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Biomedical subjects

E Balish

Publications and source records attributed to E Balish.

At least 109 records · Page 6Linked to original sources
PubMed1982

Vaginal immunization against urinary tract infection.

In an attempt to lessen susceptibility to induced urinary tract infections, rats were immunized by a non-traumatic, non-parenteral, intra-vaginal route. Up to 8 weeks following vaginal immunization against Escherichia coli O6, there was decreased adherence of viable E. coli O6 to the rats' bladder epithelium. Scanning electron microscopy of the urothelium revealed that immunized rats had less epithelial swelling, exfoliation, and surface mucin disruption than non-immunized control animals. Immunized animals also cleared an induced E. coli O6 infection from the kidneys and bladder faster than control animals. Vaginal immunization may offer a new approach to prophylaxis and treatment of ascending urinary tract infections.

Animals↗
PubMed1982

Resolution of induced urinary tract infection: an animal model to assess bladder immunization.

The resolution of an Escherichia coli urinary tract infection in the bladder and kidneys of control and immunized rats was used to assess their resistance to experimentally induced infection. Prior intravesical immunization of rats with formalin killed E. coli 06 resulted in faster resolution of an infection that had been induced with viable E. coli 06 than was observed in nonimmunized controls. The faster resolution of infection after immunization correlates with our previous findings of decreased adherence of bacteria to urothelium of immunized rats and supports the hypothesis that local immune responses in the urinary tract may play a role in resistance to recurrent urinary tract infections.

Animals↗
PubMed1982

Origin of excess urinary nitrate in the rat.

The ability of intestinal microorganisms to N-oxidize nitrogenous compounds to nitrite or nitrate was evaluated both in vivo and in vitro. Nitrate balance studies with germ-free and conventional rats indicated that the host and not the microbial flora is responsible for excess urinary nitrate. In vitro studies showed that most intestinal microorganisms are not able to N-oxidize nitrogenous compounds to nitrite. Although the metabolic pathway for endogenous nitrate formation remains unknown, the capacity of the rats to N-oxidize acetohydroxamate and hydroxylamine to nitrate indicates that such compounds could be intermediates in nitrate synthesis.

Amino Acids↗
PubMed1981

Evaluation of nitrate synthesis by intestinal microorganisms in vivo.

The nitrate balance of germfree and conventional rats was assessed to determine whether the intestinal flora produces nitrate in vivo. The results indicate that there can be excess nitrate in the urine of germfree as well as conventional rats. This nitrate is apparently of host origin, and the presence of intestinal flora decreases the output of nitrate in urine.

Animals↗
PubMed1981

Pathogenesis of Listeria monocytogenes for gnotobiotic rats.

Listeria monocytogenes colonized the gastrointestinal tract of adult germfree rats (10(10) to 10(11)/g, dry weight) within 24 h after oral exposure. Between 3 and 14 days after monoassociation, L. monocytogenes caused a self-limiting pseudomembranous colitis, bacteremia, and infection of the spleen and liver. Monoassociation of rats with Listeria for 8 weeks stimulated 32- and 4-fold increases in serum immunoglobulin A (IgA) and IgG, respectively, whereas serum IgM decreased 2-fold. The normal microbial flora was inhibitory to Listeria colonization, since L. monocytogenes was cleared from the gastrointestinal tract of formerly monoassociated rats within 20 days after conventionalization and did not colonize the gastrointestinal tract of conventional rats after intragastric instillation of 10(8) viable L. monocytogenes. Listeria-monoassociated rats delivered large litters of healthy pups whose gastrointestinal tracts were slowly colonized with L. monocytogenes. between 3 and 60 days of age, Listeria-monoassociated rat pups exhibited eight- and fourfold increases in serum IgG and IgM, respectively; however, serum IgA was elevated (16-fold) only at 9 to 15 days of age. Adult Listeria-monoassociated rats had acquired cellular resistance to intravenous challenge with L. monocytogenes. Prolonged monoassociation of L. monocytogenes in rats attenuated its virulence for conventional rats.

Animals↗
PubMed1981

Interaction of rat platelets with Listeria monocytogenes.

Listeria monocytogenes induced aggregation of rat platelets in vitro and stimulated the nonlytic release of [3H]serotonin. Listeria-induced platelet aggregation and serotonin release required the presence of intact Listeria, was maximal at a 1:1 Listeria/platelet ratio, required a plasma cofactor, and was not inhibited by indomethacin, acetylsalicylic acid, or apyrase. Aggregation either of platelets in platelet-rich plasma with adenosine diphosphate or of washed platelets with thrombin resulted in the release of a listericidin from the platelets; however, direct interaction of L. monocytogenes with platelet-rich plasma did not kill Listeria. The ability of rats to clear an intravenous challenge of L. monocytogenes (0.005 50% lethal dose), as determined by the recovery of viable L. monocytogenes from the spleen and liver, was unaffected by prior treatment with antiplatelet serum.

Adenosine Diphosphate↗
PubMed1981

Killing of Listeria monocytogens by conventional and germfree rat sera.

Serum from both germfree and conventional rats, but not plasma or plasma serum, killed Listeria monocytogenes in vitro by a calcium-dependent mechanism that was independent of either complement or lysozyme and was not inhibited by the addition of iron. The listericidin was purified by passing either rat serum or platelet lysate through a nitrocellulose filter (0.2 micrometer) and eluting the activity from the filter with 0.02 N HCl. The partially purified listericidin was heat stable (56 degrees C for 30 min), removed by absorption with zymosan or bentonite, sensitive to treatment with trypsin or pronase, and inhibited by the addition of citrate (0.045 M), suggesting that the serum listericidin is a cationic protein. The development of serum listericidal activity, which could be important in the innate resistance of rats to L. monocytogenes, was dependent on both age and microbial status. Although some discrepancies exist between the serum listericidin and previous descriptions of serum beta-lysin, we believe that the rat serum listericidin is a similar cationic protein.

Aging↗
PubMed1981

Lysosomal enzyme activity in pulmonary alveolar macrophages from conventional, germfree, monoassociated, and conventionalized rats.

Pulmonary alveolar macrophages (PAM) were harvested from conventional (CONV), germfree (GF), conventionalized, and monoassociated (MA) rats. Germfree rats had significantly fewer PAM than did their CONV, conventionalized or MA counterparts. The bronchopulmonary wash from the CONV and conventionalized rats contained higher lysosomal specific activity for beta-glucuronidase and cathepsin D than did similar washes from GF rats. Cellular and subcellular PAM fractions from GF rats also showed decreased enzyme activity in comparison with similar fractions from the PAM or CONV rats. Colonization of GF rats with one (MA) or more bacterial species (conventionalized) increased the beta-glucuronidase and cathepsin D activity of their PAM as well as total PAM. These data suggest that the intestinal flora not only enhances PAM proliferation but also is associated with an increase in their lysosomal enzyme activity.

Animals↗
PubMed1980

Trichophyton mentagrophytes dermatophytosis in germfree guinea pigs.

Primary and secondary Trichophyton mentagrophytes dermatophytosis was studied in germfree and conventionally-reared Strain 2 guinea pigs. Although the onset and early development of the primary cutaneous lesions appeared similar in both groups, the T. mentagrophytes monoassociated guinea pigs exhibited more severe skin ulcerations and took twice as long to heal as their conventionally-reared counterparts. Cutaneous reinfection of T. mentagrophytes monoassociated guinea pigs was also protracted; however, these lesions healed in about the same time as a primary infection on conventionally-reared guinea pigs. Germfree guinea pigs, sensitized by cutaneous infection with T. mentagrophytes, manifested 3 correlates of systemic cell-mediated immunity: (1) delayed-type hypersensitivity to intracutaneous injection of trichophytin antigen, (ii) in vitro blastogenesis of spleen and lymph node cells to polyclonal mitogens and Trichophyton antigens, and (iii) allergic contact dermatitis 48 hr following cutaneous reinfection. In an additional experiment, we observed that the time course and severity of a primary T. mentagrophytes infection of germfree guinea pigs was reduced by prior feedings with heat-killed T. mentagrophytes culture. These experiments confirm that the normal microbial skin flora is not required for initiation, development or clearance of T. mentagrophytes dermatophytosis. The disease was protracted and severe in T. mentagrophytes monoassociated guinea pigs, but was abbreviated following either active infection or feeding heat killed mentagrophytes culture. These results support the hypothesis that cutaneous T. mentagrophytes infection is a cell-mediated hypersensitivity disease similar to contact dermatitis.

Animals↗
PubMed1980

Cutaneous basophil hypersensitivity and contact sensitivity after cutaneous Trichophyton mentagrophytes infection.

The histopathology of cutaneous lesions and trichophytin skin test responses was examined by light microscopy after the infection of strain 2 guinea pigs with Trichophyton mentagrophytes. Skin biopsies were fixed and stained with procedures which allowed differentiation of the polymorphonuclear granulocytic leukocytes that were present in lesions or skin test reactions. Basophils comprised about one-third of the leukocytes infiltrating the 24 to 48-h trichophytin skin test reactions of guinea pigs sensitized by a cutaneous T. mentagrophytes infection. These results were comparable to the percentage of basophils counted in skin test lesions elicited by the contact agent dinitrochlorobenzene and are consistent with previously published descriptions of cutaneous basophil hypersensitivity. In contrast, the active T. mentagrophytes lesion in the skin of guinea pigs sacrificed at defined intervals after infection or reinfection did not appear to contain similarly elevated numbers of basophils. The early inflammation in primary T. mentagrophytes-induced skin lesions can be characterized histologically as a primary irritant dermatitis which evolves, during the course of the disease, into a chronic mononuclear inflammation. This shift apparently results from host sensitization to fungal antigens during infection and the concurrent development of acquired immunity. Reinfection of guinea pigs with T. mentagrophytes resulted in an accelerated cutaneous inflammation that was temporally and histologically similar to allergic contact dermatitis. These results support the hypothesis that contact sensitivity to T. mentagrophytes develops during the primary cutaneous infection of guinea pigs and is an early component of the hypersensitivity response to reinfection.

Animals↗