Biomedical subjects

Lon V Kendall

Publications and source records attributed to Lon V Kendall.

4 recordsLinked to original sources

PubMed2003

Detection of viral infection in the respiratory tract of virus antibody free mice: advantages of high-resolution imaging for respiratory toxicology.

Using a highly sensitive membrane permeability assay, a viral infection was discovered in the lungs of virus antibody free (VAF) Swiss-Webster mice purchased for respiratory toxicology studies. The assay is based on the uptake of a charged fluorescent compound by cells lacking an intact plasma membrane. Lungs from 74% of the untreated animals from a single vendor tested positive for injury in this assay. High-resolution histopathologic analysis of 1-microm epoxy resin sections from affected animals identified increased peribronchiolar lymphocytic infiltration and markers of epithelial cell injury. Viral particles were directly observed to be budding from the membranes of infiltrating lymphocytic cells by transmission electron microscopy. Standard histological analysis of paraffin-embedded tissues from lungs of the same mice failed to detect obvious pathology. Serological analyses failed to detect the presence of a virus in the affected mice. Therefore, we conclude that (1) a pathogenic condition was present in the respiratory systems of mice judged pathogen free by standard methodologies, (2) the observed condition produced a pattern of injury comparable to those caused by pulmonary toxicants, (3) high-resolution histopathology and advanced imaging techniques can increase the potential for detection of pathological conditions, and (4) apparently healthy animals can have unrecognized infections with the potential for confounding respiratory toxicology studies.

Animals↗

PubMed2002

Cloning and expression of a Helicobacter bilis immunoreactive protein.

In an effort to identify immunoreactive Helicobacter bilis antigens with potential for serodiagnosis, sera from mice experimentally infected with H. bilis were used to screen an H. bilis genomic DNA expression library. Among 17 immunoreactive clones, several contained sequences that encoded a predicted 167-kDa protein (P167). Five overlapping P167 peptides (P167A to P167E) of approximately 40 kDa each were generated and tested. Immune sera reacted with fragments P167C and P167D at dilutions of 1:1,600 and 1:6,400, respectively, and reacted with an H. bilis membrane extract at a dilution of 1:800 in an enzyme-linked immunosorbent assay. Sera from mice experimentally infected with H. hepaticus did not react with P167C and P167D. Sera from mice naturally infected with H. bilis but not sera from mice naturally infected with H. hepaticus reacted with P167C and P167D. Hyperimmune sera against P167C peptide reacted with recombinant P167C and with a 120-kDa band in H. bilis lysates but did not react with a protein of the same size on immunoblots prepared from H. hepaticus, H. muridarum, or unrelated Borrelia burgdorferi and Campylobacter jejuni whole-cell lysates. Nevertheless, the P167A, P167B, P167C, and P167D primers, but not the P167E primers, amplified DNA from H. hepaticus, and all five primer sets amplified DNA from H. muridarum. These results suggest that P167 is an immunodominant, H. bilis-specific antigen that may have potential for use in serodiagnosis.

Animals↗

PubMed2002

Characterization of lymphocyte subsets in the bronchiolar lymph nodes of BALB/c mice infected with cilia-associated respiratory bacillus.

Cilia-associated respiratory (CAR) bacillus is an unclassified, gram-negative, extracellular bacterium that causes chronic respiratory tract disease in rodents. Infected mice develop microscopic lesions characterized by a primary lymphocytic response followed by macrophage and neutrophilic infiltration. To characterize the lymphocytic subsets that respond to CAR bacillus infection, BALB/c mice were inoculated with 10(5) CAR bacillus bacteria. At seven weeks after inoculation, mice were euthanized and the tracheobronchiolar and hilar lymph nodes were collected and stained for cell surface markers to T cells (CD3, CD4, and CD8), B cells (B220, CD5), natural killer (NK) cells (pan-NK) and intracellular interleukin 10 (IL-10) and interferon-gamma (IFN-gamma). Flow cytometric analysis of lymph nodes from CAR bacillus-infected mice revealed 11% increase in frequency of B cells (R220+), 12% increase in the frequency of double-negative (CD4-CD8-CD3+) T cells, and slight increase in the B-1 subset of B cells (B220+CD5+). There was no change in the frequency of NK cells. The CAR bacillus-infected mice had an overall decrease in the frequency of T cells. Intracellular cytokine staining revealed distinct populations of T cells producing IL-10 and IFN-gamma, and IL-10 production from B cells; NK cells were not a substantial source of IFN-gamma. To our knowledge, this is the first characterization of lymphocytic responses and suggestion that B cells and double-negative T cells may be principally responsible for the lesions associated with CAR bacillus infection.

Animals↗

PubMed2002

Flow cytometry.

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Flow Cytometry↗