PMID- 23285227
OWN - NLM
STAT- MEDLINE
DCOM- 20130723
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 12
DP  - 2012
TI  - Opposite role of tumor necrosis factor receptors in dextran sulfate 
      sodium-induced colitis in mice.
PG  - e52924
LID - 10.1371/journal.pone.0052924 [doi]
LID - e52924
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a key factor for the pathogenesis of 
      inflammatory bowel diseases (IBD), whose function is known to be mediated by TNF 
      receptor 1 (TNFR1) or 2. However, the precise role of the two receptors in IBD 
      remains poorly understood. Herein, acute colitis was induced by dextran sulfate 
      sodium (DSS) instillation in TNFR1 or 2-/- mice. TNFR1 ablation led to 
      exacerbation of signs of colitis, including more weight loss, increased 
      mortality, colon shortening and oedema, severe intestinal damage, and higher 
      levels of myeloperoxidase compared to wild-type counterparts. While, TNFR2 
      deficiency had opposite effects. This discrepancy was reflected by alteration of 
      proinflammatory cytokine and chemokine production in the colons. Importantly, 
      TNFR1 ablation rendered enhanced apoptosis of colonic epithelial cells and TNFR2 
      deficiency conferred pro-apoptotic effects of lamina propria (LP)-immune cells, 
      as shown by the decreased ratio of Bcl-2/Bax and enhanced nuclear factor (NF)-kappaB 
      activity.
FAU - Wang, Ke
AU  - Wang K
AD  - Department of Immunology, School of Basic Medical Sciences, Central South 
      University, Changsha, P. R. China.
FAU - Han, Gencheng
AU  - Han G
FAU - Dou, Yan
AU  - Dou Y
FAU - Wang, Yi
AU  - Wang Y
FAU - Liu, Guijun
AU  - Liu G
FAU - Wang, Renxi
AU  - Wang R
FAU - Xiao, He
AU  - Xiao H
FAU - Li, Xinying
AU  - Li X
FAU - Hou, Chunmei
AU  - Hou C
FAU - Shen, Beifen
AU  - Shen B
FAU - Guo, Renfeng
AU  - Guo R
FAU - Li, Yan
AU  - Li Y
FAU - Shi, Yanchun
AU  - Shi Y
FAU - Chen, Guojiang
AU  - Chen G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121228
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9042-14-2 (Dextran Sulfate)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/genetics
MH  - Cells, Cultured
MH  - Dextran Sulfate/pharmacology
MH  - Inflammatory Bowel Diseases/chemically induced/genetics/*metabolism
MH  - Intestinal Mucosa/drug effects/metabolism/physiology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Receptors, Tumor Necrosis Factor, Type I/genetics/*physiology
MH  - Receptors, Tumor Necrosis Factor, Type II/genetics/metabolism/*physiology
MH  - Survival Analysis
MH  - Tumor Necrosis Factor-alpha/pharmacology/physiology
MH  - Weight Loss/genetics
PMC - PMC3532169
COIS- Competing Interests: The authors have the following interests. Renfeng Guo is an 
      employee of InflaRx GmbH. There are no patents, products in development or 
      marketed products to declare. This does not alter the authors' adherence to all 
      the PLOS ONE policies on sharing data and materials, as detailed online in the 
      guide for authors.
EDAT- 2013/01/04 06:00
MHDA- 2013/07/24 06:00
PMCR- 2012/12/28
CRDT- 2013/01/04 06:00
PHST- 2012/09/21 00:00 [received]
PHST- 2012/11/21 00:00 [accepted]
PHST- 2013/01/04 06:00 [entrez]
PHST- 2013/01/04 06:00 [pubmed]
PHST- 2013/07/24 06:00 [medline]
PHST- 2012/12/28 00:00 [pmc-release]
AID - PONE-D-12-28897 [pii]
AID - 10.1371/journal.pone.0052924 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(12):e52924. doi: 10.1371/journal.pone.0052924. Epub 2012 Dec 28.