Aerosolized Staphylococcal Enterotoxin B-Induced Pulmonary Lesions in Rhesus Monkeys (Macaca mulatta)
| Autor: | Catherine L. Wilhelmsen, Anthony J. Johnson, R E Hunt, Marc E. Mattix, Wallace B. Baze |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Pathology
medicine.medical_specialty 040301 veterinary sciences medicine.medical_treatment Bacterial Toxins Vascular permeability Biology Toxicology 030226 pharmacology & pharmacy Pathology and Forensic Medicine 0403 veterinary science Hemolysin Proteins 03 medical and health sciences 0302 clinical medicine Edema Adventitia medicine Animals Type-I Pneumocytes Lung Molecular Biology Aerosols 04 agricultural and veterinary sciences Cell Biology Pulmonary edema medicine.disease Immunohistochemistry Macaca mulatta Endothelial stem cell Sphingomyelin Phosphodiesterase Cytokine medicine.anatomical_structure Immunology medicine.symptom |
| Zdroj: | Toxicologic Pathology. 23:262-268 |
| ISSN: | 1533-1601 0192-6233 |
| DOI: | 10.1177/019262339502300304 |
| Popis: | The pathology of aerosolized staphylococcal enterotoxin B (SEB) was studied in the nonhuman primate. Six juvenile rhesus monkeys that received multiple lethal inhaled doses of SEB developed diarrhea and vomiting within 24 hr followed by depression, dyspnea, and shock. Three of 6 animals died by 52 hr. The most striking gross lesion in all 6 monkeys was diffuse severe pulmonary edema. Histologically, edema fluid was present within the peribronchiolar, peribronchial, and perivascular interstitium, alveolar septa, and alveoli. The adventitia of pulmonary vessels was infiltrated by lymphocytes, macrophages, and fewer neutrophils. Numerous large lymphocytes with occasional mitotic figures were within pulmonary vessels, often occluding alveolar capillaries. These cells were strongly immunoreactive with monoclonal antibodies against CD3, establishing them as T cells. Ultrastructurally, endothelial cell junctions were intact, and endothelial cells and type I pneumocytes contained numerous pinocytotic vesicles. Alveolar septal interstitial spaces were expanded by edema. The mechanism of these SEB-induced pulmonary lesions was not determined. We hypothesize that cytokine production by activated T cells may have caused vascular permeability changes leading to widespread pulmonary edema and shock. |
| Databáze: | OpenAIRE |
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