Eosinophil-mediated inflammation in the absence of eosinophilia

Miyabe, Yui; Kobayashi, Yoshiki; Fukuchi, Mineyo; Saga, Akiko; Moritoki, Yuki; Saga, Tomoo; Akuthota, Praveen; Ueki, Shigeharu

doi:10.5415/apallergy.2021.11.e30

Cited by 17 publications

(14 citation statements)

References 174 publications

(174 reference statements)

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“…Tissue deposition of granule proteins in the absence of eosinophil accumulation has been reported in various conditions such as Hodgkin disease, parasitic infection, chronic urticaria, atopic dermatitis, and endomyocardial disease [ 8 ]. The mechanism of extracellular MBP deposition in the absence of eosinophils may involve cytolytic EETosis.…”

Section: Discussionmentioning

confidence: 99%

“…However, a chronic Th2-type reaction is thought to be involved in EGIDs [ 6 ]. The eosinophils contain four major cationic proteins, including the major basic protein (MBP), which play important roles in eosinophil-mediated inflammation [ 7 8 ]. The eosinophils release these granule proteins via piecemeal degranulation, exocytosis, and cytolysis.…”

Section: Introductionmentioning

confidence: 99%

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Case of hypereosinophilic syndrome with gastrointestinal involvement showing tissue eosinophil cytolysis

Hagiwara

Ueki

Watanabe

et al. 2022

Asia Pacific Allergy

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Hypereosinophilic syndrome (HES), which is characterized by eosinophilia in the peripheral blood, often causes various organ disorders, including those of the gastrointestinal (GI) tract. The eosinophils play a key role in inflammation in eosinophilic GI disorders (EGIDs), including HES with GI involvement. Here, we report a case of HES with GI involvement that showed major basic proteins (MBPs) deposition in the absence of marked eosinophilic infiltration in the mucosa of the GI tract. An 11-year-old boy presented with nausea and epigastric pain for one week. He had a history of idiopathic HES with eosinophilic cystitis, diagnosed at the age of 2 years. He had been taking a low dose of corticosteroids for 9 years. The peripheral blood eosinophil count was 2,254/μL. Endoscopy revealed a swelling of the duodenal bulb mucosa. Histological findings of the duodenal mucosa revealed chronic inflammation, but no evidence of significant eosinophil infiltration and we could not diagnose him with HES with GI involvement or EGID. Immunofluorescent staining for MBP and galectin-10 was performed to detect intact and cytolytic eosinophils (eosinophil extracellular trap cell death: EETosis). Marked MBP deposition was evident in a small number of intact eosinophils in tissues from the duodenum, gastric antrum, and terminal ileum. The current case illustrates the utility of immunostaining for the detection of persistent eosinophilic inflammation, especially when cytolytic eosinophils are dominant.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Case of hypereosinophilic syndrome with gastrointestinal involvement showing tissue eosinophil cytolysis

Hagiwara

Ueki

Watanabe

et al. 2022

Asia Pacific Allergy

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“…Eosinophils also release their total cellular content through so-called cytolysis, which is distinct from apoptosis and necrosis. Cytolysis in inflamed tissues is associated with deposition of granular proteins and occurs in 30–80% of eosinophils [ 53 , 54 , 55 , 56 ]. Recent evidence has shown that cytolysis is an active cell death program that releases a net-like chromatin structure (i.e., extracellular trap cell death [ETosis]) [ 36 , 57 , 58 , 59 ].…”

Section: Release Of Galectin-10 Is Not Mediated Through Secretory Sys...mentioning

confidence: 99%

“…Pathological studies of patients with allergies or eosinophilic diseases have frequently shown abundant eosinophilic granule deposition, even in the absence of intact eosinophil infiltration [ 53 ]. Our laboratory has performed tissue immunostaining for galectin-10 and MBP in various diseases.…”

Section: Detection Of Cytolytic Etosis Using Immunohistochemical Stai...mentioning

confidence: 99%

Galectin-10 as a Potential Biomarker for Eosinophilic Diseases

et al. 2022

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Galectin-10 is a member of the lectin family and one of the most abundant cytoplasmic proteins in human eosinophils. Except for some myeloid leukemia cells, basophils, and minor T cell populations, galectin-10 is exclusively present in eosinophils in the human body. Galectin-10 forms Charcot–Leyden crystals, which are observed in various eosinophilic diseases. Accumulating studies have indicated that galectin-10 acts as a new biomarker for disease activity, diagnosis, and treatment effectiveness in asthma, eosinophilic esophagitis, rhinitis, sinusitis, atopic dermatitis, and eosinophilic granulomatosis with polyangiitis. The extracellular release of galectin-10 is not mediated through conventional secretory processes (piecemeal degranulation or exocytosis), but rather by extracellular trap cell death (ETosis), which is an active cell death program. Eosinophils undergoing ETosis rapidly disintegrate their plasma membranes to release the majority of galectin-10. Therefore, elevated galectin-10 levels in serum and tissue suggest a high degree of eosinophil ETosis. To date, several studies have shown that galectin-10/Charcot–Leyden crystals are more than just markers for eosinophilic inflammation, but play functional roles in immunity. In this review, we focus on the close relationship between eosinophils and galectin-10, highlighting this protein as a potential new biomarker in eosinophilic diseases.

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“…Several studies have reported the presence of lysed eosinophils, as well as the presence of both free eosinophil granules and extracellular DNA in tissues in several eosinophilic diseases and models [ 4 , 5 , 6 , 7 , 8 , 9 , 10 ]. Notably, the presence of free eosinophil granules has been associated with epithelial damage in the airways [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

Autophagy Protects against Eosinophil Cytolysis and Release of DNA

Esnault

Fichtinger

Barretto

et al. 2022

Cells

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The presence of eosinophils in the airway is associated with asthma severity and risk of exacerbations. Eosinophils deposit their damaging products in airway tissue, likely by degranulation and cytolysis. We previously showed that priming blood eosinophils with IL3 strongly increased their cytolysis on aggregated IgG. Conversely, IL5 priming did not result in significant eosinophil cytolysis in the same condition. Therefore, to identify critical events protecting eosinophils from cell cytolysis, we examined the differential intracellular events between IL5- and IL3-primed eosinophils interacting with IgG. We showed that both IL3 and IL5 priming increased the eosinophil adhesion to IgG, phosphorylation of p38, and production of reactive oxygen species (ROS), and decreased the phosphorylation of cofilin. However, autophagic flux as measured by the quantification of SQSTM1-p62 and lipidated-MAP1L3CB over time on IgG, with or without bafilomycin-A1, was higher in IL5-primed compared to IL3-primed eosinophils. In addition, treatment with bafilomycin-A1, an inhibitor of granule acidification and autophagolysosome formation, enhanced eosinophil cytolysis and DNA trap formation in IL5-primed eosinophils. Therefore, this study suggests that increased autophagy in eosinophils protects from cytolysis and the release of DNA, and thus limits the discharge of damaging intracellular eosinophilic contents.

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Eosinophil-mediated inflammation in the absence of eosinophilia

Cited by 17 publications

References 174 publications

Case of hypereosinophilic syndrome with gastrointestinal involvement showing tissue eosinophil cytolysis

Case of hypereosinophilic syndrome with gastrointestinal involvement showing tissue eosinophil cytolysis

Galectin-10 as a Potential Biomarker for Eosinophilic Diseases

Autophagy Protects against Eosinophil Cytolysis and Release of DNA

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