PMID- 26014805
OWN - NLM
STAT- MEDLINE
DCOM- 20160712
LR  - 20150925
IS  - 1600-0625 (Electronic)
IS  - 0906-6705 (Linking)
VI  - 24
IP  - 10
DP  - 2015 Oct
TI  - Impairment of skin barrier function via cholinergic signal transduction in a 
      dextran sulphate sodium-induced colitis mouse model.
PG  - 779-84
LID - 10.1111/exd.12775 [doi]
AB  - Dry skin has been clinically associated with visceral diseases, including liver 
      disease, as well as for our previously reported small intestinal injury mouse 
      model, which have abnormalities in skin barrier function. To clarify this 
      disease-induced skin disruption, we used a dextran sulphate sodium (DSS)-induced 
      colitis mouse model. Following treatment with DSS, damage to the colon and skin 
      was monitored using histological and protein analysis methods as well as the 
      detection of inflammatory mediators in the plasma. Notably, transepidermal water 
      loss was higher, and skin hydration was lower in DSS-treated mice compared to 
      controls. Tumor necrosis factor-alpha (TNF-alpha), interleukin 6 and NO2-/NO3- levels 
      were also upregulated in the plasma, and a decrease in body weight and colon 
      length was observed in DSS-treated mice. However, when administered TNF-alpha 
      antibody or an iNOS inhibitor, no change in skin condition was observed, 
      indicating that another signalling mechanism is utilized. Interestingly, the 
      number of tryptase-expressing mast cells, known for their role in immune function 
      via cholinergic signal transduction, was elevated. To evaluate the function of 
      cholinergic signalling in this context, atropine (a muscarinic cholinoceptor 
      antagonist) or hexamethonium (a nicotinic cholinergic ganglion-blocking agent) 
      was administered to DSS-treated mice. Our data indicate that muscarinic 
      acetylcholine receptors (mAChRs) are the primary receptors functioning in 
      colon-to-skin signal transduction, as DSS-induced skin disruption was suppressed 
      by atropine. Thus, skin disruption is likely associated with DSS-induced colitis, 
      and the activation of mast cells via mAChRs is critical to this association.
CI  - (c) 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Yokoyama, Satoshi
AU  - Yokoyama S
AD  - Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Mie, 
      Japan.
FAU - Hiramoto, Keiichi
AU  - Hiramoto K
AD  - Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Mie, 
      Japan.
FAU - Koyama, Mayu
AU  - Koyama M
AD  - Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Mie, 
      Japan.
FAU - Ooi, Kazuya
AU  - Ooi K
AD  - Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, Mie, 
      Japan.
LA  - eng
PT  - Journal Article
DEP - 20150818
PL  - Denmark
TA  - Exp Dermatol
JT  - Experimental dermatology
JID - 9301549
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Interleukin-6)
RN  - 0 (Muscarinic Antagonists)
RN  - 0 (Nicotinic Antagonists)
RN  - 0 (Nitrates)
RN  - 0 (Receptors, Muscarinic)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 3C9PSP36Z2 (Hexamethonium)
RN  - 7C0697DR9I (Atropine)
RN  - 9042-14-2 (Dextran Sulfate)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - S7G510RUBH (Nitrogen Dioxide)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/pharmacology
MH  - Atropine/pharmacology
MH  - Cell Count
MH  - Colitis/chemically induced/complications/*physiopathology
MH  - Colon/pathology/*physiopathology
MH  - Dextran Sulfate
MH  - Disease Models, Animal
MH  - Enzyme Inhibitors/pharmacology
MH  - Hexamethonium/pharmacology
MH  - Interleukin-6/blood
MH  - Male
MH  - Mast Cells
MH  - Mice
MH  - Muscarinic Antagonists/pharmacology
MH  - Nicotinic Antagonists/pharmacology
MH  - Nitrates/blood
MH  - Nitric Oxide Synthase Type II/antagonists & inhibitors/metabolism
MH  - Nitrogen Dioxide/blood
MH  - Organ Size
MH  - Receptors, Muscarinic/drug effects/*metabolism
MH  - Signal Transduction/*drug effects
MH  - Skin Diseases/etiology/pathology/*physiopathology
MH  - Skin Physiological Phenomena/*drug effects
MH  - Tumor Necrosis Factor-alpha/blood/immunology
MH  - Water Loss, Insensible
MH  - Weight Loss
OTO - NOTNLM
OT  - acetylcholine receptor
OT  - colitis
OT  - mast cell
OT  - skin hydration
OT  - transepidermal water loss
EDAT- 2015/05/28 06:00
MHDA- 2016/07/13 06:00
CRDT- 2015/05/28 06:00
PHST- 2015/05/19 00:00 [accepted]
PHST- 2015/05/28 06:00 [entrez]
PHST- 2015/05/28 06:00 [pubmed]
PHST- 2016/07/13 06:00 [medline]
AID - 10.1111/exd.12775 [doi]
PST - ppublish
SO  - Exp Dermatol. 2015 Oct;24(10):779-84. doi: 10.1111/exd.12775. Epub 2015 Aug 18.