PMID- 25152078
OWN - NLM
STAT- MEDLINE
DCOM- 20160329
LR  - 20211021
IS  - 2042-0226 (Electronic)
IS  - 1672-7681 (Print)
IS  - 1672-7681 (Linking)
VI  - 12
IP  - 4
DP  - 2015 Jul
TI  - HMGB1 contributes to allergen-induced airway remodeling in a murine model of 
      chronic asthma by modulating airway inflammation and activating lung fibroblasts.
PG  - 409-23
LID - 10.1038/cmi.2014.60 [doi]
AB  - The pro-inflammation factor high-mobility group box protein 1 (HMGB1) has been 
      implicated in the pathogenesis of asthma. In this study, we used a murine model 
      of chronic asthma to evaluate the effects of HMGB1 on airway remodeling. Female 
      BALB/c mice were randomly divided into four groups: control, ovalbumin (OVA) 
      asthmatic, OVA+isotype antibody and OVA+anti-HMGB1 antibody. Anti-HMGB1 antibody 
      therapy was started on day 21 and was administered three times per week for 6 
      weeks before intranasal challenge with OVA. In this mouse model, HMGB1 expression 
      is significantly elevated. The anti-HMGB1 antibody group exhibited decreased 
      levels of immunoglobulin E (IgE) and inflammatory mediators and reduced 
      inflammatory cell accumulation, airway hyperresponsiveness (AHR), mucus 
      synthesis, smooth muscle thickness and lung collagen content compared with the 
      OVA groups. Treatment with HMGB1 increased proliferation, migration, collagen 
      secretion and alpha-smooth muscle actin (SMA) expression in MRC-5 cells. Treatment 
      with the HMGB1/IL-1beta complex significantly increased the expression and secretion 
      of transforming growth factor (TGF-beta1), matrix metalloproteinase (MMP)-9 and 
      vascular endothelial growth factor (VEGF). Altogether, these results suggest that 
      blocking HMGB1 activity may reverse airway remodeling by suppressing airway 
      inflammation and modulating lung fibroblast phenotype and activation.
FAU - Hou, Changchun
AU  - Hou C
FAU - Kong, Jinliang
AU  - Kong J
FAU - Liang, Yue
AU  - Liang Y
FAU - Huang, Hong
AU  - Huang H
FAU - Wen, Hanchun
AU  - Wen H
FAU - Zheng, Xiaowen
AU  - Zheng X
FAU - Wu, Lihong
AU  - Wu L
FAU - Chen, Yiqiang
AU  - Chen Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140825
PL  - China
TA  - Cell Mol Immunol
JT  - Cellular & molecular immunology
JID - 101242872
RN  - 0 (Actins)
RN  - 0 (HMGB1 Protein)
RN  - 0 (HMGB1 protein, mouse)
RN  - 0 (IL1B protein, mouse)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Tgfb1 protein, mouse)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (vascular endothelial growth factor A, mouse)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
RN  - EC 3.4.24.35 (Mmp9 protein, mouse)
SB  - IM
MH  - Actins/immunology
MH  - Animals
MH  - Asthma/chemically induced/*immunology/pathology
MH  - Cell Line
MH  - Cell Movement/*immunology
MH  - *Cell Proliferation
MH  - Chronic Disease
MH  - Disease Models, Animal
MH  - Female
MH  - Fibroblasts/*immunology/pathology
MH  - HMGB1 Protein/*immunology
MH  - Immunoglobulin E/immunology
MH  - Inflammation Mediators/immunology
MH  - Interleukin-1beta/immunology
MH  - Lung/*immunology/pathology
MH  - Matrix Metalloproteinase 9/immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Transforming Growth Factor beta1/immunology
MH  - Vascular Endothelial Growth Factor A/immunology
PMC - PMC4496537
EDAT- 2014/08/26 06:00
MHDA- 2016/03/30 06:00
PMCR- 2015/07/01
CRDT- 2014/08/26 06:00
PHST- 2013/12/18 00:00 [received]
PHST- 2014/06/11 00:00 [revised]
PHST- 2014/06/15 00:00 [accepted]
PHST- 2014/08/26 06:00 [entrez]
PHST- 2014/08/26 06:00 [pubmed]
PHST- 2016/03/30 06:00 [medline]
PHST- 2015/07/01 00:00 [pmc-release]
AID - cmi201460 [pii]
AID - 10.1038/cmi.2014.60 [doi]
PST - ppublish
SO  - Cell Mol Immunol. 2015 Jul;12(4):409-23. doi: 10.1038/cmi.2014.60. Epub 2014 Aug 
      25.