The Development of Emphysema in Cigarette Smoke-exposed Mice Is Strain Dependent

Guerassimov, Alexei; Hoshino, Yuma; Takubo, Yasutaka; Turcotte, Antony; Yamamoto, Midori; Ghezzo, Heberto; Triantafillopoulos, Alexandra; Whittaker, K. B.; Hoidal, John R.; Cosio, Manuel G.

doi:10.1164/rccm.200309-1270oc

Cited by 261 publications

(263 citation statements)

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“…For example, inbred mice varied significantly in their susceptibility to cigarette smokeinduced emphysema. 43,44 Further studies will be required to analyze genetic mechanisms for differences in inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Relationship of strain-dependent susceptibility to experimentally induced acute pancreatitis with regulation of Prss1 and Spink3 expression

Wang

Ohmuraya

Suyama

et al. 2010

Laboratory Investigation

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To analyze susceptibility to acute pancreatitis, five mouse strains including Japanese Fancy Mouse 1 (JF1), C57BL/6J, BALB/c, CBA/J, and C3H/HeJ were treated with either a cholecystokinin analog, cerulein, or a choline-deficient, ethioninesupplemented (CDE) diet. The severity of acute pancreatitis induced by cerulein was highest in C3H/HeJ and CBA/J, moderate in BALB/c, and mildest in C57BL/6J and JF1. Basal protein expression levels of the serine protease inhibitor, Kazal type 3 (Spink3) were higher in JF1 and C57BL/6J mice than those of the other three strains under normal feeding conditions. After treatment with cerulein, expression level of Spink3 increased remarkably in JF1 and mildly in C57BL/6J, BALB/c, CBA/J, and C3H/HeJ strains. Increased proteinase, serine, 1 (Prss1) protein expression accompanied by increased trypsin activity with cerulein treatment was observed in susceptible strains such as CBA/J and C3H/HeJ. Similar results were obtained with a CDE diet. In the 3 kb Spink3 promoter region, 92 or 8 nucleotide changes were found in JF1 or C3H vs C57BL/6J, respectively, whereas in the Prss1 promoter region 39 or 46 nucleotide changes were found in JF1 or C3H vs C57BL/6J, respectively. These results suggest that regulation of Prss1 and Spink3 expression is involved in the susceptibility to experimentally induced pancreatitis. The JF1 strain, which is derived from the Japanese wild mouse, will be useful to examine new mechanisms that may not be found in other laboratory mouse strains. Over 450 inbred strains of mice have been described, 1 providing a wealth of different genotypes and phenotypes for studying human diseases. Actually, the use of various breeding strategies in combination with positional cloning and positional candidate gene approach has led to the discovery of many genes that underlie human disease. 2 The Japanese wild mouse, belonging to Mus musculus molossinus, has several genetic characteristics clearly distinguishable from the European wild mouse, derived from M.m. domesticus. These subspecies were separated about one million years ago and about 1% of their genome sequences are different. [3][4][5][6][7][8] Therefore, strains MSM/Ms 9 and Japanese Fancy Mouse 1 (JF1), 10 which were established from M.m. molossinus, are powerful genetic resources to analyze disease processes.Many inbred strains have been bred for specific phenotypes. C57BL/6J mice are susceptible to high-fat diet-induced type II diabetes. 11 JF1 mice are especially sensitive to high-fat diet-induced diabetes and obesity, whereas MSM/Ms mice are resistant. 12 To date, however, there is little information about the difference in severity of pancreatitis among inbred strains of mice.Acute pancreatitis is an important disease that can be triggered by a variety of factors, including excessive alcohol consumption, 13-16 obstruction of the ampulla of Vater by gall stones, 17,18 and genetic factors. 19,20 Hereditary chronic pancreatitis is a rare form of early onset chronic pancreatitis, characterized by the onset of recurrent...

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Section: Discussionmentioning

confidence: 99%

Relationship of strain-dependent susceptibility to experimentally induced acute pancreatitis with regulation of Prss1 and Spink3 expression

Wang

Ohmuraya

Suyama

et al. 2010

Laboratory Investigation

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“…This study characterized the effects of CS on strains of mice known to have differing susceptibilities to CS-induced inflammatory lung pathology [31]. CS exposure was associated with both RF and autoantibodies against HSP70 primarily in the AKR/J strain most susceptible to inflammatory LD.…”

Section: Discussionmentioning

confidence: 99%

“…The RF response appeared to correlate with susceptibility to smoke-induced inflammatory LD [31], with the AKR/J mice being most susceptible. Circulating IgA and/or IgM RFs may be a marker of a genetic susceptibility to smoke-induced inflammatory LD.…”

Section: Cs Exposure Induces the Rfsmentioning

confidence: 96%

“…Sera from male AKR/J, A/J, and C57BL/6 mice were collected after exposure to room air or CS from two 2R1 unfiltered research cigarettes per day, 5 days a week, for up to 9 months as previously described [31]. Cytokine expression in lung tissues and the histology of smoke-induced LD in the mice used in the study was previously reported [31].…”

Section: Animals and Cs Exposurementioning

confidence: 99%

“…Cytokine expression in lung tissues and the histology of smoke-induced LD in the mice used in the study was previously reported [31]. The animal studies were approved by the McGill Animal Care Committee in compliance with the regulations of the Canadian Council for Animal Care.…”

Section: Animals and Cs Exposurementioning

confidence: 99%

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Chronic smoke exposure induces rheumatoid factor and anti‐heat shock protein 70 autoantibodies in susceptible mice and humans with lung disease

et al. 2012

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The impact of cigarette smoke (CS), a risk factor for rheumatoid arthritis (RA), on autoantibody production was studied in humans and mice with and without chronic lung disease (LD). Rheumatoid factor (RF), anti-cyclic citrullinated peptides (CCPs), and anti-HSP70 autoantibodies were measured in several mouse strains and in cohorts of smokers and nonsmokers with and without autoimmune disease. Chronic smoking-induced RFs in AKR/J mice, which are most susceptible to LD. RFs were identified in human smokers, preferentially in those with LD. Anti-HSP70 autoantibodies were identified in CS-exposed AKR/J mice but not in ambient air exposed AKR/J controls. Whereas inflammation could induce anti-HSP70 IgM, smoke exposure promoted the switch to anti-HSP70 IgG autoantibodies. Elevated anti-CCP autoantibodies were not detected in CS-exposed mice or smokers. AKR/J splenocytes stimulated in vitro by immune complexes (ICs) of HSP70/anti-HSP70 antibodies produced RFs. The CD91 scavenger pathway was required as anti-CD91 blocked the HSP70-IC-induced RF response. Blocking Toll-like receptors did not influence the HSP70-IC-induced RFs. These studies identify both anti-HSP70 and RFs as serological markers of smoke-related LD in humans and mice. Identification of these autoantibodies could suggest a common environmental insult, namely CS, in a number of different disease settings.Keywords: Autoantibodies r Heat shock protein 70 r Lung disease r Rheumatoid factor IntroductionSmoking is a very strong environmental risk factor that is linked to rheumatoid arthritis (RA) [1,2] and other autoimmune disCorrespondence: Dr. Marianna M. Newkirk e-mail: Marianna.newkirk@mcgill.ca eases [3][4][5]. Furthermore, there is little information on the association between the most common smoke-induced lung disease (LD), chronic obstructive pulmonary disease (COPD), and serological markers associated with autoimmunity.In North American Native (NAN) populations the prevalence of RA can be three times that of Caucasians [6]. Whereas smoking rates have decreased in the past decade in Caucasians, with 18% of Canadians >15 years of age smoking, 60-70% C 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu1052 Marianna M. Newkirk et al. Eur. J. Immunol. 2012. 42: 1051-1061 of NANs (residing mostly on reservations) smoke (Health Canada). Although smoking cessation can lower RA risk and disease burden, the risk continues 10 years after cessation [1] and similarly, prolonged smoking cessation is critical for the reduction of lung cancer [7]. Lung inflammation, oxidative stress, and protease burden remain elevated for several months after smoking cessation [8]. Early diagnosis of those at risk of smoking-related diseases ideally by the use of informative biomarkers is critical with sustained cessation an important goal. Rheumatoid factor (RF), used in the diagnosis of RA [9], is an autoantibody of any isotype that binds IgG Fc. Epidemiological studies have shown that RF-positive RA patients are most associated with an increased risk conferred f...

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Cigarette Smoke Exposure as a Model of Inflammation Associated with COPD

2013

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Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation resulting from inflammation-driven pathologies in the lungs that are a consequence of smoking over many years. Given that the disease is increasing globally, understanding the mechanism by which cigarette smoke (CS) causes lung inflammation and exploiting that knowledge to develop effective treatments is urgently required. Animal models of CS exposure are commonly used to examine the inflammatory processes that may be involved in the development of COPD. The protocols described in this unit detail the development of preclinical models of CS-driven lung inflammation. These systems can be utilized to investigate the role of various biological pathways in CS-mediated inflammation and to assess the efficacy of new therapeutic strategies for treating COPD.

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The Development of Emphysema in Cigarette Smoke-exposed Mice Is Strain Dependent

Cited by 261 publications

References 40 publications

Relationship of strain-dependent susceptibility to experimentally induced acute pancreatitis with regulation of Prss1 and Spink3 expression

Relationship of strain-dependent susceptibility to experimentally induced acute pancreatitis with regulation of Prss1 and Spink3 expression

Chronic smoke exposure induces rheumatoid factor and anti‐heat shock protein 70 autoantibodies in susceptible mice and humans with lung disease

Cigarette Smoke Exposure as a Model of Inflammation Associated with COPD

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