Autophagy deficiency in myeloid cells exacerbates eosinophilic inflammation in chronic rhinosinusitis

Choi, Go Eun; Yoon, Seung-Yong; Kim, Jiyun; Kang, Do‐Young; Jang, Yong Ju; Kim, Hun Sik

doi:10.1016/j.jaci.2017.10.038

Cited by 35 publications

(67 citation statements)

References 65 publications

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“…65 In addition, impaired autophagy in myeloid cells was reported to aggravate eosinophilia, epithelial hyperplasia, and mucosal thickening in mice with eosinophilic CRS. 66 Decreased expression of antimicrobial S100 proteins in the epithelium of patients with CRS might lead to diminished innate immune responses and barrier function. 67,68 …”

Section: Epithelial Barrier Defect and Reduced Innate Immunity In Crsmentioning

confidence: 99%

Pathophysiologic mechanisms of chronic rhinosinusitis and their roles in emerging disease endotypes

Cao

Wang

Schleimer

et al. 2019

Annals of Allergy, Asthma & Immunology

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Objective: Chronic rhinosinusitis (CRS) is a heterogeneous disorder with distinct pathophysiologic mechanisms. Based on the transcription factor expression and cytokine production patterns in different types of innate lymphoid cells (ILCs), in parallel with those of adaptive CD4+ T helper (Th) cells and CD8+ cytotoxic T (Tc) cells, new perspectives on endotypes of patients are emerging around the immune response deviation into type 1 (orchestrated by ILC1s, Tc1 and Th1 cells), type 2 (characterized by ILC2s, Tc2 and Th2 cells), and type 3 (mediated by ILC3s, Tc17 and Th17 cells) responses. Additionally, cluster analysis has been applied to the endotyping of CRS in recent years, which has provided additional novel insights into the CRS pathogenesis. This article aims to review pathological mechanisms of CRS on the basis of type 1, type 2, and type 3 immune responses and how they inform us to begin to understand CRS endotypes. This article also reviews the recent cluster analysis studies of CRS endotypes. Finally, the impact of endotype on therapeutic management of CRS is summarized. Data Sources: Review of published literature. Study Selections: Relevant literature concerning CRS endotypes and the possible underlying mechanisms were obtained from a PubMed search and summarized here. Results and Conclusion: Both CRSwNP and CRSsNP are comprised of distinct endotypes with distinct deviated immune responses, pathogenic mechanisms, and different responses to medical and surgical treatment. An endotype of CRS with prominent type 2 immune responses is the most well studied endotype, and generally can benefit from treatment with steroids and specific type 2 disrupting biologics.

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Section: Epithelial Barrier Defect and Reduced Innate Immunity In Crsmentioning

confidence: 99%

Pathophysiologic mechanisms of chronic rhinosinusitis and their roles in emerging disease endotypes

Cao

Wang

Schleimer

et al. 2019

Annals of Allergy, Asthma & Immunology

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“…The same study showed that BMMC lacking Atg7 or 12 have normal granule formation, but defective IgE-mediated degranulation, demonstrating the importance of autophagic machinery in granule movement and release. Furthermore, dysregulation of autophagy in mast cells has been shown in various disease states such as systemic sclerosis, chronic rhinosinusitis, and asthma ( 48 – 50 ). Overall, research on mast cell survival, apoptosis, and autophagy pathways suggests that these pathways are important for both maintenance and function in both health and disease.…”

Section: Mast Cell Growth Survival and Apoptosismentioning

confidence: 99%

Controlling Mast Cell Activation and Homeostasis: Work Influenced by Bill Paul That Continues Today

et al. 2018

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Mast cells are tissue resident, innate immune cells with heterogenous phenotypes tuned by cytokines and other microenvironmental stimuli. Playing a protective role in parasitic, bacterial, and viral infections, mast cells are also known for their role in the pathogenesis of allergy, asthma, and autoimmune diseases. Here, we review factors controlling mast cell activation, with a focus on receptor signaling and potential therapies for allergic disease. Specifically, we will discuss our work with FcεRI and FγR signaling, IL-4, IL-10, and TGF-β1 treatment, and Stat5. We conclude with potential therapeutics for allergic disease. Much of these efforts have been influenced by the work of Bill Paul. With many mechanistic targets for mast cell activation and different classes of therapeutics being studied, there is reason to be hopeful for continued clinical progress in this area.

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“…The JACI advances in 2018 examined both the factors leading to tissue eosinophilia and the effect of eosinophils on the inflammatory process itself. In a novel study examining the role of the prostaglandin pathway in chronic rhinosinusitis (CRS), Choi et al 1 deleted the autophagy-related gene Atg7 in the myeloid lineage of mice challenged with a mixture of Aspergillus species protease and ovalbumin to induce CRS. 1 They not only observed an increase in eosinophilic inflammation in the Atg7-deficient mice but also associated dysregulation of the prostaglandin D 2 pathway.…”

Section: Eosinophils and Allergic Inflammationmentioning

confidence: 99%

“…In a novel study examining the role of the prostaglandin pathway in chronic rhinosinusitis (CRS), Choi et al 1 deleted the autophagy-related gene Atg7 in the myeloid lineage of mice challenged with a mixture of Aspergillus species protease and ovalbumin to induce CRS. 1 They not only observed an increase in eosinophilic inflammation in the Atg7-deficient mice but also associated dysregulation of the prostaglandin D 2 pathway. Macrophage autophagy and IL-1 played a major role in this process, highlighting a potential new therapeutic approach for CRS.…”

Section: Eosinophils and Allergic Inflammationmentioning

confidence: 99%

Advances in eosinophilic diseases in 2018

Klion

Rothenberg

2019

Journal of Allergy and Clinical Immunology

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Interest in eosinophil biology and eosinophilic diseases is increasing, as reflected in a doubling of the number of annual articles focused on this topic published in the Journal of Allergy and Clinical Immunology over the past decade. Although the majority of these publications relate to eosinophilic asthma, a growing proportion of them focus on breakthroughs in the diagnosis, treatment, and pathogenesis of other eosinophilic disorders, most notably eosinophilic esophagitis. This review highlights advances in our understanding of eosinophilia and eosinophilic disorders (excluding asthma) published in the

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Autophagy deficiency in myeloid cells exacerbates eosinophilic inflammation in chronic rhinosinusitis

Abstract: Our results suggest that impaired autophagy in myeloid cells, particularly macrophages, has a causal role in eosinophilic inflammation and ECRS pathogenesis.

Cited by 35 publications

References 65 publications

Pathophysiologic mechanisms of chronic rhinosinusitis and their roles in emerging disease endotypes

Pathophysiologic mechanisms of chronic rhinosinusitis and their roles in emerging disease endotypes

Controlling Mast Cell Activation and Homeostasis: Work Influenced by Bill Paul That Continues Today

Advances in eosinophilic diseases in 2018

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