PMID- 18541446
OWN - NLM
STAT- MEDLINE
DCOM- 20081110
LR  - 20181201
IS  - 1065-6995 (Print)
IS  - 1065-6995 (Linking)
VI  - 32
IP  - 9
DP  - 2008 Sep
TI  - Inhibition of lipopolysaccharide-mediated rat alveolar macrophage activation in 
      vitro by antiflammin-1.
PG  - 1108-15
LID - 10.1016/j.cellbi.2008.04.023 [doi]
AB  - Antiflammin-1 (AF-1) is a synthetic nonapeptide with a similar sequence to the 
      conserved sequence of CC10 secreted by lung Clara cells. Studies suggest that it 
      is potent inhibitor of inflammation. We investigated the effects and possible 
      mechanisms of AF-1 on LPS-induced alveolar macrophage (AM) activation in vitro. 
      AMs harvested from the BALF of Sprague-Dawley (SD) rat were treated with various 
      concentrations of AF-1 both simultaneously and after LPS stimulation. The 
      concentrations of the cytokines IL-1beta, IL-6, and IL-10 in the supernatant were 
      detected by an enzyme-linked immunosorbent assay. The mRNA expression levels of 
      these cytokines in AMs were analyzed using quantitative RT-PCR. To investigate 
      more fully the possible mechanisms by which AF-1 modulates the expression of 
      cytokines, cells were pretreated with anti-IL-10 antibody. Toll-like receptor-4 
      (TLR-4) expression on the cell surface was also detected using flow cytometry. 
      The results showed that AF-1 suppressed mRNA expression and protein production of 
      IL-1beta and IL-6, while it promoted IL-10 expression in LPS-stimulated AMs, in a 
      dose-dependent manner. The inhibitory effects of AF-1 on IL-1beta were 
      significantly decreased when endogenous production of IL-10 was blocked. AF-1 
      also showed an effect on downregulated TLR-4 expression in LPS-stimulated AMs. 
      The data show for the first time that AF-1 modulates the AM response to LPS by 
      regulating TLR-4 expression and upregulating IL-10 secretion, which could be 
      another important mechanism in the AF-1 inhibiting effect on inflammation.
FAU - Han, Jianzhong
AU  - Han J
AD  - Department of Physiology, Xiang-Ya Medical School, Central South University, 110 
      Xiangya Road, Changsha, PR China.
FAU - Li, Chen
AU  - Li C
FAU - Liu, Huijun
AU  - Liu H
FAU - Fen, Dandan
AU  - Fen D
FAU - Hu, Wanxiang
AU  - Hu W
FAU - Liu, Yong
AU  - Liu Y
FAU - Guan, Chaxiang
AU  - Guan C
FAU - Luo, Zi-Qiang
AU  - Luo ZQ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080502
PL  - England
TA  - Cell Biol Int
JT  - Cell biology international
JID - 9307129
RN  - 0 (Cytokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Peptide Fragments)
RN  - 0 (RNA, Messenger)
RN  - 0 (Toll-Like Receptor 4)
RN  - 118850-71-8 (antiflammin P1)
RN  - 9060-09-7 (Uteroglobin)
SB  - IM
MH  - Animals
MH  - Cell Membrane/drug effects/metabolism
MH  - Cytokines/genetics/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Flow Cytometry
MH  - Gene Expression Regulation/drug effects
MH  - Inflammation Mediators/metabolism
MH  - Lipopolysaccharides/*pharmacology
MH  - Macrophage Activation/*drug effects
MH  - Macrophages, Alveolar/*cytology/*drug effects/metabolism
MH  - Peptide Fragments/*pharmacology
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Toll-Like Receptor 4/metabolism
MH  - Uteroglobin/*pharmacology
EDAT- 2008/06/11 09:00
MHDA- 2008/11/11 09:00
CRDT- 2008/06/11 09:00
PHST- 2007/12/13 00:00 [received]
PHST- 2008/03/11 00:00 [revised]
PHST- 2008/04/25 00:00 [accepted]
PHST- 2008/06/11 09:00 [pubmed]
PHST- 2008/11/11 09:00 [medline]
PHST- 2008/06/11 09:00 [entrez]
AID - S1065-6995(08)00442-3 [pii]
AID - 10.1016/j.cellbi.2008.04.023 [doi]
PST - ppublish
SO  - Cell Biol Int. 2008 Sep;32(9):1108-15. doi: 10.1016/j.cellbi.2008.04.023. Epub 
      2008 May 2.