Murine models of COPD

Brusselle, Guy; Bracke, Ken R.; Maes, Tania; D’hulst, An I.; Moerloose, Katrien; Joos, Guy; Pauwels, Romain

doi:10.1016/j.pupt.2005.06.001

Cited by 90 publications

(57 citation statements)

References 98 publications

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“…It is validated as a model to examine smoke-induced respiratory diseases. 38 Although no animal model can perfectly mimic human disease, this model offers important advantages over established models for assessing smoke-induced changes in the gut. Furthermore, the use of a murine model enabled us to investigate the ileum, a region that is less evident than the colon to study in human beings, as it is less accessible and PP are often difficult to identify endoscopically.…”

Section: Smoking Alters Intestinal Apoptosis and Galtmentioning

confidence: 99%

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Verschuere

Bracke

Demoor

et al. 2011

Laboratory Investigation

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Smokers have a twofold increased risk to develop Crohn's disease (CD). However, little is known about the mechanisms through which smoking affects CD pathogenesis. Especially Crohn's ileitis is negatively influenced by smoking. Interestingly, the ileum and, more in particular, the Peyer's patches in the terminal ileum are also the sites where the first CD lesions are found. Several chemokines are implicated in the pathogenesis, among which is the CCL20-CCR6 pathway. Here, we studied the gut-associated lymphoid tissue in C57BL/6 wild-type mice and in CCR6-deficient mice after exposure to air or cigarette smoke for 24 weeks. Apoptotic index of the follicle-associated epithelium overlying the Peyer's patches was evaluated. We found that chronic smoke exposure induced apoptosis in the follicle-associated epithelium. Furthermore, immune cell numbers and differentiation along with chemokine expression were determined in Peyer's patches. Important changes in immune cell composition were observed: total dendritic cells, CD4 þ T cells (including regulatory T cells) and CD8 þ T cells increased significantly after smoke exposure. The CD11b þ dendritic cell subset almost doubled. Interestingly, these changes were accompanied by an upregulated mRNA expression of the chemokines CCL9 and CCL20. However, no differences in the increase of dendritic cells were observed between wild-type and CCR6-deficient mice. Our results show that cigarette smoke exposure increases apoptosis in the follicle-associated epithelium and is associated with immune cell accumulation in Peyer's patches.

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Section: Smoking Alters Intestinal Apoptosis and Galtmentioning

confidence: 99%

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Verschuere

Bracke

Demoor

et al. 2011

Laboratory Investigation

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“…Although in genetic mouse models of emphysema, alveolar remodeling is progressive and related to the activation of alveolar macrophages and inflammation rather than developmental abnormalities, 57 the lack of alveoli formation in Hoxa5 Ϫ/Ϫ lungs favors the view that the inflammatory response is secondary to developmental defects. In Hoxa5 mutants, activated macrophages are abundantly found in the lung as early as birth and most of them express MMP12.…”

Section: Contribution Of Inflammatory Stimuli To Alveolar Defects In mentioning

confidence: 99%

Impact of the Loss of Hoxa5 Function on Lung Alveogenesis

Mandeville

Aubin

LeBlanc

et al. 2006

The American Journal of Pathology

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The involvement of genes controlling embryonic processes in the etiology of diseases often escapes attention because of the focus given to their inherent developmental role. Hoxa5 belongs to the Hox gene family encoding transcription factors known for their role in skeletal patterning. Hoxa5 is required for embryonic respiratory tract morphogenesis. We now show that the loss of Hoxa5 function has severe repercussions on postnatal lung development. Hoxa5؊/؊ lungs present an emphysema-like morphology because of impaired alveogenesis. Chronic inflammation characteristics, including goblet cell hyperplasia, mucus hypersecretion, and recruitment of inflammatory cells, were also observed. Altered cell specification during lung morphogenesis triggered goblet cell anomalies. In addition, the defective motility of alveolar myofibroblast precursors in the embryonic lung led to the mispositioning of the alveolar myofibroblasts and to abnormal elastin deposition postnatally. Both goblet cell hyperplasia and elastic fiber abnormalities contributed to the chronic physiopathological features of Hoxa5 ؊/؊ lungs. They constituted an attractive stimulus to recruit activated macrophages that in turn generated a positive feedback loop that perpetuated macrophage accumulation in the lung. The present work corroborates the notion that altered Hox gene expression may predispose to lung pathologies. Lung morphogenesis relies on finely orchestrated processes that initiate from the outpocketing and the elongation of the foregut endoderm into the surrounding mesenchyme. The lung bud then branches extensively giving rise to saccules that expend and subdivide to ultimately produce alveoli. In the mouse, the main stem bronchi form at approximately embryonic day (E) 9.5, and ramification organized by signaling centers shapes the respiratory tree during the pseudoglandular period that extends from E14.0 to E16.5. At late gestational stages, saccules are found at the end of each terminus of the pulmonary tree. The last step of lung morphogenesis occurs between postnatal day (P) 5 and P30, and it aims at multiplying the respiratory surface for vital gas exchanges after birth by modifying the distal lung architecture through the process of alveogenesis. During each step of lung development, the concerted action of transcriptional regulators, signaling molecules, their associated receptors and downstream effectors governs branching morphogenesis and lung maturation by integrating cellular proliferation, differentiation, apoptosis, and migration.

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“…The exposure to cigarette smoke is implicated in abnormal immune responses as well as the acute damage of lungs (Taylor, 2010). Hence, cigarette smoke has been used to induce of the pulmonary diseases as the main source (Brusselle et al, 2006;Chan et al, 2009;Zheng et al, 2009). Lipopolysaccaride (LPS) is a compound of cigarette smoke which has been used to induce acute pulmonary diseases in murine models (Brusselle et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Hence, cigarette smoke has been used to induce of the pulmonary diseases as the main source (Brusselle et al, 2006;Chan et al, 2009;Zheng et al, 2009). Lipopolysaccaride (LPS) is a compound of cigarette smoke which has been used to induce acute pulmonary diseases in murine models (Brusselle et al, 2006). Some studies have induced acute respiratory diseases using cigarette smoke and LPS (Doz et al, 2008;Le Quement et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Ligustrum lucidum Fruits Extract Inhibits Acute Pulmonary Inflammation in Mice

Kwak

Lim²

2013

Korean Journal of Medicinal Crop Science

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: Traditionally, Ligustrum lucidum fruits (LL) is one of the well-known oriental herb used in the treatment of skin and lung inflammation. This study investigated anti-inflammatory effects of LL in the pathogenesis of acute pulmonary inflammation in mice. Acute pulmonary inflammation was induced by intratracheal instillation of cigarette smoke condensate (CSC) and lipopolysaccharide (LPS) 5 times within 12 days in mice. LL extract was administered orally at a dose of 50 or 200 ㎎/㎏. Administration of LPS and CSC significantly elevated airway hyperresponsiveness (AHR) to mice, and increased in the levels of inflammatory cells and mediators in mice. However, the LL extract significantly reduced the elevated AHR, and the increase of neutrophils, CD4 + /CD3+ cells and CD8 + /CD3 + cells, along with reducing the expression of TNF-α, IL-6, and MIP-2. Moreover, the LL extract alleviated the infiltration of inflammatory cells in expanded airway walls histologically. These results indicate that the LL extract has an inhibitory effects on acute pulmonary inflammation and AHR in murine model, and plays a crucial role as a immunomodulator which possess anti-inflammatory property.

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Murine models of COPD

Cited by 90 publications

References 98 publications

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Impact of the Loss of Hoxa5 Function on Lung Alveogenesis

Ligustrum lucidum Fruits Extract Inhibits Acute Pulmonary Inflammation in Mice

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