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Tissue Culture Studies of Cellular Hypersensitivity in Rheumatic Fever

III. A Reexamination of Tuberculin Hypersensitivity in Tissue Culture by a Study of the Response to Old Tuberculin of Human White Blood Cells and Fibroblasts from Human and Guinea Pig Skin¹

From the Department of Preventive Medicine and Public Health, University of Colorado School of Medicine, the Department of Health and Hospitals, and the Colorado Foundation for Research in Tuberculosis, Denver, Colorado

Abstract

The growth of fibroblasts from human skin, the migration and spindling of certain elements of white blood cells from tuberculous and tuberculin-negative human beings were compared in their tissue culture responses to various concentrations of old tuberculin. The growth of fibroblasts from skin of guinea pigs before and after sensitization with killed human tubercle bacilli was compared in various concentrations of old tuberculin.

Fibroblastic growth was significantly depressed by old tuberculin in the group of 5 guinea pigs after sensitization. In any single experiment, however, the results were never sufficiently decisive to make it possible always to distinguish a sensitized from a nonsensitized animal.

In contrast to this observation, even the grouped data in the human experiments did not show a difference between patients with active tuberculosis and tuberculin-negative individuals.

When human tissues from individuals with and without rheumatic fever were tested with streptococcal products under similar experimental conditions (1, 2), evaluation of combined data suggested some inhibition in vitro of fibroblasts, though not of white blood cells from patients with rheumatic fever. However, it was not possible to classify correctly any individual case. A statistically demonstrable hypersensitivity to streptococcal filtrates and disintegrated streptococci may exist in rheumatic fever; however, an individually measurable one does not exist under these experimental conditions.

Cellular sensitivity, if the phenomenon observed in tissue culture could be interpreted as such, was more evident in rheumatic fever than in human tuberculosis.

Footnotes

¹ We wish to thank Dr. Gardner Middlehrook who supplied us with the old tuberculin, and the National Jewish Hospital which was the source of most of the skin specimens and white blood cells from patients with clinically active cases of tuberculosis, as well as some with tuberculin-negative cases. Dr. Thad P. Sears from the Denver Veterans' Hospital also supplied us with blood from some of the tuberculin-negative patients that had been admitted to that hospital. Our thanks also extend to some of our tuberculin-negative medical students who supplied us with blood for these studies.