A light and electron microscopic study was conducted to investigate nuclear changes observed in specimens obtained from various sites by computed tomographic (CT)-guided fine needle aspiration (FNA) biopsy. These changes, which consisted of a disappearance of the nuclear chromatin and a disruption of the nuclear membrane, were found in 70% of 10 FNA specimens obtained with CT guidance, in 26% of 15 specimens obtained with fluoroscopic guidance and in 0% of 10 specimens obtained without x-ray imaging techniques. Although the number of cases studied was small and the mechanisms responsible for these changes are not clear, cytopathologists should be aware of alterations in evaluating FNA specimens obtained with the guidance of x-ray imaging techniques.
Pneumocystis carinii infection is characterized by the attachment of P. Carinii to host alveolar type I cell and propagation of the organism with corticosteroid administration. We have examined the effects of corticosteroids on the cell surface glycocalyx of the pulmonary alveolus in rats by ultrastructural histochemistry using cationized ferritin, ruthenium red and concanavalin A-horseradish peroxidase techniques. In rats treated for 4 and 6 weeks, the amount of the alveolar cell surface glycocalyx was markedly decreased by all three techniques. The changes were most pronounced at the cell surface of the type I pneumocyte, and this may be important in the pathogenesis of P. carinii pneumonia.
Tumor necrosis factor alpha (TNF-alpha) mediates components of the acute-phase response, stimulates granulocyte metabolism, and induces endothelial cell surface changes. We studied whether human recombinant TNF-alpha (rTNF-alpha) could increase pulmonary edema formation and pulmonary vascular permeability. Rabbits preinfused with 125I-albumin were administered rTNF-alpha or saline. Animals were sacrificed, and lung wet/dry weight ratios as well as bronchoalveolar lavage fluid and plasma 125I activities were determined. rTNF-alpha increased lung wet/dry weight ratios by 151% (P less than 0.02) and bronchoalveolar lavage fluid/plasma 125I activity ratios by 376% (P less than 0.01) compared with values for saline controls. Electron microscopy of lung sections demonstrated endothelial injury, perivascular edema, and extravasation of an ultrastructural permeability tracer. To demonstrate that rTNF-alpha could directly increase pulmonary vascular endothelial permeability in vitro, we studied albumin transfer across cultured porcine pulmonary artery endothelial cell monolayers. rTNF-alpha induced time-dependent dose-response increments in transendothelial albumin flux in the absence of granulocyte effector cells. These observations suggest that rTNF-alpha can provoke acute pulmonary vascular endothelial injury in vivo as well as in vitro.
Pneumocystis carinii pneumonia was produced in eight different strains of mice by the administration of corticosteroids, low (8%)-protein diet, and tetracycline in the drinking water. Heavier degrees of P. carinii infection were most consistently found in C3H/HeN mice; intermediate levels occurred in BALB/c AnN, C57BL/6N, B10.A(2R), AKR/J, and Swiss Webster mice; lighter degrees were found in DBA/2N and DBA/IJ mice. Histopathologically, P. carinii organisms were morphologically indistinguishable from human and rat P. carinii, and elicited a predominantly mononuclear response that was similar among the various mouse strains. The optimal cortisone acetate regimen was 1 mg injected subcutaneously twice weekly. Higher doses shortened the life span of the mice, presumably by inducing overwhelming bacterial infection. This problem occurred not only in different strains of mice, but also in the same strain of mice obtained from different breeders. Thus, cortisonized mice should be useful in the study of experimental P. carinii infection. Success of this model depends on the corticosteroid dose, as well as the strain, source, general health, and preexisting microbial flora of the mice chosen for study.
Pneumocystis carinii was tightly attached to host alveolar type I cells, as judged by freeze-fracture electron microscopy. In contrast to other organisms studied by this technique, no changes in the cell membranes of P. carinii or the host cells could be demonstrated. These data suggest that P. carinii attaches in an unusual manner.
Journal Article Mechanism of Killing of Pneumococci by Lysozyme Get access J. Donald Coonrod, J. Donald Coonrod Departments of Medicine and Pathology, VA and University of Kentucky Medical Centers, Lexington Search for other works by this author on: Oxford Academic PubMed Google Scholar Robin Varble, Robin Varble Departments of Medicine and Pathology, VA and University of Kentucky Medical Centers, Lexington Search for other works by this author on: Oxford Academic PubMed Google Scholar Kokichi Yoneda Kokichi Yoneda Departments of Medicine and Pathology, VA and University of Kentucky Medical Centers, Lexington Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 164, Issue 3, September 1991, Pages 527–532, https://doi.org/10.1093/infdis/164.3.527 Published: 01 September 1991 Article history Received: 03 October 1990 Revision received: 17 April 1991 Published: 01 September 1991
