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Biomedical subjects

H C Bartlema

Publications and source records attributed to H C Bartlema.

9 recordsLinked to original sources
PubMed1978

Effect of ozone on lysosomal enzymes of alveolar macrophages engaged in phagocytosis and killing of inhaled Staphylococcus aureus.

The role of lysosomal enzymes in the inactivation of inhaled bacteria by alveolar macrophages was studied in rats infected with aerosols of Staphylococcus aureus and then exposed for 5 hr to 2.5 ppm of ozone to determine whether pollutant-induced defects in phagocytic killing were associated with reduction in enzyme activity. Rates of bacterial ingestion and the activities of cellular acid phosphatase and beta-glucuronidase were measured simultaneously in in situ perfused right lungs by sequential staining of frozen sections for enzyme and bacteria. Quantitative measurements of enzyme activity within macrophages without ingested bacteria were made with a computer-controlled cytospectrophotometry system. Exposure to ozone resulted in diminished rates of bacterial clearance and ingestion, large increases in numbers of intra- and extracellular staphylococcal microcolonies, and an absence of enzyme activity for macrophages containing bacterial microcolonies. Enzyme activity was unimpaired in macrophages without ingested bacteria. These results, in which absence of enzyme activity occurred only in macrophages subjected to the dual insults of ozone exposure and ingested bacteria, prove a relationship between impairment in bactericidal capacity and cellular activities of lysosomal enzymes.

Acid Phosphatase↗
PubMed1972

Studies on respiratory immunization with tetanus toxoid: the role of adjuvants.

Aerosol vaccination of mice with purified plain tetanus toxoid does not induce an immune response unless a suitable adjuvant is added.Aluminium phosphate is without effect by aerosol treatment. Killed cells of Klebsiella pneumoniae, although effective, are unsatisfactory owing to the long inhalation period needed.Killed Bordetella perussis cells were found to be an excellent adjuvant. A single aerosol treatment with a toxoid-B. pertussis mixture during a moderate exposure period evoked a considerable immune response. With repeated aerosol treatment of primed mice the addition of adjuvant is not required; booster treatment with plain toxoid is at least as effective.Extracts from B. pertussis cells exert as good an adjuvant effect as the whole-cell vaccine. The remaining cell-wall debris also appears to be an active adjuvant.In combination with constant doses of adjuvant (10(8)B. pertussis cells), the 50% protective doses (ED 50) of toxoid were determined by inhalation and by s.c. injection and were found to be 0.1875 and 0.0625 LFU respectively. This would imply that, as a result of the adjuvant action, the s.c. ED 50 is reduced by approximately a factor of 20; whereas the respiratory ED 50 is decreased by at least a factor of 100.It is suggested that the much more pronounced adjuvant activity in aerosol immunization is associated with the induction of strong cell-mediated hypersensitivity in the respiratory tract.

Adjuvants, Immunologic↗
PubMed1966

Discussion.

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Journal Article↗
PubMedDate not supplied

Role of the alveolar macrophage in pulmonary bacterial defense.

This review concerns the role of the alveolar macrophage as part of the coordinated mucociliary, macrophge and immune bacterial defense mechanisms of the lung. Alveolar macrophages are end-stage phagocytes that are derived from two precursor sources; an uncommitted pleuripotential hematopoietic stem cell, and a committed differentiated pulmonary precursor which can renew itself, as well as mature into functional alveolar macrophages. Sufficient numbers of alveolar macrophages are distributed throughout the lungs to ensure their proximity to any bacteria that penetrates alveolar regions. Studies with rodents have shown that these alveolar macrophages ingest, inactivate, and degrade inhaled microorganisms within eight hours of their entrance into alveolar regions. The biochemical mechanisms responsible for this antibacterial function involve the elaboration of chemotactic factors consequent to the interaction of bacteria, antibody, and complement, and the presence of bactericidal substances within the macrophage itself. Normally, these cellular mechanisms enable the alveolar macrophage system to maintain the lungs bacteria-free. However, if macrophage function is impaired due to pollutant or viral exposure, the host-parasite balance is upset and bacterial proliferation ensues. In such circumstances, polymorphonuclear leucocytes and additional macrophages enter the area of bacterial proliferation to produce the classical inflammatory reaction of pneumonia.

Animals↗