Skip to main content

Advertisement

Log in

A case with eosinophilic gastroenteritis exhibiting enhanced TNF-α and IL-6 responses

  • Case Report
  • Published:
Clinical Journal of Gastroenterology Aims and scope Submit manuscript

Abstract

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.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Fig. 1
Fig. 2
Fig. 3

Similar content being viewed by others

References

  1. Walker MM, Potter M, Talley NJ. Eosinophilic gastroenteritis and other eosinophilic gut diseases distal to the oesophagus. Lancet Gastroenterol Hepatol. 2018;3:271–80.

    Article  Google Scholar 

  2. Kinoshita Y, Oouchi S, Fujisawa T. Eosinophilic gastrointestinal diseases - Pathogenesis, diagnosis, and treatment. Allergol Int. 2019;68:420–9.

    Article  CAS  Google Scholar 

  3. 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.

    Google Scholar 

  4. 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.

    Article  Google Scholar 

  5. Tanaka T, Narazaki M, Kishimoto T. IL-6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol. 2014;6:a016295.

    Article  Google Scholar 

  6. 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.

    Article  Google Scholar 

  7. 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.

    Article  CAS  Google Scholar 

  8. 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.

    Article  Google Scholar 

  9. 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.

    Article  Google Scholar 

  10. 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.

    Article  PubMed  Google Scholar 

  11. 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.

    Article  Google Scholar 

  12. 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.

    Article  Google Scholar 

  13. Caminero A, Meisel M, Jabri B, et al. Mechanisms by which gut microorganisms influence food sensitivities. Nat Rev Gastroenterol Hepatol. 2019;16:7–18.

    Article  CAS  Google Scholar 

  14. 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.

    Article  Google Scholar 

Download references

Funding

This work was supported by a Grant-in-Aid for Scientific Research (19K08455) from the Japan Society for the Promotion of Science and grants from the Takeda Science Foundation, Smoking Research Foundation, Yakult Bio-Science Foundation, and SENSHIN Medical Research Foundation.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Tomohiro Watanabe.

Ethics declarations

Conflict of interest

Ikue Sekai, Tomohiro Watanabe, Keisuke Yoshikawa, Ryutaro Takada, Akane Hara, Tomoe Yoshikawa, Ken Kamata, Kosuke Minaga, and Masatoshi Kudo declare that they have no conflicts of interest.

Human and animal rights

All the procedures followed have been performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments.

Informed consent

Informed consent was obtained from the patient for being included in the study.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Sekai, I., Watanabe, T., Yoshikawa, K. et al. A case with eosinophilic gastroenteritis exhibiting enhanced TNF-α and IL-6 responses. Clin J Gastroenterol 14, 511–516 (2021). https://doi.org/10.1007/s12328-020-01320-3

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s12328-020-01320-3

Keywords

Navigation