title: Apoptosis contributes to the decrement in numbers of alveolar macrophages from rats with polymicrobial sepsis.
abstract: To investigate the effects of sepsis-related acute lung injury on the events of alveolar macrophages apoptosis and phagocytosis, cecal-ligated-and-punctured male Sprague-Dawley rats were employed as sepsis model. At the early (9 h) and late (20 h) stages of sepsis, cecal-ligated-and-punctured and sham-operated animals were sacrificed and their lungs were removed. Alveolar macrophages were isolated by bronchoalveolar lavage and counted. The results showed that the purity of alveolar macrophages from both groups was over 98% as stained by Giemsa. The number of alveolar macrophages in late-stage septic rats significantly decreased. Alveolar macrophages apoptosis was then evaluated by labeling with fluorescein-conjugated annexin-V and exclusion of propidium iodide. There were minimal levels of baseline apoptosis in sham-operated rats. Compared with that of sham-operated rats, cecalligated-and-puncture operation resulted in 2.5- and 3.2-fold time-dependent increases in the amount of apoptotic alveolar macrophages in early- and late-stage septic animals, respectively. Among cecal-ligated-and-punctured and sham-operated rats of 9 and 20 h, the ability of alveolar macrophages to phagocytize opsonized fluorescence particles did not change significantly. However, the total alveolar macrophages phagocytic capacity of septic animals reduced due to the decrease in the number of alveolar macrophages. We conclude that apoptosis contributes to the decrement in the number of alveolar macrophages in cecal-ligated-and-punctured rats. Considering that alveolar macrophages have important roles in the defense and immunoregulation of the lungs, these results suggest that the defensive ability of septic lungs may be reduced, and could explain, at least in part, the increased susceptibility of septic lungs to superimposed infections.
authors.affiliation: Department of Physiology, School of Medicine, China Medical College, Taichung, Taiwan, ROC. luminchi@mail.cmc.edu.tw
authors.forename: Min-Chi
authors.initials: MC
authors.lastname: Lu
authors.forename: Tzu-An
authors.initials: TA
authors.lastname: Liu
authors.forename: Miau-Rong
authors.initials: MR
authors.lastname: Lee
authors.forename: Lina
authors.initials: L
authors.lastname: Lin
authors.forename: Weng-Cheng
authors.initials: WC
authors.lastname: Chang
mesh_terms: D000818:Animals; D017209:Apoptosis; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002432:Cecum / Q000382:microbiology / Q000473:pathology; D002452:Cell Count; D005434:Flow Cytometry; D016676:Macrophages, Alveolar / Q000166:cytology* / Q000276:immunology; D008297:Male; D010587:Phagocytosis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology