ArticleImmunology2004
Danger signals derived from stressed and necrotic epithelial cells activate human eosinophils.
Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- The Role of Alarmins in the Pathogenesis of Asthma.Biomolecules · 2025Review
- Beyond Eosinophilic Esophagitis: Eosinophils in Gastrointestinal Disease-New Insights, "New" Diseases.Journal of the Canadian Association of Gastroenterology · 2023Review
- Distinct Epithelial-Innate Immune Cell Transcriptional Circuits Underlie Airway Hyperresponsiveness in Asthma.American journal of respiratory and critical care medicine · 2023Article
- Disturbed microbiota-metabolites-immune interaction network is associated with olfactory dysfunction in patients with chronic rhinosinusitis.Frontiers in immunology · 2023Article
- Research trends in the field of the gut-brain interaction: Functional dyspepsia in the spotlight - An integrated bibliometric and science mapping approach.Frontiers in neuroscience · 2023Review
- Epithelial microRNA-30a-3p targets RUNX2/HMGB1 axis to suppress airway eosinophilic inflammation in asthma.Respiratory research · 2022Article
- Silicone Oil-Based Nanoadjuvants as Candidates for a New Formulation of Intranasal Vaccines.Vaccines · 2021Article
- Eosinophil prognostic scores for patients with head and neck squamous cell carcinoma treated with nivolumab.Cancer science · 2021Article
- Eosinophils as Major Player in Type 2 Inflammation: Autoimmunity and Beyond.Advances in experimental medicine and biology · 2021Review
- IL-33 reduces tumor growth in models of colorectal cancer with the help of eosinophils.Oncoimmunology · 2020Article
- Possible Mechanisms of Eosinophil Accumulation in Eosinophilic Pneumonia.Biomolecules · 2020Review
- Eosinophils in Eosinophilic Esophagitis: The Road to Fibrostenosis is Paved With Good Intentions.Frontiers in immunology · 2020Review
- Article
- Cancer cachexia induces morphological and inflammatory changes in the intestinal mucosa.Journal of cachexia, sarcopenia and muscle · 2019Article
- Eosinophils in the gastrointestinal tract and their role in the pathogenesis of major colorectal disorders.World journal of gastroenterology · 2019Review
- Synergy of Interleukin (IL)-5 and IL-18 in eosinophil mediated pathogenesis of allergic diseases.Cytokine & growth factor reviews · 2019Review
- Inhibition of the dipeptidyl peptidase DPP4 (CD26) reveals IL-33-dependent eosinophil-mediated control of tumor growth.Nature immunology · 2019Article
- Involvement and Possible Role of Eosinophils in Asthma Exacerbation.Frontiers in immunology · 2018Review
- IL-4-secreting eosinophils promote endometrial stromal cell proliferation and preventProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Eosinophils in Autoimmune Diseases.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eosinophilic granulocytes are found in tissues with an interface with the external environment, such as the gastrointestinal, genitourinary and respiratory tracts. These leucocytes have been associated with tissue damage in a variety of diseases. The aim of this study was to evaluate whether necrotic epithelial cells can activate eosinophils. The danger theory postulates that cells of the innate immune system primarily recognize substances that signal danger to the host. We damaged epithelial cell lines derived from the genital (HeLa cells), respiratory (HEp-2 cells) and intestinal tracts (HT29 cells) and assessed their capacity to cause eosinophilic migration, release of putative tissue-damaging factors, such as eosinophil peroxidase (EPO) and eosinophil cationic protein (ECP), as well as secretion of tissue-healing factors, e.g. fibroblast growth factors (FGF)-1 and -2 and transforming growth factor (TGF)-beta1. We found that necrotic intestinal cells induced chemotaxis in human eosinophils. EPO release was elicited in eosinophils stimulated with necrotic cells derived from all cell lines, as well as from viable HEp-2 and HT29 cells. Release of ECP was only seen in eosinophils incubated with necrotic intestinal or genital cells, not viable ones. Both necrotic intestinal and genital cells elicited FGF-2 secretion from eosinophils. TGF-beta1 was released from eosinophils exposed to viable and necrotic HT29 cells. These findings indicate that eosinophils are able to recognize and be activated by danger signals released from damaged epithelial cells, which may be of importance in understanding the role of eosinophils in the various inflammatory conditions in which they are involved.
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