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. 2019 Feb 11;19(1):28.
doi: 10.1186/s12876-019-0937-9.

Plasma levels of TNF-α, IL-6, IFN-γ, IL-12, IL-17, IL-22, and IL-23 in achalasia, eosinophilic esophagitis (EoE), and gastroesophageal reflux disease (GERD)

Steven Clayton  1 , Elliot Cauble  2 , Ambuj Kumar  2 , Nirav Patil  3 , Dennis Ledford  4 , Narasaiah Kolliputi  4 , Maria F Lopes-Virella  5 , Donald Castell  6 , Joel Richter  2
Affiliations

Plasma levels of TNF-α, IL-6, IFN-γ, IL-12, IL-17, IL-22, and IL-23 in achalasia, eosinophilic esophagitis (EoE), and gastroesophageal reflux disease (GERD)

Steven Clayton et al. BMC Gastroenterol. .

Abstract

An elevation of serum inflammatory biomarkers in achalasia patients compared with controls recently was demonstrated. It has not been determined whether the elevation of inflammatory cytokines is unique to achalasia or occurs with other diseases involving the esophagus. The primary aim of our study was to compare the differences in plasma immunological profiles (TNF- α receptor, IL-6, IFN-γ, IL-12, IL-17, IL-22, and IL-23) of patients with achalasia, eosinophilic esophagitis (EoE), and gastroesophageal reflux disease (GERD). A secondary aim of this study was to classify these same plasma cytokine profiles in the three achalasia subtypes.

Methods: Plasma from 53 patients with achalasia, 22 with EoE, and 20 with GERD (symptoms plus esophagitis or + reflux study) were analyzed.

Exclusion criteria: malignancy, autoimmune condition, immunodeficiency disorder, and treatment with steroids/immune modulating drugs. Cytokine levels were assayed via multiplex enzyme-linked immunosorbent assay (ELISA).

Results: Our key finding revealed significant elevations in IL- 6 (p = 0.0158) in achalasia patients compared with EoE patients. Overall, plasma inflammatory biomarker patterns were not different in the three subtypes of achalasia.

Conclusion: There were no differences between the cytokine levels of any of the measured biomarkers between the achalasia and GERD groups suggesting that luminal stasis does increase biomarker levels for any of the cytokines examined in our study. While these results are an early first step towards clarifying some aspects of the pathogenesis of achalasia, they bring about many more questions that require further investigation and expansion. Further investigation with a larger cohort and a broader panel of biomarkers is needed.

Keywords: Achalasia; Eosinophilic esophagitis; GERD; IL-6; Inflammatory cytokines.

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Conflict of interest statement

Ethics approval and consent to participate

This study was approved by the institutional review board of The University of South Florida IRB#:Pro00013748. Following a detailed explanation of the study, a written informed consent was obtained from all participants prior to their enrollment in the study.

Consent for publication

Not applicable

Competing interest

None of the contributing authors have any potential personal or financial conflict of interests. No funding sources to declare.

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References

    1. Abassa KK, Lin XY, Xuan JY, Zhou HX, Guo YW. Diagnosis of eosinophilic gastroenteritis is easily missed. World J Gastroenterol. 2017;23:3556–3564. doi: 10.3748/wjg.v23.i19.3556. - DOI - PMC - PubMed
    1. Blanchard C, Mingler MK, Vicario M, Abonia JP, Wu YY, Lu TX, Collins MH, Putnam PE, Wells SI, Rothenberg ME. IL-13 involvement in eosinophilic esophagitis: transcriptome analysis and reversibility with glucocorticoids. J Allergy Clin Immunol. 2007;120:1292–1300. doi: 10.1016/j.jaci.2007.10.024. - DOI - PubMed
    1. Blanchard C, Wang N, Stringer KF, Mishra A, Fulkerson PC, Abonia JP, Jameson SC, Kirby C, Konikoff MR, Collins MH, Cohen MB, Akers R, Hogan SP, Assa'ad AH, Putnam PE, Aronow BJ, Rothenberg ME. Eotaxin-3 and a uniquely conserved gene-expression profile in eosinophilic esophagitis. J Clin Invest. 2006;116:536–547. doi: 10.1172/JCI26679. - DOI - PMC - PubMed
    1. Boeckxstaens GE, Zaninotto G, Richter JE. Achalasia. Lancet (London, England) 2014;383:83–93. doi: 10.1016/S0140-6736(13)60651-0. - DOI - PubMed
    1. Cauble EW, Rife C, Singh ER, Arevalo LF, Freeman J, Lopes-Virella MF, Castell DO. 432 evidence that achalasia involves a systemic inflammatory response. Gastroenterology. 2012;142:97.