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Biomedical subjects

D E Gardner

Publications and source records attributed to D E Gardner.

At least 37 records · Page 2Linked to original sources
PubMed1982

Use of experimental airborne infections for monitoring altered host defenses.

The success or failure of the respiratory system to defend itself against airborne infectious agents largely depends upon the efficiency of the pulmonary defenses to maintain sterility and to dispose of unwanted substances. Both specific and nonspecific host defenses cooperate in the removal and inactivation of such agents. Several studies have shown that these defenses are vulnerable to a wide range of environmental agents and that there is a good relationship between exposure to pollutant and the impaired resistance to pulmonary disease. There are numerous immunological, biochemical and physiological techniques that are routinely used to identify and to characterize individual impairments of these defenses. Based on these effects, various hypotheses are proposed as to what health consequences could be expected from these effects. The ultimate test is whether the host, with its compromised defense mechanisms, is still capable of sustaining the total injury and continuing to defend itself against opportunistic pathogens. This paper describes the use of an experimental airborne infectious disease model capable of predicting subtle changes in host defenses at concentrations below which there are any other overt toxicological effects. Such sensitivity is possible because the model measure not just a single "health" parameter, but instead is capable of reflecting the total responses caused by the test chemical.

Air Microbiology↗
PubMed1981

Effects of exposure to ozone on susceptibility to experimental tuberculosis.

Exposure of mice to 1.96 mg/m3 ozone (O3) 3 h/day, 5 days/week, for up to 8 weeks beginning at 1 or 2 weeks after challenge with Mycobacterium tuberculosis R1Rv resulted in significant enhancement of bacterial titers in the lungs at 5 through 8 weeks after challenge when compared to mice exposed to filtered air. Exposure to lower concentrations of O3 did not produce any significant changes compared to controls. Exposure of guinea pigs to 2.9 mg/m3O3 for 3 h immediately after challenge with M. tuberculosis resulted in a suppression of the cutaneous delayed hypersensitivity response, without affecting the serum hemagglutination antibody titers. However, exposure of guinea pigs to 0.98 mg/m3 O3 3h/day for 5 days, initiated within 3 h after the infectious challenge, enhanced hemagglutination antibody titers initially, but the delayed hypersensitivity reaction did not differ from controls.

Animals↗
PubMed1981

Effects of exposure to peroxyacetyl nitrate on susceptibility to acute and chronic bacterial infection.

A significant increase in mortality due to acute respiratory pneumonia caused by inhalation of Streptococcus pyogenes aerosol was seen after a single 3-h exposure of mice to 14.8-28.4 mg/m3 peroxyacetyl nitrate (PAN). The excess mortality ranged from 8 to 39% and the decrease in survival time from 2.4 to 7.9 d. A single exposure to 25.0 mg/m3 PAN resulted in a significant increase in total number of cells lavaged from the lungs but somewhat decreased levels of adenosine triphosphate (ATP) in alveolar macrophages. Exposure to 7.4 mg/m3 PAN for 3 h/d, 5 d/wk, for 2 wk resulted in a reduced total count of free pulmonary cells and a significant reduction of ATP levels in alveolar macrophages but had no effect on mortality or survival rate. Scanning electron microscopic observations of the respiratory tract after both single and multiple exposures to PAN showed raised and sloughing nonciliated cells in the nasal cavities and tracheas and presence of excess mucus. Six daily 3-h exposures to 25.0 mg/m3 PAN did not produce any marked changes in a chronic respiratory infection in mice as measured by Mycobacterium tuberculosis lung titers.

Acetates↗
PubMed1981

Effects of cell source, mouse strain, and immunosuppressive treatment on production of virulent and attenuated murine cytomegalovirus.

Murine cytomegalovirus pools from various in vitro and in vivo sources were compared for virulence in suckling mice in an effort to identify the conditions which were necessary for the production of virulent and attenuated viruses. Virus passaged in tracheal ring and salivary gland organ cultures, where virus is produced primarily by epithelial cells, was even more attenuated than virus passaged in mouse embryo fibroblasts. The attenuation observed after passage in all three of these in vitro systems did not appear to be due to defective interfering particles. We also found that virus produced in vivo in salivary glands became attenuated with time after infection. Virus harvested from salivary glands 5 to 6 weeks after infection was highly attenuated compared with both salivary gland-passaged virus harvested 2 to 3 weeks after infection and tissue culture-passaged virus. The attenuation of salivary gland-passaged virus with time was reversed when animals were treated with cyclophosphamide before the virus was harvested. A comparison of virus pools harvested from susceptible and resistant mouse strains indicated that the mouse strain had little effect on the virulence of the virus produced. When the various sources of virus tested in this study were ranked in terms of the virulence of the virus produced, salivary glands in intact mice either 2 to 3 weeks after infection or after cyclophosphamide treatment produced the most virulent virus, followed by mouse embryo fibroblast cultures, tracheal ring and salivary gland organ cultures, and, finally, salivary glands in intact mice 5 to 6 weeks after infection.

Animals↗
PubMed1981

Correlation of effects of inhaled versus intratracheally injected males on susceptibility to respiratory infection in mice.

Effects of intratracheally administered air pollutant chemicals on susceptibility of mice to infection by aerosolized bacteria were compared with effects of the same chemical previously studied by the inhalation route. Out of 22 compounds previously studied by inhalation, the same 3 (CdSO4, CuSO4, and ZnSO4) that caused significantly increased mortality because of infection after a 3-h exposure to 1 to 2 mg/m3 showed large (greater than or equal to 40% over sham injected) mortality increases when administered by intratracheal injection at lung concentrations calculated to be equivalent to those achieved during inhalation exposures (0.6 to 1.2 microgram). Dose-effect curves of these compounds were similar by the 2 routes. Five of the compounds caused a moderate (20 to 30%) enhancement in the mean excess mortality at concentrations of 2 to 3 microgram/animal. The remaining compounds, which showed no significant effect by inhalation, also showed no effect when given by intratracheal injection. Thus, similar effects on susceptibility to lung bacterial infection were seen whether chemicals were deposited in te lung by inhalation or by intratracheal injection.

Aerosols↗
PubMed1980

Alterations in the facial skeleton of the guinea pig following a lesion of the trigeminal motor nucleus.

In thirty-three of sixty-six guinea pigs of the Topeka strain small, unilateral, electrolytic lesions were produced in the motor nucleus of the trigeminal nerve. Unoperated animals and the side contralateral to the muscle paralysis served as controls. Lesions were created when animals were 15 days or 75 days of age, and the animals were killed 15, 30, 45, or 60 days postoperatively. Each animal was subjected to dry skull preparations or radiographic and histologic techniques. Alterations in craniofacial form were noted in both the growing animals and the animals with little growth remaining. Alterations in form and function included paralysis and atrophy of the muscles of mastication on the lesion side, hypereruption of teeth, and reduction in growth of facial bones on the lesion side. Remodeling changes were evident in the glenoid fossa, the condylar process, and the coronoid process on the operated side but were not apparent in the contralateral control or the unoperated control animal.

Animals↗
PubMed1980

Extrapulmonary effects of NO2 as reflected by pentobarbital-induced sleeping time in mice.

The influence of nitrogen dioxide (NO2) on pentobarbital (PEN)-induced sleeping time (S.T.) was investigated in mice. Acute exposure to concentractions as low as 470 microgram NO2/m3 (0.25 ppm) caused a significant increase in PEN-induced S.T. No significant effects on PEN-induced S.T. were detected after 1 or 2 days (3 h/day) exposure to 235 microgram NO2/m3 (0.125 ppm). None of the exposure regimens affected the time required for the drug to induce sleep. When the effects of repeated daily exposures (3 h/day) to 9400 microgram NO2/m3 (5 ppm) were compared in male and female mice, the females had a significantly increased PEN-induced S.T. after 1 and 2 days of exposure. However, an increase in PEN-induced S.T. was not observed in males until the 3rd day of exposure. Since the duration of PEN-induced S.T. is primarily determined by hepatic mixed function oxidase activity, it is possible that NO2 may alter some aspects of xenobiotic metabolism.

Animals↗
PubMed1980

Biochemical changes in pulmonary cells following manganese oxide inhalation.

Inhalation of manganese oxide (Mn dose, 879.0 micrograms/m3) for 2 h reduced the total number of alveolar macrophages obtained by endotracheal lavage in pulmonary cell populations, slightly reduced cellular viability, and reduced both phagocytic capability and total protein in sonicated pulmonary cells. Increases in intracellular adenosine triphosphate and acid phosphatase specific activity were also exhibited by the pulmonary cells, but sonicated cells obtained from the exposed mice showed no change in lactic acid dehydrogenase specific activity. A slight increase in extracellular protein in the fluid phase of the lavage suspension was observed after manganese oxide exposure.

Adenosine Triphosphate↗
PubMed1980

Decreased resistance to infection in exercised mice exposed to NO2 and O3.

A mechanized wheel was constructed for use in evaluating the interaction of exercise and gaseous pollutants such as O3 and NO2. Immediately after the pollutant exposure, both exercised and nonexercised female mice (CD-1) were combined with controls, challenged with an aerosol of viable Streptococcus pyogenes (group C), and then observed over a 15-d period for incidence of mortality. Exposure to O3 at 196 micrograms/m3 (0.1 ppm) or 590 micrograms/m3 (0.3 ppm) while exercising yielded mortality rates that were significantly higher than those observed in the O3 groups that were not exercised. With exposure to NO2 at 5640 micrograms/m3 (3 ppm), exercise produced a significant enhancement in mortality over the other treatment groups. These studies show that exercise can affect the mortality observed in this model system and indicate the need for establishing safe exposure levels of pollutants as a function of the activity level of the exposed population.

Air Pollutants↗
PubMed1980

Acute exposure of laboratory mice to manganese oxide.

An acute inhalation exposure of laboratory mice to respirable Mn3O4 aerosols is described. The generation system consisted of a Wright dust generator which produced 1.40 micrometer aerosols. A non-linear loss of deposited manganese from mouse lungs over the inital 24-hour post-exposure period was observed. Systemic distribution of the manganese was observed in various tissues following exposure.

Air Pollutants↗
PubMed1980

Experimental infection of the respiratory tract with Mycoplasma pneumoniae.

M. pneumoniae, a common human respiratory pathogen, has been studied experimentally for years using intranasal inoculation of the golden Syrian hamster. Because of recent evidence outlining the role in pulmonary immune development of particle size and depth of mycoplasma deposition in the hamster lung, we developed an aerosol chamber for the reproducible aerosolization of radiolabeled M. pneumoniae. Organisms were labeled to high specific activity by the incorporation of 3H-oleic acid and aerosolized under airflow and humidity conditions creating a mean particle diameter of 2.0 micrometers. Under these conditions, viable mycoplasmas were reproducibly and evenly distributed to all major lobes of the lung. Examination of radioactive clearance and organism viability within the lung during the first 48 hr after aerosolization have suggested a minimal role for macrophage mycoplasmacidal activity and a more prominent role for ciliary clearance. Data from aerosol infections of hamsters with radio-labeled M. pneumoniae should provide a unique opportunity to examine in a highly controlled manner the effects of air pollutants on the initial stages of infection as well as effects on the development of pulmonary immunity and histologic alterations.

Aerosols↗