PMID- 19528036
OWN - NLM
STAT- MEDLINE
DCOM- 20100408
LR  - 20220310
IS  - 1468-3288 (Electronic)
IS  - 0017-5749 (Print)
IS  - 0017-5749 (Linking)
VI  - 59
IP  - 1
DP  - 2010 Jan
TI  - Local B cells and IgE production in the oesophageal mucosa in eosinophilic 
      oesophagitis.
PG  - 12-20
LID - 10.1136/gut.2009.178020 [doi]
AB  - BACKGROUND: Eosinophilic oesophagitis (EO) is an emerging yet increasingly 
      prevalent disorder characterised by a dense and selective eosinophilic 
      infiltration of the oesophageal wall. While EO is considered an atopic disease 
      primarily triggered by food antigens, disparities between standard allergen 
      testing and clinical responses to exclusion diets suggest the participation of 
      distinct antigen-specific immunoglobulin E (IgE) in the pathophysiology of EO. 
      AIM: To find evidence for a local IgE response. METHODS: Endoscopic biopsies of 
      the distal oesophagus of atopic and non-atopic EO and control individuals (CTL) 
      were processed for immunohistochemistry and immunofluorescence to assess the 
      presence of B cells, mast cells, and IgE-bearing cells. Oesophageal RNA was 
      analysed for the expression of genes involved in B cell activation, class switch 
      recombination to IgE and IgE production, including germline transcripts (GLTs), 
      activation-induced cytidine deaminase (AID), IgE heavy chain (Cepsilon) and 
      mature IgE mRNA using polymerase chain reaction and microarray analysis. RESULTS: 
      Regardless of atopy, EO showed increased density of B cells (p<0.05) and of 
      IgE-bounded mast cells compared to CTL. Both EO and CTL expressed muGLT, 
      epsilonGLT, gamma4GLT, AID, Cepsilon and IgE mRNA. However, the frequency of 
      expression of total GLTs (p = 0.002), epsilonGLT (p = 0.024), and Cepsilon (p = 
      0.0003) was significantly higher in EO than in CTL, independent of the atopic 
      status. CONCLUSION: These results support the heretofore unproven occurrence of 
      both local immunoglobulin class switching to IgE and IgE production in the 
      oesophageal mucosa of EO patients. Sensitisation and activation of mast cells 
      involving local IgE may therefore critically contribute to disease pathogenesis.
FAU - Vicario, M
AU  - Vicario M
AD  - Division of Allergy and Immunology, Department of Pediatrics, Cincinnati 
      Children's Hospital Medical Center, University of Cincinnati College of Medicine, 
      Cincinnati, Ohio, USA.
FAU - Blanchard, C
AU  - Blanchard C
FAU - Stringer, K F
AU  - Stringer KF
FAU - Collins, M H
AU  - Collins MH
FAU - Mingler, M K
AU  - Mingler MK
FAU - Ahrens, A
AU  - Ahrens A
FAU - Putnam, P E
AU  - Putnam PE
FAU - Abonia, J P
AU  - Abonia JP
FAU - Santos, J
AU  - Santos J
FAU - Rothenberg, M E
AU  - Rothenberg ME
LA  - eng
GR  - Z01 NR000014/ImNIH/Intramural NIH HHS/United States
GR  - R37 AI045898/AI/NIAID NIH HHS/United States
GR  - R01 AI045898/AI/NIAID NIH HHS/United States
GR  - U19 AI070235/AI/NIAID NIH HHS/United States
GR  - R01 DK076893/DK/NIDDK NIH HHS/United States
GR  - R21 AI079874/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Gut
JT  - Gut
JID - 2985108R
RN  - 0 (Interleukin-13)
RN  - 0 (RNA, Messenger)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
CIN - Gut. 2010 Jan;59(1):6-7. PMID: 20007954
MH  - Adolescent
MH  - B-Lymphocytes/*immunology
MH  - Cell Count
MH  - Child
MH  - Child, Preschool
MH  - Eosinophilia/*immunology
MH  - Esophagitis/*immunology
MH  - Esophagus/immunology
MH  - Female
MH  - Humans
MH  - Hypersensitivity, Immediate/*immunology
MH  - Immunoglobulin E/*biosynthesis/genetics
MH  - Interleukin-13/biosynthesis
MH  - Interleukin-4/biosynthesis
MH  - Lymphocyte Activation/immunology
MH  - Male
MH  - Mast Cells/immunology
MH  - Mucous Membrane/immunology
MH  - Oligonucleotide Array Sequence Analysis/methods
MH  - Polymerase Chain Reaction/methods
MH  - RNA, Messenger/genetics
MH  - Retrospective Studies
MH  - Transcription, Genetic
PMC - PMC2791234
COIS- Competing interests: MER receives financial and/or stock compensation as a 
      consultant and/or speaker for Merck, Ception Therapeutics, Novartis, Nycomed, and 
      Centocor. The other authors have no competing interests.
EDAT- 2009/06/17 09:00
MHDA- 2010/04/09 06:00
PMCR- 2009/06/14
CRDT- 2009/06/17 09:00
PHST- 2009/06/17 09:00 [entrez]
PHST- 2009/06/17 09:00 [pubmed]
PHST- 2010/04/09 06:00 [medline]
PHST- 2009/06/14 00:00 [pmc-release]
AID - gut.2009.178020 [pii]
AID - gt178020 [pii]
AID - 10.1136/gut.2009.178020 [doi]
PST - ppublish
SO  - Gut. 2010 Jan;59(1):12-20. doi: 10.1136/gut.2009.178020.