PMID- 22288595
OWN - NLM
STAT- MEDLINE
DCOM- 20120322
LR  - 20211021
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 167
IP  - 3
DP  - 2012 Mar
TI  - Surfactant protein D inhibits lipopolysaccharide-induced monocyte chemoattractant 
      protein-1 expression in human renal tubular epithelial cells: implication for 
      tubulointerstitial fibrosis.
PG  - 514-22
LID - 10.1111/j.1365-2249.2011.04521.x [doi]
AB  - Surfactant protein D (SP-D), a member of the C-type lectin (collectin) protein 
      family, plays a critical role in innate host defence against various microbial 
      pathogens and in the modulation of inflammatory responses in the lung. However, 
      little is known about its expression and biological function in the kidney. In 
      this work, we studied SP-D expression in human kidney and cultured human renal 
      proximal tubular epithelial cells (HK-2), and examined the effect of SP-D on 
      proinflammatory cytokine production after lipopolysaccharide (LPS) stimulus. We 
      observed the expression of both SP-D mRNA and protein in human kidney and 
      in-vitro HK-2 cells by immunohistochemistry, Western blot analysis, reverse 
      transcription-polymerase chain reaction (RT-PCR) and real-time PCR. To explore 
      the potential role of SP-D in the pathogenesis of tubulointerstitial fibrosis in 
      kidney infection, we examined the production of monocyte chemoattractant 
      protein-1 (MCP-1) in HK-2 cells after LPS treatment. Results showed that the 
      level of MCP-1 in the conditioned medium increased significantly when HK-2 cells 
      were cultured with LPS (>0.1 microg/ml) for 8 h. Of interest, LPS treatment inhibited 
      SP-D expression in HK-2 cells. Furthermore, over-expression of SP-D reduced 
      significantly the LPS-induced expression of MCP-1 in transfected cells. These 
      findings suggest that SP-D in the kidney functions as an anti-inflammatory factor 
      in renal tubular epithelial cells and may modulate tubulointerstitial fibrosis in 
      kidney.
CI  - (c) 2011 The Authors. Clinical and Experimental Immunology (c) 2011 British Society 
      for Immunology.
FAU - Hu, F
AU  - Hu F
AD  - Division of Nephrology, Department of Medicine, Renmin Hospital of Wuhan 
      University, Wuhan, China.
FAU - Liang, W
AU  - Liang W
FAU - Ren, Z
AU  - Ren Z
FAU - Wang, G
AU  - Wang G
FAU - Ding, G
AU  - Ding G
LA  - eng
GR  - R21 HL096007/HL/NHLBI NIH HHS/United States
GR  - HL096007/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Pulmonary Surfactant-Associated Protein D)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Proteins)
SB  - IM
MH  - Base Sequence
MH  - Cell Line
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Culture Media, Conditioned
MH  - Epithelial Cells/drug effects/immunology/metabolism
MH  - Fibrosis
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Kidney Diseases/etiology/genetics/metabolism/pathology
MH  - Kidney Tubules/cytology/drug effects/*immunology/*metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Pulmonary Surfactant-Associated Protein D/genetics/*metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Recombinant Proteins/genetics/metabolism
MH  - Transfection
PMC - PMC3374284
EDAT- 2012/02/01 06:00
MHDA- 2012/03/23 06:00
PMCR- 2013/03/01
CRDT- 2012/02/01 06:00
PHST- 2012/02/01 06:00 [entrez]
PHST- 2012/02/01 06:00 [pubmed]
PHST- 2012/03/23 06:00 [medline]
PHST- 2013/03/01 00:00 [pmc-release]
AID - 10.1111/j.1365-2249.2011.04521.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2012 Mar;167(3):514-22. doi: 10.1111/j.1365-2249.2011.04521.x.