Identification of potential inflammation markers for outgrowth of cow’s milk allergy
Issued Date
2025-09-01
Resource Type
eISSN
19326203
Scopus ID
2-s2.0-105015681492
Pubmed ID
40929127
Journal Title
Plos One
Volume
20
Issue
9 September
Rights Holder(s)
SCOPUS
Bibliographic Citation
Plos One Vol.20 No.9 September (2025)
Suggested Citation
Hendrickx D.M., Long M., Wopereis H., van der Molen R.G., Belzer C., Chatchatee P., Nowak-Wegrzyn A., Lange L., Benjaponpitak S., Chong K.W., Sangsupawanich P., van Ampting M.T.J., Oude Nijhuis M.M., Harthoorn L.F., Langford J.E., Knol J., Knipping K., Garssen J., Trendelenburg V., Pesek R., Davis C.M., Muraro A., Erlewyn-Lajeunesse M., Fox A.T., Michaelis L.J., Beyer K., Noimark L., Stiefel G., Schauer U., Hamelmann E., Peroni D., Boner A. Identification of potential inflammation markers for outgrowth of cow’s milk allergy. Plos One Vol.20 No.9 September (2025). doi:10.1371/journal.pone.0331462 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/112112
Title
Identification of potential inflammation markers for outgrowth of cow’s milk allergy
Author(s)
Hendrickx D.M.
Long M.
Wopereis H.
van der Molen R.G.
Belzer C.
Chatchatee P.
Nowak-Wegrzyn A.
Lange L.
Benjaponpitak S.
Chong K.W.
Sangsupawanich P.
van Ampting M.T.J.
Oude Nijhuis M.M.
Harthoorn L.F.
Langford J.E.
Knol J.
Knipping K.
Garssen J.
Trendelenburg V.
Pesek R.
Davis C.M.
Muraro A.
Erlewyn-Lajeunesse M.
Fox A.T.
Michaelis L.J.
Beyer K.
Noimark L.
Stiefel G.
Schauer U.
Hamelmann E.
Peroni D.
Boner A.
Long M.
Wopereis H.
van der Molen R.G.
Belzer C.
Chatchatee P.
Nowak-Wegrzyn A.
Lange L.
Benjaponpitak S.
Chong K.W.
Sangsupawanich P.
van Ampting M.T.J.
Oude Nijhuis M.M.
Harthoorn L.F.
Langford J.E.
Knol J.
Knipping K.
Garssen J.
Trendelenburg V.
Pesek R.
Davis C.M.
Muraro A.
Erlewyn-Lajeunesse M.
Fox A.T.
Michaelis L.J.
Beyer K.
Noimark L.
Stiefel G.
Schauer U.
Hamelmann E.
Peroni D.
Boner A.
Author's Affiliation
Charité – Universitätsmedizin Berlin
Wageningen University & Research
Ruhr-Universitat Bochum
Radboud University Medical Center
Mahidol University
Chulalongkorn University
NYU Langone Health
Guy's and St Thomas' NHS Foundation Trust
Prince of Songkla University
Texas Children's Hospital
Uniwersytet Warminsko-Mazurski w Olsztynie
The Royal London Hospital
University Hospital Southampton NHS Foundation Trust
Azienda Ospedale Università Padova
Azienda Ospedaliera Universitaria Integrata Verona
Leicester Royal Infirmary
Utrechts Instituut voor Farmaceutische Wetenschappen
KK Women's And Children's Hospital
Arkansas Children's Hospital
Great North Children's Hospital
Nutricia Research, Netherlands
St. Marien Hospital, Bonn
Wageningen University & Research
Ruhr-Universitat Bochum
Radboud University Medical Center
Mahidol University
Chulalongkorn University
NYU Langone Health
Guy's and St Thomas' NHS Foundation Trust
Prince of Songkla University
Texas Children's Hospital
Uniwersytet Warminsko-Mazurski w Olsztynie
The Royal London Hospital
University Hospital Southampton NHS Foundation Trust
Azienda Ospedale Università Padova
Azienda Ospedaliera Universitaria Integrata Verona
Leicester Royal Infirmary
Utrechts Instituut voor Farmaceutische Wetenschappen
KK Women's And Children's Hospital
Arkansas Children's Hospital
Great North Children's Hospital
Nutricia Research, Netherlands
St. Marien Hospital, Bonn
Corresponding Author(s)
Other Contributor(s)
Abstract
Immunoglobulin E (IgE)-mediated cow’s milk allergy (CMA) is an immune-mediated reaction to cow’s milk (CM). Non-IgE-mediated CMA resolves in most children in the first years of life, whereas IgE-mediated CMA outgrowth is often later or not at all. The exact mechanisms underlying resolution of IgE-mediated CMA are not fully understood. We aim to gain insight in the immunological mechanisms underlying resolution of IgE-mediated CMA by analyzing unique saliva samples of allergic infants using the Olink<sup>®</sup> Target 96 Inflammation panel. Twenty-four children who outgrew their CMA after 12 months were compared to 15 with persistent CMA. Persistent CMA was accompanied by an increase in interleukin-15 receptor subunit alpha in the first 6 months, followed by a decrease, hinting towards an initial increased T cell response. At the same time caspase-8 was increased and interleukin-7 was decreased in persistent CMA. For CMA resolution, we found elevated levels of delta and notch-like epidermal growth factor-related receptor. Furthermore, adenosine deaminase (ADA) increased significantly between 0 and 12 months in resolved CMA, but not in persistent CMA. KEGG pathway analysis suggests mainly the TNF signaling pathway to be important in the resolution of CM allergy. Our findings show that Olink<sup>®</sup> Target 96 Inflammation panel analysis of saliva samples can reveal potential immunological markers and mechanisms involved in CMA resolution.
