Association of neuropeptides with Th1/Th2 balance and allergic sensitization in children.
BACKGROUND
Among neurogenic factors, the neuropeptides have an important regulatory influence on immune system activity and may lead to allergic sensitization.


OBJECTIVE
The aim of our study was to investigate the relationship of the neuropeptides vasoactive intestinal peptide (VIP), somatostatin (SOM) and substance P (SP) on modulation of Th1/Th2 balance and allergic sensitization in children.


METHODS
Within the LISAplus (Life style-Immune system-Allergy) study, blood samples of 321 six-year-old children were analysed for concentration of neuropeptides, Th1 and Th2 cytokines, transcription factors for T cell regulation and suppressors of cytokine signalling. In addition, samples were screened for specific IgE against inhalant and food allergens.


RESULTS
Children with high SOM values showed a Th2 polarization and a reduced expression of FOXP3, the marker for regulatory T cells. High (VIP) levels correlated inversely with the expression of T cell transcription factors (Tbet and SOCS3). In contrast, elevated levels of SP were associated with reduced GATA3 and SOCS3 expression and with increased IFN-gamma concentrations. Allergic sensitization was more prevalent in children with higher SOM and VIP concentrations but not associated with SP levels.


CONCLUSIONS
Our data reveal an association between neuropeptides and modulatory effects on immune cells in vivo, especially on Th1/Th2 balance with a correlation to allergic sensitization in children. We suggest that elevated SOM and VIP concentrations and the inducing factors should be considered as allergy risk factors.
Herberth
G
G
Department of Environmental Immunology, UFZ Centre for Environmental Research Leipzig-Halle, Leipzig, Germany. gunda.herberth@ufz.de
Daegelmann
C
C
Weber
A
A
Röder
S
S
Giese
T
T
Krämer
U
U
Schins
R P F
RP
Behrendt
H
H
Borte
M
M
Lehmann
I
I
D015415:Biomarkers / Q000097:blood; D002648:Child; D005260:Female; D005512:Food Hypersensitivity / Q000276:immunology; D051858:Forkhead Transcription Factors / Q000235:genetics; D050990:GATA3 Transcription Factor / Q000235:genetics; D006801:Humans; D006967:Hypersensitivity / Q000097:blood*; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D015847:Interleukin-4 / Q000097:blood / Q000235:genetics; D015848:Interleukin-5 / Q000097:blood; D016906:Interleukin-9 / Q000097:blood; D016015:Logistic Models; D008297:Male; D009479:Neuropeptides / Q000097:blood*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013004:Somatostatin / Q000097:blood; D013373:Substance P / Q000097:blood; D000071222:Suppressor of Cytokine Signaling 1 Protein; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics; D018417:Th1 Cells / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology*; D014660:Vasoactive Intestinal Peptide / Q000097:blood
D015415:Biomarkers; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D050990:GATA3 Transcription Factor; C494749:GATA3 protein, human; D015848:Interleukin-5; D016906:Interleukin-9; D009479:Neuropeptides; D012333:RNA, Messenger; C108944:SOCS1 protein, human; C106644:SOCS3 protein, human; D000071222:Suppressor of Cytokine Signaling 1 Protein; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D015847:Interleukin-4; D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D007073:Immunoglobulin E; D013004:Somatostatin; D007371:Interferon-gamma