounds were found to decrease host resistance, while three did not have this property, although all eight compounds were highly antiinflammatory. The compounds capable of decreasing host resistance were (I) hydrocortisone acetate; (III) 9α-fluoro, 16α-methylprednisolone acetate; (IV) 9α-fluoro, 16α-hydroxyprednisolone; (V) 9α-fluoro, 16α-hydroxyprednisolone, 16α–17α-acetonide; and (VII) 9α-fluoro, 16α-hydroxypredmsolone, 16α-, 17α-acetonide, 21 disodium phosphate. Following a single injection of 10 mg of any of these compounds, latent corynebacterial infection was provoked into active pseudotuberculosis. Also, mice injected with these corticosteroids were more susceptible to infection with Corynebacterium kutscheri, Staphylococcus aureus, Klebsiella pneumoniae, or Listeria monocytogenes. These same corticosteroids inhibited the ability of mouse peritoneal macrophages to spread on glass surfaces. The three compounds incapable of decreasing host resistance, although highly antiinflammatory, were: (II) 6α-methylprednisolone, 21 sodium hemisuccinate: (VI) 9α-fluoro, 16α-hydroxyprednisolone, 16α-, 17α-acetonide, 21 hemisuccinate; and (VIII) 9α-fluoro, 16α-hydroxyprednisolone, 16, 21 dihemisuccinate. These three compounds were also unable to inhibit the spreading of macrophages on glass. The importance of succinate group bound to the corticosteroid molecule as hemisuccinate is emphasized since it is seen that the infection-provoking property can be dissociated from the antiinflammatory property. This finding may be of practical consequence in selecting a corticosteroid for treatment in disease, and also shows that one cannot use, indifferently, corticosteroids only on the basis of their common antiinflammatory property

TLR-dependent cross talk between human Kupffer cells and NK cells

The liver protects the host from gut-derived pathogens yet is tolerant of antigenic challenge from food and commensal sources. Innate responses involving liver macrophages (Kupffer cells) and effector liver natural killer (NK) cells form the first line in this defense. We address the impact of Toll-like receptor (TLR) signaling on the cross talk between these two cells, and reveal how the liver displays a down-regulated inflammatory response to constitutive bacterial elements through the secretion of interleukin (IL) 10 yet retains a vigorous response to viral challenge. The data support the model that (a) human liver Kupffer cells respond to TLR ligands and indirectly activate NK cells; (b) the activation depends on cell–cell contact; (c) the Kupffer cells synthesize NK cell activating signals, among which IL-18 is critical, and NK cell inhibitory factors, including IL-10; (d) ligands that signal via myeloid differentiation factor 88 induce IL-10, giving a blunted response in the NK cells; and (e) ligands that signal via the Toll–IL-1 receptor domain–containing adaptor inducing interferon (IFN) β–IFN regulatory factor 3 pathway induce less IL-10, and also directly potentiate the stimulatory effect of IL-18 on NK cells, resulting in enhanced activation. Subversion of cellular mechanisms of innate immune response against viruses may be important for hepatotropic viruses (e.g., hepatitis B and C) to develop persistence

Radiative effect of clouds on tropospheric chemistry in a global three‐dimensional chemical transport model

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94988/1/jgrd12465.pd

Short Communication Bcl-2 Expression Inhibits Liver Carcinogenesis and Delays the Development of Proliferating Foci

Tumor development is thought to require both increased proliferation and inhibition of apoptosis. However , the relationship between cell replication and cell death in liver tumorigenesis is complex because both proliferation and apoptosis increase during hepatocarcinogenesis. To investigate the effect of the anti-apoptotic gene Bcl-2 in liver carcinogenesis, we established a line of double transgenic mice that express transforming growth factor-␣ (TGF-␣) , a liver mitogen , and Bcl-2. Double transgenic mice , TGF-␣ and Bcl-2 single transgenics , and wild type received an injection of diethylnitrosamine at 15 days of age. This alkylating agent induces liver carcinogenesis and its effect is greatly enhanced by TGF-␣. We report that Bcl-2 expression inhibited diethylnitrosamine-induced liver carcinogenesis and counteracted the enhancing effect of TGF-␣. Bcl-2 delayed the growth of proliferative foci at the early stages of carcinogenesis and inhibited cell proliferation in these foci. The effect of Bcl-2 on liver carcinogenesis is consistent with its reported ability to interfere with cell replication. The data demonstrate that the expression of an antiapoptotic gene during liver carcinogenesis causes a delay rather than an increase in tumorigenesis. The discovery that overexpression of Bcl-2 in follicular lymphomas, caused by a chromosomal translocation, inhibits apoptosis without increasing cell proliferation established a new mode of action for oncogenes