Biomedical subjects

A M Hooke

Publications and source records attributed to A M Hooke.

4 recordsLinked to original sources

PubMed1991

Oral immunization of mice with temperature-sensitive Pseudomonas aeruginosa enhances pulmonary clearance of the wild-type.

DBA/2J mice were immunized daily for 3 days per os with 10(8)-10(9) colony forming units (c.f.u.) of two different temperature-sensitive (TS) mutants of Pseudomonas aeruginosa. At varying times after the final immunization the animals were exposed to aerosols of the parental immunotype 1, and the ability of the immunized and control mice to clear their lungs of the wild-type (WT) challenge was measured 4 h later. The number of c.f.u. remaining in the lungs of mice immunized with one mutant, D/1/8, was significantly less (p less than 0.01) than the number remaining in the lungs of control mice and mice immunized with a second TS mutant, E/9/9.

Administration, Oral↗

PubMed1991

Immunization with temperature-sensitive mutants of Salmonella typhi induces protection in mice.

Temperature-sensitive (TS) mutants of Salmonella typhi were isolated following mutagenesis with nitrosoguanidine and two cycles of enrichment with penicillin and D-cycloserine. Several of the TS mutants were characterized with respect to growth profiles at permissive (29 degrees C) and non-permissive (36 degrees C) temperatures, reversion rates, and the potential for inducing protection against challenge in an animal model. All three TS mutants tested were immunogenic in mice; antibodies measured by enzyme-linked immunosorbent assay were produced following intraperitoneal (i.p.) immunization with three different doses of each of the mutants; i.p. immunization with the same mutants also induced highly significant protection (100%) from i.p. wild-type challenge; and oral immunization with one of the mutants significantly reduced shedding of the wild-type following oral challenge.

Animals↗

PubMed1978

Ideal target organism for quantitative bactericidal assays.

We have developed a target organism which permits quantitative bactericidal assays. The organism is an Escherichia coli mutant which cannot grow at the temperature of the assay (37 degrees C), but retains full colony-forming potential for subsequent quantitation at 25 degrees C. We show that quantitative data on the bactericidal capacity of polymorphonuclear leukocytes and alveolar macrophages can be obtained when this mutant is used as a target. The procedure used to generate the strain is described in detail and should be applicable to many bacterial species. Characterization of the properties of the mutant indicates that it has a strong potential for use in other in vivo and in vitro investigations of host responses to microbial invasion.

Animals↗

PubMedDate not supplied

The effect of liposomal cefoperazone against Pseudomonas aeruginosa in a granulocytopenic mouse model of acute lung infection.

The therapeutic efficacy of liposomal cefoperazone against Pseudomonas aeruginosa was investigated in a granulocytopenic mouse model of acute lung infection. Granulocytopenia was induced in mice by intraperitoneal (i.p.) injection of 200 mg/kg cyclophosphamide. Mice were challenged by exposure to an aerosol containing P. aeruginosa and were treated i.p. with liposomal cefoperazone prepared by the dehydration-rehydration method. The half-life of free cefoperazone in the lungs following i.p. administration of the liposomal drug was significantly lengthened (13 min vs. 261 min), and the cefoperazone activity in the lungs remained above the MIC longer after administration of liposomal cefoperazone than after treatment with cefoperazone. Liposomal cefoperazone was more effective than cefoperazone alone in preventing death of granulocytopenic mice from lethal pulmonary challenge with P. aeruginosa (75% vs. 38% survival, p = 0.031). Finally, P. aeruginosa was cleared faster from the lungs of mice treated with liposomal cefoperazone when compared with those treated with cefoperazone. This study shows that incorporation of cefoperazone into liposomes enhances the activity of the antibiotic against P. aeruginosa in a granulocytopenic host.

Acute Disease↗