bromochloroacetic-acid and Respiratory-Tract-Infections

The adenovirus is a non-enveloped DNA virus which may lead to severe diseases of the respiratory tract. In order to study the influence of virus infection on primary cultured peribronchial submucosal gland cells, we performed in vitro infection with human adenovirus type 3. Peribronchial submucosal glands are the main source of tracheobronchial mucus and, therefore, play a major pathophysiological role in common pulmonary diseases such as bronchial asthma, chronic obstructive pulmonary disease and cystic fibrosis. The success of infection was verified by means of immunofluorescence and transmission electron microscopy. Infection follows a certain timetable with a climax of paracristalline intranuclear virus inclusions after 48 h of infection. Virus particles could be detected in the nucleus as well as in peripheral and perinuclear cytoplasmatic vacuoles. The release of virus capsids from the nucleus could be visualized using transmission electron microscopy and immunofluorescence with antibodies against hexon proteins. Two different kinds of mechanisms of transition of newly synthesized virus capsids from the nucleus into the cytoplasm could be identified. Due to an increasing cytopathic effect, viruses spread from cytoplasm after longer terms of infection. Cytopathic effects and cytoskeleton aspects under this virus infection could be characterized using immunofluorescence with several monoclonal antibodies against different cytokeratins.

Topics: Adenovirus Infections, Human; Adenoviruses, Human; Antibodies, Monoclonal; Bronchi; Cell Nucleus; Cytopathogenic Effect, Viral; Cytoplasm; Epithelial Cells; Fluorescent Antibody Technique; Humans; Keratins; Microscopy, Confocal; Microscopy, Electron; Respiratory Tract Infections; Vacuoles; Virion

Seventy patients with olfactory disorders following upper respiratory viral infection (URVI) were studied clinically, and the olfactory mucosa of 13 patients was biopsied using special biopsy forceps. The specimens were examined using immunohistochemical staining for neuron-specific enolase (NSE), S-100 protein (S-100), cytokeratin (CK), and proliferating cell nuclear antigen (PCNA). Although the clinical course of URVI-olfactory disorders was not very good, overall a high proportion of Alinamin intravenous injection test-positive patient's recovered their sense of smell. Immunohistochemical study of the biopsy specimens revealed a decrease in the number of olfactory receptor cells and nerve bundles. In a few cases the olfactory neuroepithelium was replaced by metaplastic squamous epithelium. Sometimes different types of degeneration were found in the same specimen. No PCNA-immunoreactivity was detected in the olfactory epithelium. The result generally correlated with the degree of degeneration of the olfactory mucosa, because regeneration of the olfactory receptor cells is suspected to be extremely slow or rare in humans. Alinamin test-positive patients had many olfactory receptor cells. These findings suggest that olfactory mucosal biopsy and the Alinamin intravenous injection test are useful methods of determining the prognosis in post-URVI olfactory disorders.

Topics: Adult; Aged; Female; Humans; Immunohistochemistry; Keratins; Male; Middle Aged; Olfactory Mucosa; Phosphopyruvate Hydratase; Proliferating Cell Nuclear Antigen; Respiratory Tract Infections; S100 Proteins; Sensory Thresholds; Smell; Virus Diseases

Keratotic and squamous changes characteristic of vitamin A deficiency were minimal even in chicks which were malnourished and growth stunted and had no vitamin A in their diet. However, when these chicks were infected with Newcastle disease virus (NDV), keratotic changes appeared, most markedly in areas regenerating after infection. In chicks raised on full nutrient diets lacking only vitamin A, keratotic changes appeared in several areas of nasal mucosa but were absent from the mucosa of the inner (under) surface of the maxillary turbinate. Following NDV infection, such changes did appear in the inner lining epithelia. It is suggested that depletion of vitamin A causes regenerating epithelial cells to keratinize. Other effects of combined lack of vitamin A plus NDV infection were exhaustion of lymphoid cells from cranial bone marrow and exhaustion of lymphoid cell systems locally from the nose and paranasal glands.

Topics: Acute Disease; Animal Nutritional Physiological Phenomena; Animals; Bone Marrow; Bone Marrow Cells; Chickens; Diet; Harderian Gland; Keratins; Newcastle Disease; Newcastle disease virus; Plasma Cells; Respiratory Tract Infections; Turbinates; Vitamin A Deficiency