Presentation Title

Comparison of Alveolar Macrophage Populations in Fatal Asthma Subjects & Controls

Location

Nova Southeastern University, Davie, Florida, USA

Format

Podium Presentation

Start Date

21-2-2020 8:30 AM

End Date

21-2-2020 4:00 PM

Abstract

Objective. Determine the macrophage populations in alveoli of fatal asthmatics and controls. Background. We hypothesize that macrophage number would differ in healthy and asthmatic subjects. Methods. Stratified, random samples of lung parenchyma were examined and macrophage number was determined. (20 high mag fields/subject). Macrophage counts were expressed as number per mm2. Results. In fatal asthma lungs (12), there was a considerable variation of macrophage numbers averaging 49.14 ±29.82 STD v.s. 5.16 ±2.91 STD / mm2 in (6) non-asthmatics (P<0.05). Discussion. Detailed examination of the lung in this study revealed a confounding variation of morphological changes, from hyperemia, edema, atelectasis to hemorrhage. These represent the compartmentalized and extreme variation of the pathological severity. Although the classical involvement of granulocytes and lymphocytes in asthma pathogenesis is relatively well established, there is a staggering heterogeneity of asthma signs and responses to treatments. As lung parenchyma is challenged, the resulting debris increases with each asthma episode, the immigrating macrophages increase in numbers, indicating their participation in asthma pathogenesis. Conclusion. The future exploration of macrophage abundance, activation and suppression will yield a fertile ground in elucidating the specific clinical and inflammatory asthma varieties and improve their diagnosis and focused treatment. Grant. NSU Faculty Research Grant.

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Feb 21st, 8:30 AM Feb 21st, 4:00 PM

Comparison of Alveolar Macrophage Populations in Fatal Asthma Subjects & Controls

Nova Southeastern University, Davie, Florida, USA

Objective. Determine the macrophage populations in alveoli of fatal asthmatics and controls. Background. We hypothesize that macrophage number would differ in healthy and asthmatic subjects. Methods. Stratified, random samples of lung parenchyma were examined and macrophage number was determined. (20 high mag fields/subject). Macrophage counts were expressed as number per mm2. Results. In fatal asthma lungs (12), there was a considerable variation of macrophage numbers averaging 49.14 ±29.82 STD v.s. 5.16 ±2.91 STD / mm2 in (6) non-asthmatics (P<0.05). Discussion. Detailed examination of the lung in this study revealed a confounding variation of morphological changes, from hyperemia, edema, atelectasis to hemorrhage. These represent the compartmentalized and extreme variation of the pathological severity. Although the classical involvement of granulocytes and lymphocytes in asthma pathogenesis is relatively well established, there is a staggering heterogeneity of asthma signs and responses to treatments. As lung parenchyma is challenged, the resulting debris increases with each asthma episode, the immigrating macrophages increase in numbers, indicating their participation in asthma pathogenesis. Conclusion. The future exploration of macrophage abundance, activation and suppression will yield a fertile ground in elucidating the specific clinical and inflammatory asthma varieties and improve their diagnosis and focused treatment. Grant. NSU Faculty Research Grant.