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On the model of the septic mouse infected with mice pathogenic Erysipelothrix strain NaSCN had a protective effect (lower and delayed lethality in the doses of 64 and 256 mg/kg, given once a day intraperitoneally prophylactically or simultaneously to the infection.
Infection of mouse L cells with mengovirus resulted in the activation of a protein kinase (PK) that selectively phosphorylated the small, 38,000-molecular-weight alpha subunit of eucaryotic initiation factor 2 (eIF-2) in vitro. The mengovirus-activated kinase was detected in vitro approximately 3 h after virus adsorption. The ratio of phosphorylated to unphosphorylated eIF-2 also increased in vivo between 3 and 7 h after adsorption. The virus-activated kinase fractionated with the ribosomal pellet and had a high affinity for DEAE-cellulose and Mono Q ion-exchange columns. Gel electrophoresis of the kinase activity eluting from the Mono Q column and silver staining of the gel revealed only one protein band with a molecular mass of 70 kilodaltons. The optimal assay conditions for the mengovirus-activated kinase paralleled those of the double-stranded RNA-activated PK (dsRNA-PK). Lysates from infected cells contained elements capable of activating partially purified dsRNA-PK. These elements were identified as double-stranded RNA by their sensitivity to double-stranded RNase. The phosphorylation of the alpha subunit of eIF-2 coincided with the synthesis of dsRNA in infected cells, suggesting that the mengovirus-activated kinase is the dsRNA-PK. The phosphorylation of the alpha subunit of eIF-2 correlated with the global inhibition of protein synthesis that occurs at late times after infection.
Infection of arrested mouse kidney cells by polyoma virus results in the induction of the cellular 6-8S DNA polymerase activity. Levels of this enzyme increase two- to threefold in the cytoplasm but seven- to tenfold in nuclei and nuclear extract, suggesting an accumulation of the enzyme in the nucleus. Experiments using the inhibitor of DNA synthesis, fluordeoxyuridine, indicate that this accumulation is linked to active DNA synthesis. The activity and cellular distribution of the small 3.4S DNA polymerase remains unchanged.
Mice (C57BL) infected with the intestinal nematode Nematospiroides dubius showed depressed delayed type hypersensitivity responses to ovalbumin administered subcutaneously in Freund's complete adjuvant. IgG and IgM responses to this inoculum were unaffected. It is unlikely that the depression arose from impairment of the ear test response because responses to an extract of the adult parasite were measurable and ear testing with lipopolysaccharide yielded normal responses in infected mice. Furthermore, mice immunized on the day of infection responded normally, whilst long term infected mice ear challenged with antigen pulsed macrophages gave depressed responses. The in vitro proliferative responses of cells from the spleens and from the lymph nodes draining the site of immunization were enhanced marginally by N. dubius infection. Furthermore, these cells induced normal or elevated adoptive delayed-type hypersensitivity and IgG responses in irradiated recipients. These findings suggest that N. dubius does not compromise the development of ovalbumin specific T cells involved in a delayed type hypersensitivity response. Evidence for the induction of suppressor cells by N. dubius is discussed, and the findings are compared with results obtained with Nippostrongylus brasiliensis, a parasite which is rejected rapidly from the mouse.
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The new fluorinated 4-quinolones appear to represent orally effective alternatives to parenteral and oral agents currently in use. A number of new fluorinated 4-quinolones were compared in acute systemic mouse-infection models with various Gram-positive cocci (streptococci and staphylococci), Enterobacteriaceae and Pseudomonas aeruginosa. Also included were standard oral and parenteral antimicrobial agents. CI-934 was the most potent quinolone in infections induced by Streptococcus pyogenes and Str. pneumoniae. CI-934, ciprofloxacin, enoxacin, norfloxacin, ofloxacin and pefloxacin were as effective as or superior to standard oral agents currently utilized in infections induced by the Enterobacteriaceae and staphylococci. They were active against antibiotic-susceptible strains and strains resistant to beta-lactams and gentamicin. Most were also quite potent against systemic P. aeruginosa mouse infections. These studies indicate good chemotherapeutic potential for the new generation fluorinated 4-quinolones in infections induced by the staphylococci, streptococci, Enterobacteriaceae and P. aeruginosa, including strains resistant to standard antimicrobial agents.
Immunogenicity and property of antigens obtained from Trypanosoma gambiense-infected mouse blood (IMP) were examined. A strong vaccine effect against intravenous challenges with 3 x10(3) parasites given on study day 3, 5, or 14 (day 0 = immunization) was observed in mice immunized with a combination of IMP (2 mg protein/mouse) and Freund's complete adjuvant (FCA). But when the challenge was given on day 21 or 30, per cent survival in mice dropped to the 20- and 40-per cent level, respectively. Among fractioned components of IMP, IMP-1, IMP-2, and imp-3, by gel filtration with Sephadex G-200, all of the mice immunized with IMP-1 antigen alone or together with FCA and challenged on day 5 were able to conquer intraperitoneal challenges with 1 x10(2) parasites. Mice immunized with IMP-2 or IMP-3 died within 6 days after challenge. Moreover, protection efficacy shown by IMP-1p (144,000 xg sediment of IMP-1) antigen in mice was similar to that by IMP and IMP-1 antigens. IMP-3 yielded a single precipitin line against mouse anti-IMP serum by Ouchterlony double diffusion method but this response was eliminated when the antiserum was absorbed by IMP-1p. No precipitin line was identified between mouse anti-IMP serum and IMP-1 or IMP-2. From electron microscopic observations, elements of IMP-1 and IMP-1p are possibly corresponded to the fragments of filopodia of the parasites.
BALB/cfC3H females neonatally infected with mammary tumor virus (MTV) possess spleen cells capable of significant cytotoxic activity against target MTV-induced mammary tumor cells in microcytotoxicity assay. Spleen cells from supposedly MTV-free BALB/c females are also specifically reactive, as a result of horizontal transmission of MTV antigens. No quantitative differences in reactivity exist between females not susceptible to the development of mammary tumors (BALB/c) and those that may develop or already have tumors (multiparous BALB/cfC3H). However, there are qualitative differences in response between those at risk and those not at risk.
Amoxycillin was significantly more active than ampicillin in the treatment of intraperitoneal mouse infections when administered by oral and parenteral routes, although the causal bacteria were equally susceptible in vitro to the two penicillins. Amoxycillin produced higher antibiotic blood concentrations in mice than ampicillin after oral administration, and this was a possible explanation for the superior oral activity of amoxycillin. In contrast, antibiotic blood concentrations were the same for both compounds after subcutaneous injection, but it was demonstrated that amoxycillin was more effective than ampicillin by this route in reducing bacterial counts in the peritoneal cavity and in the blood of mice infected with Escherichia coli. Amoxycillin was also significantly more active than ampicillin in the treatment of infection by intraperitoneal dosing as a result of greater bactericidal activity in infected mice together with the production of higher antibiotic blood levels. The results of these studies on the effects of parental treatment of experimental infections with the two penicillins show that the superior chemotherapeutic activity of amoxycillin was associated with the greater bactericidal activity of amoxycillin in vivo and with differences in the distribution of the two penicillins in the infected animal.
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At 100 microM 5'-S-isobutyladenosine (SIBA) inhibits polyoma virus production in infected mouse embryo fibroblasts and in mouse kidney cells, as measured by plaque formation and by haemagglutination assays. SIBA has no significant effect on the synthesis of T and V antigens as well as on viral DNA synthesized in infected cells. Analysis of virus production on CsCl gradients on CsCl gradients showed that in the presence of SIBA reduced amount of heavy viral particles is produced and that part of these particles are pseudovirions containing low density DNA instead of supercoiled viral DNA.
51Cr-labelled uninfected cells, separated from Plasmodium berghei-infected mouse blood using the fluorescence-activated cell sorter, were cleared more rapidly than normal mouse erythrocytes after intravenous injection into normal mice.
The rates of release of salivary amylase and esterase from normal and polyoma virus infected mouse submandibular glands were measured in a continuous flow perifusion system. Following stimulation by epinephrine, the rate of release of esterase by the infected glands was significantly greater than that from control glands. The rate of amylase release, while greater from infected glands, was not significantly different. The total enzyme contents from infected and control tissues were similar. Cyclic GMP was found to be higher in the infected glands than the control glands, suggesting one possible mechanism for the higher rates of enzyme release by infected tissues.
UNLABELLED: Experimental infection models are widely used to investigate host-microbe interactions, often under the assumption that bacterial populations are genetically uniform. Here, we examined population heterogeneity in the widely used Helicobacter pylori strain PMSS1 and its relationship to variation in mouse infectivity. Single-colony isolates derived from PMSS1 displayed substantial differences in colonization efficiency, indicating that pre-existing variation within the population contributes to infection outcomes. To distinguish the effects of initial population heterogeneity from changes arising during infection, we analyzed PMSS2, a genetically homogeneous reference strain derived from PMSS1 that exhibited consistent infection phenotypes across independently isolated clones. Comparative genomic analysis of isolates recovered from infected mice revealed differences in the extent and patterns of genomic variation between PMSS1- and PMSS2-derived populations. These results demonstrate that variability in infection outcomes can arise from pre-existing heterogeneity within bacterial populations and highlight the importance of considering population composition when interpreting experimental infection studies. IMPORTANCE: Animal infection models are widely used to study how bacterial pathogens cause disease and change during infection. These studies often assume that the bacteria used for infection are genetically uniform. Our study shows that this assumption may not always hold. We found that a commonly used Helicobacter pylori strain contains hidden genetic diversity that leads to large differences in how well bacteria infect mice. By comparing this strain with a genetically uniform derivative, we show how differences present before infection can shape infection outcomes and influence the genetic changes observed during infection. Our findings highlight the importance of considering starting population diversity when interpreting experimental infection studies and are broadly relevant to research on microbial pathogenesis.
Standardized bacterial and viral mouse infection models have been developed. Infections with extracellular bacteria (K. pneumoniae, S. pneumoniae, S. pyogenes A) were produced by either of two routes: via the intravenous route (i.v.) resulting in septicaemia and the intranasal route (i.n.) giving infections confined to the respiratory apparatus. Infections with intracellular bacteria (L. monocytogenes, S. typhimurium) were produced only by the i.v. route. Two types of viral infection, mild and severe, were produced. Infection with influenza virus was by aerosol and herpes virus HSV-1 by the intraperitoneal route. All infection models produced under strictly controlled conditions were shown to be characterized by a remarkable reproducibility regarding both the pattern of development and death rate. The infection models lend themselves to estimation of the efficacy of a drug as well as the designing of new therapeutic strategies.
The mechanism of cooperation between the L3T4+ and Lyt-2+ T cell subsets in effective clearance of Sendai virus from infected mouse lungs was studied by adoptive cell transfer using nude mice. Simultaneous transfer of a long-term-cultured Sendai virus-specific L3T4+ T cell line with L3T4+ cell-depleted immune spleen cell (L3T4-) fraction to infected nude mice could result in viral clearance, although single injection with either of these cells was not effective. Instead of the L3T4+ T cells, culture supernatants of the L3T4- T cell line or concanavalin A-stimulated mouse spleen cells and mouse serum immunized with the virus were also active in the cooperative viral clearance with L3T4- fraction. The role of the Sendai virus-sensitized L3T4- cell fraction in cooperative viral clearance with humoral factors could be replaced by neither T cell-deprived immune spleen cell fraction nor normal spleen cells. The 1,500 units of recombinant mouse interleukin 2 (IL-2), which was more than 12 times the IL-2 activity present in the supernatants of the T cell line or concanavalin A-stimulated spleen cells, failed to clear the virus in combination with the L3T4- fraction. Monoclonal antibodies to Sendai or mouse hepatitis viruses were also effective in the cooperative antiviral activity. IL-2 activity was not detected in these monoclonal antibodies and the mouse immune serum. Single injection of any humoral factors failed to clear the virus. These results indicate that Sendai virus-sensitized Lyt-2+ subset of T cells acts cooperatively with humoral factor(s) other than IL-2 or Sendai virus-specific antibody present in supernatants of the T cell line, of concanavalin A-stimulated spleen cells or hybridomas, and in mouse serum immunized with the virus.
Effects of DNA hypomethylating agents on reactivation of herpes simplex virus from latently infected mouse ganglia in vitro were examined. L-ethionine and 5-azacytidine increased the incidence of reactivation. Dimethylsulphoxide and 5-azacytidine allowed earlier detection of virus.
The induction of DNA polymerase activity and of DNA synthesis in polyoma virus-infected mouse kidney cells is inhibited by actinomycin D and cycloheximide, even in cells that are already T-antigen positive. This indicates that the induction of the DNA-synthesizing apparatus requires transcription and translation. The increase in cellular DNA polymerase activity and in the DNA synthesizing capacity follows the appearance of T-antigen only after a characteristic lag period of several hours.