Summary of Study ST002355

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001512. The data can be accessed directly via it's Project DOI: 10.21228/M8812G This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002355
Study TitleStool short chain fatty acid (SCFA) levels in peanut allergy
Study SummaryPrior evidence supports differential levels of short chain fatty acids in the stool of human beings with allergy and murine models of allergy. Here we performed a targeted study of selected short chain fatty acid levels in stool samples collected from children with allergy risk factors. Sample processing included homogenization of stool samples, inclusion of internal standards, and derivitization for liquid chromatography tandem mass spectrometry.
Institute
Icahn School of Medicine at Mount Sinai
Last NameBunyavanich
First NameSupinda
Address1 Gustave L. Levy Pl, New York, NY 10029
Emailsupinda.bunyavanich@mssm.edu
PhoneStool metabolite levels in individuals with peanut allergy were measured.
Submit Date2022-11-08
Raw Data AvailableYes
Raw Data File Type(s)mzXML
Analysis Type DetailLC-MS
Release Date2023-12-08
Release Version1
Supinda Bunyavanich Supinda Bunyavanich
https://dx.doi.org/10.21228/M8812G
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:

Project:

Project ID:PR001512
Project DOI:doi: 10.21228/M8812G
Project Title:Stool metabolites in peanut allergy
Project Summary:Rising rates of peanut allergy motivate investigations of its development to inform prevention and therapy. Microbiota and the metabolites they produce shape food allergy risk. We performed a longitudinal, multi-center, integrative study of the gut microbiome and metabolome of 122 infants with allergy risk factors but no peanut allergy who were followed through mid childhood. 28.7% of infants developed peanut allergy by mid-childhood. Lower infant gut microbiome diversity was associated with peanut allergy development (P=0.014). Peanut allergy-bound children had different abundance trajectories of Clostridium sensu stricto 1 sp. (FDR=0.015) and Bifidobacterium sp. (FDR=0.033), with butyrate (FDR=0.045) and isovalerate (FDR=0.036) decreasing over time. Metabolites associated with peanut allergy development clustered within the histidine metabolism pathway. Positive correlations between microbiota, butyrate, and isovalerate and negative correlations with histamine marked the peanut allergy free network. The temporal dynamics of the gut microbiome and metabolome in early childhood are distinct for children who develop peanut allergy.
Institute:Icahn School of Medicine at Mount Sinai
Last Name:Bunyavanich
First Name:Supinda
Address:1 Gustave L. Levy Pl, New York, NY 10029
Email:supinda.bunyavanich@mssm.edu
Phone:212-241-5548

Subject:

Subject ID:SU002444
Subject Type:Human
Subject Species:Homo sapiens
Taxonomy ID:9606

Factors:

Subject type: Human; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Treatment
SA236736100003306control_infant
SA236737100003322control_infant
SA236738100003016control_infant
SA236739100008020control_infant
SA236740100003423control_infant
SA236741100003757control_infant
SA236742100004390control_infant
SA236743100004274control_infant
SA236744100003178control_infant
SA236745100039012control_infant
SA236746100003157control_infant
SA236747100005050control_infant
SA236748100005108control_infant
SA236749100005426control_infant
SA236750100009111control_infant
SA236751100003336control_infant
SA236752100003417control_infant
SA236753100009308control_infant
SA236754100004372control_infant
SA236755100007026control_infant
SA236756100007013control_infant
SA236757100039015control_infant
SA236758100004304control_infant
SA236759100008017control_infant
SA236760100009114control_infant
SA236761100002299control_infant
SA236762100005009control_infant
SA236763100002095control_infant
SA236764100005379control_infant
SA236765100003774control_infant
SA236766100004316control_infant
SA236767100009066control_infant
SA236768100002101control_infant
SA236769100006030control_infant
SA236770100005348control_infant
SA236771100005117control_infant
SA236772100003337control_infant
SA236773100007042control_infant
SA236774100004422control_infant
SA236775100003162control_infant
SA236776120091160control_mid-childhood
SA236777120091162control_mid-childhood
SA236778120091142control_mid-childhood
SA236779120091168control_mid-childhood
SA236780120091011control_mid-childhood
SA236781120091016control_mid-childhood
SA236782120091000control_mid-childhood
SA236783120091161control_mid-childhood
SA236784120091077control_mid-childhood
SA236785120091056control_mid-childhood
SA236786120091076control_mid-childhood
SA236787120091063control_mid-childhood
SA236788120091152control_mid-childhood
SA236789120091039control_mid-childhood
SA236790120091036control_mid-childhood
SA236791120091173control_mid-childhood
SA236792120091174control_mid-childhood
SA236793120091111control_mid-childhood
SA236794120091007control_mid-childhood
SA236795120091003control_mid-childhood
SA236796120091096control_mid-childhood
SA236797120091121control_mid-childhood
SA236798120091019control_mid-childhood
SA236799120091052control_mid-childhood
SA236800120091025control_mid-childhood
SA236801120091123control_mid-childhood
SA236802120091030control_mid-childhood
SA236803120091050control_mid-childhood
SA236804120091178control_mid-childhood
SA236805120091015control_mid-childhood
SA236806120091070control_mid-childhood
SA236807120091075control_mid-childhood
SA236808120091159control_mid-childhood
SA236809120091135control_mid-childhood
SA236810120091153control_mid-childhood
SA236811120091130control_mid-childhood
SA236812120091094control_mid-childhood
SA236813120091029control_mid-childhood
SA236814120091129control_mid-childhood
SA236815120091128control_mid-childhood
SA236816120091013control_mid-childhood
SA236817120091104control_mid-childhood
SA236818120091149control_mid-childhood
SA236819120091017control_mid-childhood
SA236820120091020control_mid-childhood
SA236821120091034control_mid-childhood
SA236822120091059control_mid-childhood
SA236823120091132control_mid-childhood
SA236824120091176control_mid-childhood
SA236825120091062control_mid-childhood
SA236826120091012control_mid-childhood
SA236827120091106control_mid-childhood
SA236828120091051control_mid-childhood
SA236829120091072control_mid-childhood
SA236830120091055control_mid-childhood
SA236831120091008control_mid-childhood
SA236832120091095control_mid-childhood
SA236833120091009control_mid-childhood
SA236834120091046control_mid-childhood
SA236835120091021control_mid-childhood
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Collection:

Collection ID:CO002437
Collection Summary:Participants of this study included 122 children from the multi-center NIAID Consortium for Food Allergy Research (CoFAR) Observational Study (CoFAR2) who provided stool samples at both infancy and mid-childhood (these are the factors listed in the table). The recruitment and clinical characteristics of these CoFAR2 subjects have been previously described. Briefly, 511 children were recruited at age 3 to 15 months from five US sites (New York, NY, Baltimore, MD, Little Rock, AR, Denver, CO, Durham, NC).16 The cohort was designed as a longitudinal study of infants at high risk for developing peanut allergy, and inclusion criteria included likely egg allergy, milk allergy, and/or moderate to severe atopic dermatitis with a positive egg and/or milk skin prick test at enrollment, but no known peanut allergy. 16 Clinical phenotyping of the subjects, including assessments of peanut allergy, egg allergy, milk allergy, and atopic dermatitis, were performed at 6-12 month intervals between enrollment at infancy and mid-childhood (mean age 9 years, SD 0.6 years). All subjects provided stool samples at baseline and were invited to submit a follow up sample at mid-childhood. Stool samples were collected from 492 of the children at baseline and from 122 of the children at mid-childhood. Samples were immediately stored at -80 o C upon receipt.
Sample Type:Feces

Treatment:

Treatment ID:TR002456
Treatment Summary:Children were categorized as PA if they developed peanut allergy by mid-childhood and not peanut allergic (NPA) if they did not develop peanut allergy by mid-childhood. In study design table, subjects were sampled in infancy and then again mid childhood and placed into either PA or NPA for the purpose of this study. Peanut allergy was defined based on: (1) confirmed IgE-mediated reaction (e.g. positive doctor supervised oral food challenge to peanut and sensitization to peanut), or (2) convincing IgEmediated reaction (e.g. convincing reaction and sensitization to peanut) at any visit.16 This was “alternate definition 1” of the parent CoFAR2 study16 . We used this definition rather than the main definition to avoid inclusion of less convincing peanut allergy in case ascertainment, as the main definition16 also included those with peanut sensitization but no history of reaction.

Sample Preparation:

Sampleprep ID:SP002450
Sampleprep Summary:Stool samples were weighed into bead blaster tubes with zircon beads and homogenized in 100% methanol to a final concentration of 10mg/mL including deuterated SCFA internal standards Chun et al. p.22 (CDN Isotopes). 46 Control samples were created by combining sample homogenates into a 1mL of pooled sample (pooled control) or 1mL of methanol (instrument blank). A portion of the pooled control was then subjected to three successive rounds of extraction to deplete SCFAs but retain the insoluble particles to generate null matrix material. A standard curve for the cocktail of SCFAs was prepared in null matrix, and these samples were extracted side-by-side with the study samples and sequence blanks (either methanol or null matrix). The resulting SCFA extracts were then derivatized as described47 for liquid chromatography tandem mass spectrometry (LCMS) with methanol being used instead of acetonitrile. Samples were analyzed with a QExactive HF coupled to a Dionex Ultimate 3000. A Waters BEH C18 column (2.1 x 150mm, 1.7µm) was used with Buffer A as 0.1% formic acid in water, and Buffer B as 0.1%formic acid in acetonitrile. A gradient elution was used (15%B to 55%B in 9 min, 200µL/min) and the mass spectrometer was operated in negative ion mode (HESI, -3.5kV). The order of acquisition was randomized and several control blocks including blanks and external standards were interspersed throughout the run to assess instrument performance and quality control of the derivatization protocol. All analytes were corrected to their respective internal standard, and the resulting ratio was interpolated against the matrix-controlled standard curve to quantify the level of SCFA in each sample. The limit of detection was determined from null-matrix samples for each analyte, and this limit was imputed for any point falling below the limit of detection. The interpolated values were used for the downstream analyses, and the imputed ratio threshold values were used for samples below the limit of detection.

Combined analysis:

Analysis ID AN003846
Analysis type MS
Chromatography type Reversed phase
Chromatography system Thermo Dionex Ultimate 3000 RS
Column Waters Acquity BEH C18 (150 x 2mm,1.7um)
MS Type ESI
MS instrument type Orbitrap
MS instrument name Thermo Q Exactive HF hybrid Orbitrap
Ion Mode POSITIVE
Units Absolute Intensity

Chromatography:

Chromatography ID:CH002848
Chromatography Summary:Previously derivatized short chain fatty acids were separated using RP column in a targeted method. Intrinsic background was accessed by using derivatized blanks and null matrix blanks. Analytes were detected by direct coupling to MS in a targeted PRM method.
Instrument Name:Thermo Dionex Ultimate 3000 RS
Column Name:Waters Acquity BEH C18 (150 x 2mm,1.7um)
Solvent A:100% water; 0.1% formic acid
Solvent B:100% acetonitrile; 0.1% formic acid
Chromatography Type:Reversed phase

MS:

MS ID:MS003588
Analysis ID:AN003846
Instrument Name:Thermo Q Exactive HF hybrid Orbitrap
Instrument Type:Orbitrap
MS Type:ESI
MS Comments:All analytes were corrected to their respective internal standard, and the resulting ratio was interpolated against the matrix-controlled standard curve to quantify the level of SCFA in each sample. The limit of detection was determined from null-matrix samples for each analyte, and this limit was imputed for any point falling below the limit of detection. The interpolated values were used for the downstream analyses, and the imputed ratio threshold values were used for samples below the limit of detection
Ion Mode:POSITIVE
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