A case with eosinophilic gastroenteritis exhibiting enhanced TNF-α and IL-6 responses.
Eosinophilic gastroenteritis
IL-6
T helper type 2
TNF-α
Journal
Clinical journal of gastroenterology
ISSN: 1865-7265
Titre abrégé: Clin J Gastroenterol
Pays: Japan
ID NLM: 101477246
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
09
11
2020
accepted:
08
12
2020
pubmed:
6
1
2021
medline:
29
6
2021
entrez:
5
1
2021
Statut:
ppublish
Résumé
Eosinophilic gastroenteritis (EGE) is a chronic allergic disorder characterized by infiltration of eosinophils in the gastrointestinal (GI) tract and hypereosinophilia. Although T helper type 2 (Th2) responses play pathogenic roles in EGE, roles of innate immunity cytokines including IL-6 and TNF-α have been poorly defined. Here, we describe a case of EGE exhibiting accumulation of eosinophils in the upper GI mucosa and hypereosinophilia. Induction of remission by prednisolone reduced expression levels not only of Th2 cytokines but also of IL-6 and TNF-α in the GI mucosa. Moreover, induction of remission was accompanied by a marked reduction in serum levels of chemokine C-C motif ligand 17 (CCL17, TARC), IL-6 and TNF-α, implicating that both Th2 and innate immune responses were involved in the development of EGE in this case. Collectively, this case suggests possible involvement of IL-6 and TNF-α in the development of EGE.
Identifiants
pubmed: 33400188
doi: 10.1007/s12328-020-01320-3
pii: 10.1007/s12328-020-01320-3
doi:
Substances chimiques
Interleukin-6
0
Tumor Necrosis Factor-alpha
0
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
511-516Subventions
Organisme : Japan Society for the Promotion of Science
ID : 19K08455
Références
Walker MM, Potter M, Talley NJ. Eosinophilic gastroenteritis and other eosinophilic gut diseases distal to the oesophagus. Lancet Gastroenterol Hepatol. 2018;3:271–80.
doi: 10.1016/S2468-1253(18)30005-0
Kinoshita Y, Oouchi S, Fujisawa T. Eosinophilic gastrointestinal diseases - Pathogenesis, diagnosis, and treatment. Allergol Int. 2019;68:420–9.
doi: 10.1016/j.alit.2019.03.003
Prussin C, Lee J, Foster B. Eosinophilic gastrointestinal disease and peanut allergy are alternatively associated with IL-5+ and IL-5(-) T(H)2 responses. J Allergy Clin Immunol. 2009;124(1326–32):e6.
Ahmad S, Azid NA, Boer JC, et al. The key role of TNF-TNFR2 interactions in the modulation of allergic inflammation: a review. Front Immunol. 2018;9:2572.
doi: 10.3389/fimmu.2018.02572
Tanaka T, Narazaki M, Kishimoto T. IL-6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol. 2014;6:a016295.
doi: 10.1101/cshperspect.a016295
Ishihara S, Kinoshita Y, Schoepfer A. Eosinophilic esophagitis, eosinophilic gastroenteritis, and eosinophilic colitis: common mechanisms and differences between east and west. Inflamm Intest Dis. 2016;1:63–9.
doi: 10.1159/000445131
Watanabe T, Minaga K, Kamata K, et al. RICK/RIP2 is a NOD2-independent nodal point of gut inflammation. Int Immunol. 2019;31:669–83.
doi: 10.1093/intimm/dxz045
Kono M, Komeda Y, Sakurai T, et al. Induction of complete remission by azacitidine in a patient with myelodysplastic syndrome-associated inflammatory bowel disease. J Crohns Colitis. 2018;12:499–502.
doi: 10.1093/ecco-jcc/jjx170
Minaga K, Watanabe T, Hara A, et al. Identification of serum IFN-alpha and IL-33 as novel biomarkers for type 1 autoimmune pancreatitis and IgG4-related disease. Sci Rep. 2020;10:14879.
doi: 10.1038/s41598-020-71848-4
Honjo H, Watanabe T, Arai Y, et al. ATG16L1 negatively regulates RICK/RIP2-mediated innate immune responses. Int Immunol. 2020. https://doi.org/10.1093/intimm/dxaa062 .
doi: 10.1093/intimm/dxaa062
pubmed: 32909611
Muir A, Surrey L, Kriegermeier A, et al. Severe eosinophilic gastroenteritis in a Crohn’s disease patient treated with infliximab and adalimumab. Am J Gastroenterol. 2016;111:437–8.
doi: 10.1038/ajg.2015.438
Hayashida S, Sato S, Shimada Y, et al. Eosinophilic gastroenteritis in an ulcerative colitis patient during treatment with tumor necrosis factor-alpha antagonist. Intern Med. 2020;59:1977–81.
doi: 10.2169/internalmedicine.4554-20
Caminero A, Meisel M, Jabri B, et al. Mechanisms by which gut microorganisms influence food sensitivities. Nat Rev Gastroenterol Hepatol. 2019;16:7–18.
doi: 10.1038/s41575-018-0064-z
Arias A, Vicario M, Bernardo D, et al. Toll-like receptors-mediated pathways activate inflammatory responses in the esophageal mucosa of adult eosinophilic esophagitis. Clin Transl Gastroenterol. 2018;9:147.
doi: 10.1038/s41424-018-0017-4