PMID- 30553057
OWN - NLM
STAT- MEDLINE
DCOM- 20190430
LR  - 20190816
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 105
DP  - 2019 Jan
TI  - Anti-inflammatory action of HO-1/CO in human bronchial epithelium in response to 
      cationic polypeptide challenge.
PG  - 205-212
LID - S0161-5890(18)31004-6 [pii]
LID - 10.1016/j.molimm.2018.12.002 [doi]
AB  - Carbon monoxide (CO) is an anti-inflammatory gaseous molecule produced 
      endogenously by heme oxygenases (HOs) HO-1 and HO-2. However, the mechanisms 
      underlying the anti-inflammatory effects of CO in the human bronchial epithelium 
      are still not fully understood. In this study, the cationic peptide 
      poly-l-arginine (PLA) was utilized to induce bronchial epithelial damage and 
      subsequent pro-inflammatory cytokine release in the human bronchial epithelial 
      cell line 16HBE14o-. Expression of both HO-1 and HO-2 after PLA exposure was 
      examined. The polarized secretion of two pro-inflammatory cytokines, interleukin 
      (IL)-6 and IL-8, was determined by ELISA. The anti-inflammatory effects of CO 
      liberated from CO-releasing molecules (CORMs) were examined by both ELISA and 
      western blot analysis. Our results indicate that PLA exposure leads to 
      upregulation of HO-1 expression and p65 NF-kappaB phosphorylation, as well as IL-6 
      and IL-8 release. HO-1 induction by hemin or CORMs significantly suppressed IL-6 
      and IL-8 release. In addition, HO-1 knockdown further increased IL-6 and IL-8 
      release under basal and PLA-stimulated conditions. Our results thereby 
      demonstrate that the HO-1/CO axis exerts significant anti-inflammatory activity 
      during bronchial epithelial damage caused by cationic protein.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Zhang, Rui-Gang
AU  - Zhang RG
AD  - School of Biomedical Sciences, The Chinese University of Hong Kong, China; 
      Department of Physiology, Basic Medical School, Guangdong Medical University, 
      China.
FAU - Pan, Kewu
AU  - Pan K
AD  - School of Biomedical Sciences, The Chinese University of Hong Kong, China.
FAU - Hao, Yuan
AU  - Hao Y
AD  - School of Biomedical Sciences, The Chinese University of Hong Kong, China.
FAU - Yip, Chung-Yin
AU  - Yip CY
AD  - School of Biomedical Sciences, The Chinese University of Hong Kong, China.
FAU - Ko, Wing-Hung
AU  - Ko WH
AD  - School of Biomedical Sciences, The Chinese University of Hong Kong, China. 
      Electronic address: whko@cuhk.edu.hk.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181213
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (CXCL8 protein, human)
RN  - 0 (IL6 protein, human)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Peptides)
RN  - 25212-18-4 (polyarginine)
RN  - 7U1EE4V452 (Carbon Monoxide)
RN  - EC 1.14.14.18 (HMOX1 protein, human)
RN  - EC 1.14.14.18 (Heme Oxygenase (Decyclizing))
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
RN  - EC 1.14.14.18 (heme oxygenase-2)
SB  - IM
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Bronchi/*immunology
MH  - Carbon Monoxide/*pharmacology
MH  - Cell Line
MH  - Heme Oxygenase (Decyclizing)/genetics/immunology
MH  - Heme Oxygenase-1/genetics/*immunology
MH  - Humans
MH  - Interleukin-6/genetics/immunology
MH  - Interleukin-8/genetics/immunology
MH  - Peptides/*pharmacology
MH  - Respiratory Mucosa/*immunology
OTO - NOTNLM
OT  - Anti-inflammation
OT  - Bronchial epithelium
OT  - Carbon monoxide
OT  - Heme oxygenase
OT  - Poly-l-arginine
EDAT- 2018/12/16 06:00
MHDA- 2019/05/01 06:00
CRDT- 2018/12/16 06:00
PHST- 2018/04/23 00:00 [received]
PHST- 2018/09/26 00:00 [revised]
PHST- 2018/12/05 00:00 [accepted]
PHST- 2018/12/16 06:00 [pubmed]
PHST- 2019/05/01 06:00 [medline]
PHST- 2018/12/16 06:00 [entrez]
AID - S0161-5890(18)31004-6 [pii]
AID - 10.1016/j.molimm.2018.12.002 [doi]
PST - ppublish
SO  - Mol Immunol. 2019 Jan;105:205-212. doi: 10.1016/j.molimm.2018.12.002. Epub 2018 
      Dec 13.