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K T Schultz

Publications and source records attributed to K T Schultz.

42 records · Page 3Linked to original sources

Chemically-induced delayed hypersensitivity in the cat.

A technique to evaluate the cell mediated immune response in cats by the induction of delayed-type hypersensitivity to the strong contact sensitizer, 1-chloro, 2-4 dinitrobenzene is described. Following topical sensitization with this agent, challenge was done on the cats ear. Ear thickness measurements, the kinetics of the response and histopathologic examination of the tissue were used to assess this delayed-type hypersensitivity reaction. Based on the results it is shown that allergic contact dermatitis can be experimentally induced in the cat.

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Factors affecting phagocytosis of bacteria by neutrophils in the mare's uterus.

Ten mares, 5 resistant and 5 susceptible to bacterial endometritis, were examined for differences pertaining to the efficiency of phagocytosis of bacteria by neutrophils in the uterus. An assay for chemiluminescence was used to evaluate various schemes of opsonization and relate them to phagocytic rate. 123I-labelled albumin was used to measure protein migration to the inoculated uterus. Neutrophil numbers moving to the uterine lumen were determined. Before inoculation resistant mares were found to have substances in their uterine secretions that opsonized bacteria, resulting in effective phagocytosis. In contrast, uterine contents of susceptible mares were not effective in opsonization. The addition of serum to uterine washings significantly enhanced opsonization of bacteria in both groups. In response to intrauterine challenge with pathogenic streptococci, no differences were observed between resistant and susceptible mares in the migration of serum protein or neutrophil numbers to the site of contamination. Following inoculation, the ability of the uterine contents to opsonize bacteria was similar between groups. Clinical observations after inoculation confirmed that mares were resistant or susceptible to endometritis.

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Primary cultures of rhesus placental syncytiotrophoblasts are permissive for SIV infection.

Primary cultures of rhesus syncytiotrophoblasts incubated with SIVdeltaB670, SIVmac251, or SIVmac239 produced readily detectable virus in the supernatant for up to three weeks after infection. At four weeks, cells generally failed to release virus but placental cell lysates and placental cells cocultured for 24 hours with uninfected CEM x 174 cells were able to transmit infection. The presence of virus was confirmed by electron microscopy and PCR amplification of viral sequences from trophoblast genomic DNA. SIV p27 antigen was localized by immunostaining primarily in syncytiotrophoblasts.

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Cellular immune responses in rhesus macaques infected rectally with low dose simian immunodeficiency virus.

Monkeys infected rectally with low dose simian immunodeficiency virus (SIV) were resistant to high dose challenge with SIV. Peripheral blood mononuclear cells (PBMC) from two of four challenged monkeys were unable to support SIV replication in vitro unless cultures were depleted of CD8+ lymphocytes. Monkeys that had survived high dose rectal infection with SIV also suppressed virus replication in cultured PBMC. PBMC from uninfected monkeys supported virus replication in both unfractionated and CD8-depleted cultures. Virus-suppressive activity of PBMC may be an important correlate of protective immunity in AIDS.

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Pathogenesis of SIVmac251 after atraumatic inoculation of the rectal mucosa in rhesus monkeys.

Intrarectal inoculation of rhesus monkeys with low doses of SIVmac led to a prolonged clinical and virological latency that was not observed for high intrarectal doses or for intravenous inoculation. Animals infected intrarectally with low virus doses remained negative for serum antibody responses to SIV for at least one year even though they readily transferred SIV to naive recipients via transfusion of whole blood.

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