Cited by 27IL-33, ST2, and ILC PathwaysInflammatory Bowel DiseaseAsthma and respiratory diseases

Transcriptome profiling of mouse colonic eosinophils reveals a key role for eosinophils in the induction of s100a8 and s100a9 in mucosal healing

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Reichman, Hadar, Moshkovits, Italy, Itan, Michal, Pasmanik-Chor, Metsada, Vogl, Thomas, Roth, Johannes, Munitz, Ariel·2017·Scientific Reports

Abstract

Eosinophils are bone marrow-derived cells that have been largely implicated in Th2-associated diseases. Recent data highlights a key role for eosinophils in mucosal innate immune responses especially in the gastrointestinal (GI) tract, which is one of the largest eosinophil reservoirs in the body. Although eosinophils express and synthesize a plethora of proteins that can mediate their effector activities, the transcriptome signature of eosinophils in mucosal inflammation and subsequent repair has been considerably overlooked. We demonstrate that eosinophils are recruited to the colon in acute inflammatory stages where they promote intestinal inflammation and remain in substantial numbers throughout the mucosal healing process. Microarray analysis of primary colonic eosinophils that were sorted at distinct stages of mucosal inflammation and repair revealed dynamic regulation of colonic eosinophil mRNA expression. The clinically relevant genes s100a8 and s100a9 were strikingly increased in colonic eosinophils (up to 550-fold and 80-fold, respectively). Furthermore, local and systemic expression of s100a8 and s100a9 were nearly diminished in eosinophil-deficient ΔdblGATA mice, and were re-constituted upon adoptive transfer of eosinophils. Taken together, these data may provide new insight into the involvement of eosinophils in colonic inflammation and repair, which may have diagnostic and therapeutic implications.

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  • S100A8/A9 is recognized as both a biomarker of colitis and a promoter of inflammation-associated tumorigenesis.

    “Importantly, S100A8/A9 has been recognized as both a biomarker of colitis and a promoter of inflammation-associated tumorigenesis [16–18].”

    From Inhibition of SPI1 by ADAP Regulates S100A8/A9 Signaling in Macrophages to Control the Development of Colitis (2026) · cites this paper as [18]

    The Results and Discussion report increased S100A8/A9 expression during experimental colitis, including in colonic biopsies and serum, which supports its association with colitis but does not establish it as a validated biomarker. The Discussion links S100A8/A9 to cancer and says these proteins can facilitate cancer-cell migration; it does not establish that they promote inflammation-associated tumorigenesis. No page numbers are available in our copy. (LLM, conf=0.84)

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Authors
Reichman, H., Moshkovits, I., Itan, M., Pasmanik-Chor, M., Vogl, T., Roth, J., & Munitz, A.
Affiliations
  • Tel Aviv University (IL)
  • University of Münster (DE)
Corresponding author
Munitz, Ariel
Venue
Scientific Reports
Published
2017-08-02
Volume
7
Issue
1
Pages
7117-7117
ISSN
2045-2322 (ISSN-L)
OpenAlex
W2741128589
Cited by
27
References
61
Citations by year
2026: 1 · 2025: 4 · 2024: 4 · 2023: 3 · 2022: 5 · 2021: 5 · 2019: 3 · 2018: 2
FWCI
0.62
Type
journal article
Language
en
Open access
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Science Foundation
  • Israel Cancer Association (20150002)
  • Israel Science Foundation (886/15)
  • Tel Aviv University
  • Cancer Biology Research Center, Tel Aviv University
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
Keywords
eosinophils, S100A8, S100A9, mucosal healing, intestinal inflammation, transcriptome, eosinophil-deficient mice, adoptive transfer, type 2 inflammation, innate immunity, gene expression regulation

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