Comparison of Cigarette Smoke-Induced Acute Inflammation in Multiple Strains of Mice and the Effect of a Matrix Metalloproteinase Inhibitor on These Responses

Morris, Abigail; Kinnear, Gillian; Wan, Wing-Yan Heidi; Wyss, Daniel F.; Bahra, Parmjit; Stevenson, Christopher S.

doi:10.1124/jpet.108.140848

Cited by 54 publications

(56 citation statements)

References 23 publications

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“…Function class is intergenic (IG), intronic (IT), 5=-or 3=-untranslated region (UTR), coding synonymous (CSyn), or coding nonsynonymous (CNSyn). previously been observed upon CS exposure in BALB/cJ compared with C57Bl/6J mice (36). Accordingly, another study reported that BALB/cJ mice were the most susceptible mouse strains for developing CS-induced airway inflammation after 4 days of CS exposure compared with C57Bl/6J, 129S1/ SvlmJ, and C3H/HeJ mice, all also present in the present study (54).…”

Section: Discussionsupporting

confidence: 73%

Genetic variation associates with susceptibility for cigarette smoke-induced neutrophilia in mice

Pouwels

Heijink

Brouwer

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Section: Discussionsupporting

confidence: 73%

Genetic variation associates with susceptibility for cigarette smoke-induced neutrophilia in mice

Pouwels

Heijink

Brouwer

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…PKF242-484 dose-dependently reduced neutrophilia in BALB/C mice after cigarette smoke exposure. Strangely, PKF242-484 had no effect in C57BL/6 mice, suggesting that the role of MMPs during smoke-induced acute neutrophil inflammation is strain dependent [47]. Ilomastat also effectively attenuated the inflammation and emphysema induced by cigarette smoke in mice [48].…”

Section: Dysregulation Of Mmps In Different Lung Disorders and Its Thmentioning

confidence: 97%

A therapeutic role for matrix metalloproteinase inhibitors in lung diseases?

Vandenbroucke¹,

Dejonckheere²,

Libert³

2011

Eur Respir J

112

105

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Disruption of the balance between matrix metalloproteinases (MMPs) and their endogenous inhibitors is considered a key event in the development of pulmonary diseases such as chronic obstructive pulmonary disease, asthma, interstitial lung diseases and lung cancer. This imbalance often results in elevated net MMP activity, making MMP inhibition an attractive therapeutic strategy. Although promising results have been obtained, the lack of selective MMP inhibitors, together with limited knowledge regarding the exact functions of a particular MMP, hampers clinical application. This review discusses the involvement of different MMPs in lung disorders and future opportunities and limitations of therapeutic MMP inhibition.

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“…Further increasing smoke exposure to a maximum of five cigarettes did not significantly increase the 24 hr postexposure neutrophil count/percentage in BALF. Morris et al (2008) showed that exposure to at least four 1R3F cigarettes was needed to induce an increase in the proportion of BALF neutrophils in BALB/c mice. The discrepancy between these studies could result from differences in animal gender and the type of cigarettes used.…”

Section: Discussionmentioning

confidence: 99%

Claudin-3 and Clara Cell 10 kDa Protein as Early Signals of Cigarette Smoke–Induced Epithelial Injury along Alveolar Ducts

et al. 2012

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Smoking-associated chronic obstructive pulmonary disease is characterized by inflammation, changes affecting small airways, and development of emphysema. Various short-and long-term models have been introduced to investigate these processes. The aim of the present study was to identify markers of early epithelial injury/adaptation in a short-term animal model of cigarette smoke exposure. Initially, male BALB/c mice were exposed to smoke from one to five cigarettes and lung changes were assessed 4 and 24 hr after smoking cessation. Subsequently, animals were exposed to smoke from five cigarettes for 2 consecutive days and lungs investigated daily until the seventh postexposure day. Lung homogenates cytokines were determined, bronchioloalveolar fluid cells were counted, and lung tissue was analyzed by immunohistochemistry. Exposure to smoke from a single cigarette induced slight pulmonary neutrophilia. Smoke from two cigarettes additionally induced de novo expression of tight junction protein, claudin-3, by alveolar duct (AD) epithelial cells. Further increases in smoke exposure induced epithelial changes in airway progenitor regions. During the recovery period, the severity/frequency of epithelial reactions slowly decreased, coinciding with the switch from acute to a chronic inflammatory reaction. Claudin-3 and Clara cell 10 kDa protein were identified as possible markers of early tobacco smoke-induced epithelial injury along ADs.

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Comparison of Cigarette Smoke-Induced Acute Inflammation in Multiple Strains of Mice and the Effect of a Matrix Metalloproteinase Inhibitor on These Responses

Cited by 54 publications

References 23 publications

Genetic variation associates with susceptibility for cigarette smoke-induced neutrophilia in mice

Genetic variation associates with susceptibility for cigarette smoke-induced neutrophilia in mice

A therapeutic role for matrix metalloproteinase inhibitors in lung diseases?

Claudin-3 and Clara Cell 10 kDa Protein as Early Signals of Cigarette Smoke–Induced Epithelial Injury along Alveolar Ducts

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