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Characterization of the acute inflammatory profile and resolution of airway inflammation after Igf1r-gene targeting in a murine model of HDM-induced asthma.

Abstract Asthma is a chronic inflammatory disease characterized by bronchial hyperresponsiveness, mucus overproduction and airway remodeling. Notably, we have recently demonstrated that insulin-like growth factor 1 receptor (IGF1R) deficiency in mice attenuates airway hyperresponsiveness and mucus secretion after chronic house dust mite (HDM) exposure. On this basis, inbred C57BL/6 and Igf1r-deficient mice were given HDM extract to study the acute inflammatory profile and implication of Igf1r in acute asthma pathobiology. Additionally, Igf1r-deficiency was therapeutically induced in mice to evaluate the resolution of HDM-induced inflammation. Acute HDM exposure in inbred C57BL/6 mice led to a progressive increase in inflammation, airway remodeling and associated molecular indicators. Preventively-induced Igf1r-deficiency showed reduced neutrophil and eosinophil numbers in BALF and bone marrow, a significant reduction of airway remodeling and decreased levels of related markers. In addition, therapeutic targeting of Igf1r promoted the resolution of HDM-induced-inflammation. Our results demonstrate for the first time that Igf1r is important in acute asthma pathobiology and resolution of HDM-induced inflammation. Thus, IGF1R is suggested to be a promising candidate for future therapeutic approaches for the treatment and prevention of asthma.
PMID
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Attenuated airway hyperresponsiveness and mucus secretion in HDM-exposed Igf1r-deficient mice.

Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start


 


PMID- 29272313
OWN - NLM
STAT- In-Process
LR  - 20180111
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 12
DP  - 2017
TI  - Characterization of the acute inflammatory profile and resolution of airway
      inflammation after Igf1r-gene targeting in a murine model of HDM-induced asthma.
PG  - e0190159
LID - 10.1371/journal.pone.0190159 [doi]
AB  - Asthma is a chronic inflammatory disease characterized by bronchial
      hyperresponsiveness, mucus overproduction and airway remodeling. Notably, we have
      recently demonstrated that insulin-like growth factor 1 receptor (IGF1R)
      deficiency in mice attenuates airway hyperresponsiveness and mucus secretion
      after chronic house dust mite (HDM) exposure. On this basis, inbred C57BL/6 and
      Igf1r-deficient mice were given HDM extract to study the acute inflammatory
      profile and implication of Igf1r in acute asthma pathobiology. Additionally,
      Igf1r-deficiency was therapeutically induced in mice to evaluate the resolution
      of HDM-induced inflammation. Acute HDM exposure in inbred C57BL/6 mice led to a
      progressive increase in inflammation, airway remodeling and associated molecular 
      indicators. Preventively-induced Igf1r-deficiency showed reduced neutrophil and
      eosinophil numbers in BALF and bone marrow, a significant reduction of airway
      remodeling and decreased levels of related markers. In addition, therapeutic
      targeting of Igf1r promoted the resolution of HDM-induced-inflammation. Our
      results demonstrate for the first time that Igf1r is important in acute asthma
      pathobiology and resolution of HDM-induced inflammation. Thus, IGF1R is suggested
      to be a promising candidate for future therapeutic approaches for the treatment
      and prevention of asthma.
FAU - Pineiro-Hermida, Sergio
AU  - Pineiro-Hermida S
AD  - Lung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de
      la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, Spain.
FAU - Alfaro-Arnedo, Elvira
AU  - Alfaro-Arnedo E
AD  - Lung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de
      la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, Spain.
FAU - Gregory, Joshua A
AU  - Gregory JA
AD  - Unit of Experimental Asthma and Allergy Research, Karolinska Institutet,
      Institute of Environmental Medicine (IMM), Stockholm, Sweden.
FAU - Torrens, Raquel
AU  - Torrens R
AD  - Lung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de
      la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, Spain.
FAU - Ruiz-Martinez, Carlos
AU  - Ruiz-Martinez C
AD  - Pneumology Service, Hospital San Pedro, Logrono, Spain.
FAU - Adner, Mikael
AU  - Adner M
AD  - Unit of Experimental Asthma and Allergy Research, Karolinska Institutet,
      Institute of Environmental Medicine (IMM), Stockholm, Sweden.
FAU - Lopez, Iciar P
AU  - Lopez IP
AD  - Lung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de
      la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, Spain.
FAU - Pichel, Jose G
AU  - Pichel JG
AUID- ORCID: 0000-0001-8580-0952
AD  - Lung Cancer and Respiratory Diseases Unit, Centro de Investigacion Biomedica de
      la Rioja (CIBIR), Fundacion Rioja Salud, Logrono, Spain.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171222
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
PMC - PMC5741234
EDAT- 2017/12/23 06:00
MHDA- 2017/12/23 06:00
CRDT- 2017/12/23 06:00
PHST- 2017/10/06 00:00 [received]
PHST- 2017/12/08 00:00 [accepted]
PHST- 2017/12/23 06:00 [entrez]
PHST- 2017/12/23 06:00 [pubmed]
PHST- 2017/12/23 06:00 [medline]
AID - 10.1371/journal.pone.0190159 [doi]
AID - PONE-D-17-36069 [pii]
PST - epublish
SO  - PLoS One. 2017 Dec 22;12(12):e0190159. doi: 10.1371/journal.pone.0190159.
      eCollection 2017.