Abstract
BackgroundMarked accumulation of alveolar macrophages (AM) conferred by apoptosis resistance has been implicated in pathogenesis of chronic obstructive pulmonary disease (COPD). Apoptosis inhibitor of macrophage (AIM), has been shown to be produced by mature tissue macrophages and AIM demonstrates anti-apoptotic property against multiple apoptosis-inducing stimuli. Accordingly, we attempt to determine if AIM is expressed in AM and whether AIM is involved in the regulation of apoptosis in the setting of cigarette smoke extract (CSE) exposure.MethodsImmunohistochemical evaluations of AIM were performed. Immunostaining was assessed by counting total and positively staining AM numbers in each case (n = 5 in control, n = 5 in non-COPD smoker, n = 5 in COPD). AM were isolated from bronchoalveolar lavage fluid (BALF). The changes of AIM expression levels in response to CSE exposure in AM were evaluated. Knock-down of anti-apoptotic Bcl-xL was mediated by siRNA transfection. U937 monocyte-macrophage cell line was used to explore the anti-apoptotic properties of AIM.ResultsThe numbers of AM and AIM-positive AM were significantly increased in COPD lungs. AIM expression was demonstrated at both mRNA and protein levels in isolated AM, which was enhanced in response to CSE exposure. AIM significantly increased Bcl-xL expression levels in AM and Bcl-xL was involved in a part of anti-apoptotic mechanisms of AIM in U937 cells in the setting of CSE exposure.ConclusionsThese results suggest that AIM expression in association with cigarette smoking may be involved in accumulation of AM in COPD.
Highlights
Marked accumulation of alveolar macrophages (AM) conferred by apoptosis resistance has been implicated in pathogenesis of chronic obstructive pulmonary disease (COPD)
AM accumulation and Apoptosis inhibitor of macrophage (AIM) expression in COPD lung The number of AM was significantly increased in the lungs of COPD patients but not significant in non-COPD smoker compared to non-smoker (Figure 1A to G)
AIM expression was clearly observed in AM in lung of COPD patients and the percentages of positively staining AM were significantly increased in both COPD patients and non-COPD smoker compared to nonsmoker (Figure 1F, H)
Summary
Marked accumulation of alveolar macrophages (AM) conferred by apoptosis resistance has been implicated in pathogenesis of chronic obstructive pulmonary disease (COPD). We attempt to determine if AIM is expressed in AM and whether AIM is involved in the regulation of apoptosis in the setting of cigarette smoke extract (CSE) exposure. Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide and chronic cigarette smoke is sufficient to trigger COPD development [1]. Alveolar macrophages (AM) orchestrate innate immune responses for host defense through pattern recognition receptors (PRRs), marked increase of AM in response to cigarette smoke exposure has been widely implicated in pathogenesis of COPD via excessive. The AM specific mechanism of anti-apoptotic property for prolonged cell survival in COPD lung has not been clearly elucidated
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