ArticleThe Journal of allergy and clinical immunology2019
Apolipoprotein E is a concentration-dependent pulmonary danger signal that activates the NLRP3 inflammasome and IL-1β secretion by bronchoalveolar fluid macrophages from asthmatic subjects.
Article in The Journal of allergy and clinical immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Dementia is Associated with Severe Coronavirus Disease 2019 (COVID-19) Infection.The American journal of the medical sciences · 2021Pooled it
- Inflammasomes in respiratory diseases: from disease pathogenesis to drug development and use of multi-omics.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- ApoE impairs microglial efferocytosis by targeting Gas6/MerTK in a mouse model of acute seizure.Acta pharmacologica Sinica · 2026Article
- Critical role of keratinocytes and protease-activated receptor 2 in secondary lymphedema development.Clinical and translational medicine · 2026Article
- Cholesterol-mediated inflammation activation in alveolar macrophages.BMC biology · 2025Article
- Apolipoprotein E promoted the proliferation and function of group 2 innate lymphoid cells through low density lipoprotein receptor in allergic rhinitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Virus-associated inflammation imprints an inflammatory profile on monocyte-derived macrophages in the human liver.The Journal of clinical investigation · 2025Article
- The NLRP3 inflammasome in allergic diseases: mechanisms and therapeutic implications.Clinical and experimental medicine · 2024Review
- Neutrophil Heterogeneity Is Modified during Acute Lung Inflammation in Apoa1-/- Mice.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Three Main SCFAs Mitigate Lung Inflammation and Tissue Remodeling Nlrp3-Dependent in Murine HDM-Induced Neutrophilic Asthma.Inflammation · 2024Article
- A Marek's Disease Virus Messenger RNA-Based Vaccine Modulates Local and Systemic Immune Responses in Chickens.Viruses · 2024Article
- Mast Cells in Aspirin-Exacerbated Respiratory Disease.Current allergy and asthma reports · 2024Review
- Spatial and phenotypic heterogeneity of resident and monocyte-derived macrophages during inflammatory exacerbations leading to pulmonary fibrosis.Frontiers in immunology · 2024Article
- Evidence that Alzheimer's Disease Is a Disease of Competitive Synaptic Plasticity Gone Awry.Journal of Alzheimer's disease : JAD · 2024Review
- Cellular and molecular characterization of peripheral glia in the lung and other organs.PloS one · 2024Article
- Canonical and non-canonical functions of NLRP3.Journal of advanced research · 2023Review
- Landscape of mast cell populations across organs in mice and humans.The Journal of experimental medicine · 2023Article
- Delirium and IL-6 added to clinical scores improves their performance: a prospective analysis of CALL, PREDI-CO, MRS score applied to a population of patients admitted to internal medicine ward.Internal and emergency medicine · 2023Article
- Programmed Cell Death in Asthma: Apoptosis, Autophagy, Pyroptosis, Ferroptosis, and Necroptosis.Journal of inflammation research · 2023Review
- Role of inflammasome in severe, steroid-resistant asthma.Current research in immunology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHouse dust mite (HDM)-challenged Apoe
objectiveWe sought to characterize the pathways that induce apolipoprotein E (APOE) expression by bronchoalveolar lavage fluid (BALF) macrophages from asthmatic subjects and identify how APOE regulates IL-1β secretion.
methodsMacrophages were isolated from asthmatic BALF and derived from THP-1 cells and human monocytes.
resultsHDM-derived cysteine and serine proteases induced APOE secretion from BALF macrophages through protease-activated receptor 2. APOE at concentrations of less than 2.5 nmol/L, which are similar to levels found in epithelial lining fluid from healthy adults, did not induce IL-1β release from BALF macrophages. In contrast, APOE at concentrations of 25 nmol/L or greater induced nucleotide-binding oligomerization domain, leucine-rich repeat-containing protein (NLRP) 3 and pro-IL-1β expression by BALF macrophages, as well as the caspase-1-mediated generation of mature IL-1β secreted from cells. HDM acted synergistically with APOE to both prime and activate the NLRP3 inflammasome. In a murine model of neutrophilic airway inflammation induced by HDM and polyinosinic-polycytidylic acid, APOE reached a concentration of 32 nmol/L in epithelial lining fluid, with associated increases in BALF IL-1β levels. APOE-dependent NLRP3 inflammasome activation in macrophages was primarily mediated through a potassium efflux-dependent mechanism.
conclusionAPOE can function as an endogenous, concentration-dependent pulmonary danger signal that primes and activates the NLPR3 inflammasome in BALF macrophages from asthmatic subjects to secrete IL-1β. This might represent a mechanism through which APOE amplifies pulmonary inflammatory responses when concentrations in the lung are increased to greater than normal levels, which can occur during viral exacerbations of HDM-induced asthma characterized by neutrophilic airway inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.