Effect of Chronic Tobacco Smoke Exposure on the Function of Alveolar Macrophages in Mice

Higashimoto, Yuji; Fukuchi, Yoshinosuke; Ishida, Kohtaro; Shimada, Yoshiya; Ohata, Masahiro; Funasako, Masato; Teramoto, S; Matsuse, Takeshi; Sudo, Eiichi; Orimo, Hajime

doi:10.1159/000196298

Cited by 10 publications

(9 citation statements)

References 3 publications

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“…Studies in the early 1990s (8)(9)(10) showed that the inhalation of CS led to a transient impairment of alveolar macrophage uptake of latex beads or Candida albicans in mice. Richens and colleagues also found an impaired uptake of apoptotic cells by macrophages upon exposure to CS in vivo (11).…”

Section: Discussionmentioning

confidence: 99%

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Cigarette Smoke Inhibits Engulfment of Apoptotic Cells by Macrophages through Inhibition of Actin Rearrangement

Minematsu¹,

Blumental‐Perry²,

Shapiro³

2011

Am J Respir Cell Mol Biol

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Exposure to cigarette smoke (CS) was shown to impair the capacity of macrophages to clear bacteria and apoptotic cells. Here, we show that both the exposure of macrophages to cigarette smoke extract (CSE) in vitro and an acute single exposure to CS in vivo impair the macrophage clearance of apoptotic polymorphonuclear leukocytes (PMNs). Upon longer periods of exposure to smoke in vivo (4-12 weeks), the impaired capacity of macrophages to clear apoptotic cells persisted after the cessation of smoking, with slow recovery to normality observed 4 weeks later. With respect to the mechanism by which CS impairs the macrophage uptake of apoptotic PMNs, we did not detect altered surface expression of receptors associated with apoptotic cell clearance. We did observe the impaired phosphorylation of the guanine nucleotide exchange factor Vav1 and the downstream inhibition of Ras-related C3 botulinum toxin substrate 1 (Rac1) activation. Consistent with these findings, CS impaired the macrophage cytoskeletal changes observed after stimulation with apoptotic cells. A loss of actin occurred at the leading edge, manifested as impaired ruffling of the cell membrane and a decreased capacity to engulf apoptotic cells. The inability to clear PMNs would lead to a greater release of destructive PMN products, and would diminish the reparative phenotype induced by the macrophage clearance of apoptotic cells.

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Section: Discussionmentioning

confidence: 99%

“…The ability of alveolar macrophages to engulf apoptotic cells was impaired by smoke inhalation in animal models (11). Reversal of the effects of CS on the ability of macrophages to phagocytose apoptotic cells or microorganisms was delayed in proportion to the chronicity of smoke exposure (10,11).…”

mentioning

confidence: 99%

Cigarette Smoke Inhibits Engulfment of Apoptotic Cells by Macrophages through Inhibition of Actin Rearrangement

Minematsu¹,

Blumental‐Perry²,

Shapiro³

2011

Am J Respir Cell Mol Biol

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“…5B). Previous studies showed that the expression of Ia antigen on BAL cells increased during lung inflammation caused by silica, asbestos, or tobacco smoke (Struhar et al, 1989;Hartmann et al, 1984;Higashimoto et al, 1994). It was also reported that BAL cells from lungs inflamed by asthma showed increased expression of B7.1 and B7.2 (Burastero et al, 1999;Agea et al, 1998).…”

Section: Discussionmentioning

confidence: 92%

Exposure to ozone enhances antigen-presenting activity concentration dependently in rats

2004

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“…However, phagocytic capacity was improved in COPD subjects who had ceased smoking (ex-smokers), compared to those who were still smoking [19]. Studies in mice also support this observation in that chronic tobacco exposure of mice has been shown to decrease phagocytic capability of AM as well as LPS-induced TNF-α release, although it increased the Ia antigen expression on AM [21]. The phagocytotic activities of macrophages are triggered by their interaction with extracellular matrix components.…”

Section: Risk Factorsmentioning

confidence: 88%

Signal Transduction Pathways Linking the Activation of Alveolar Macrophages With the Recruitment of Neutrophils to Lungs in Chronic Obstructive Pulmonary Disease

Murugan

Peck

2009

Experimental Lung Research

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Chronic obstructive pulmonary disease (COPD) is a major and increasing global health problem. It is predicted by the World Health Organization to become the third most common cause of death and the fifth most common cause of disability in the world by 2020. COPD is a complex inflammatory disease involving several types of inflammatory cells and multiple inflammatory mediators. Although abnormal numbers of inflammatory cells such as macrophages, dendritic cells, neutrophils, and T lymphocytes have been documented in COPD, the relationship between these cell types and the sequence of their appearance and persistence is largely unknown. Alveolar macrophages have been identified as one of the major cell types that plays a key role in orchestrating the inflammatory events associated with the pathophysiology of COPD. One of the major functions of macrophages is the secretion of chemotactic factors and this function is markedly increased on exposure to cigarette smoke (CS). This enhanced release of chemoattractants results in increased lung neutrophil infiltration, which is thought to be a key event in the development of COPD. The molecular basis for this amplified inflammatory response is not very clear, but it could be due to an alteration in signal transduction pathways within the macrophage. Based on existing literature, an attempt has been made to create a comprehensive review of the signal transduction pathways that link the activation of macrophages with the increased recruitment of neutrophils into the airways. Some of the major stimuli that activate macrophages and cause them to secrete chemotactic factors have been identified as CS, wood smoke, ozone, bacterial endotoxin, and proinflammatory cytokines such as interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha. These stimuli seem to activate mainly redox-sensitive transcription factors such as nuclear factor (NF)-kappa B and activator protein (AP)-1, both of which play a major role in the synthesis and secretion of chemotactic factors such as IL-8 and leukotriene B(4) (LTB(4)). The pathways involved in the synthesis and secretion of other factors such as macrophage chemotactic protein-1 (MCP-1) and growth-related oncogene-alpha (Gro-alpha) have also been reviewed.

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Effect of Chronic Tobacco Smoke Exposure on the Function of Alveolar Macrophages in Mice

Cited by 10 publications

References 3 publications

Cigarette Smoke Inhibits Engulfment of Apoptotic Cells by Macrophages through Inhibition of Actin Rearrangement

Cigarette Smoke Inhibits Engulfment of Apoptotic Cells by Macrophages through Inhibition of Actin Rearrangement

Exposure to ozone enhances antigen-presenting activity concentration dependently in rats

Signal Transduction Pathways Linking the Activation of Alveolar Macrophages With the Recruitment of Neutrophils to Lungs in Chronic Obstructive Pulmonary Disease

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