Results 171 to 180 of about 50,798 (264)

PGI2 signaling metabolically reprograms CD4 Th2 cells and represses allergic airway inflammation. [PDF]

open access: yesJ Immunol
Zhou W   +10 more
europepmc   +1 more source

IL‐33 Drives Inflammatory Changes and Extracellular Trap Formation in Eosinophils Involving Oxidised LDL and Complement Pathways

open access: yesAllergy, EarlyView.
IL‐33 induces inflammatory gene signatures in eosinophils, characterised by the upregulation of cell surface markers, inflammatory mediators and regulatory factors, all of which were also observed in nasal polyp‐derived eosinophils. Ox‐LDL and complement fragments (C3a and C5a) promote eosinophil adhesion and survival.
Emiko Matsuyama   +16 more
wiley   +1 more source

Adipokines in Obese Asthma: A Complex Relationship Influenced More by Sex, Weight, and Oral Steroid Treatment Than Disease Severity

open access: yesAllergy, EarlyView.
Adipokine secretion from adipose tissue may be involved in obesity‐related asthma, but it is unknown how adipokine levels relate to asthma characteristics. Plasma adipokines were measured in well‐characterized lean, overweight or obese patients with mild‐to‐moderate or severe asthma.
Lars I. Andersson   +20 more
wiley   +1 more source

MrgprC11<sup>+</sup> Jugular Neurons Control Airway Hyperresponsiveness in Allergic Airway Inflammation. [PDF]

open access: yesAm J Respir Cell Mol Biol
Xing Y   +7 more
europepmc   +1 more source

Iron Physiology and Its Impact on Atopic Diseases: An EAACI Taskforce Report

open access: yesAllergy, EarlyView.
ABSTRACT Iron is essential for oxygen transport, energy metabolism, and immune regulation. Yet iron deficiency is the most common micronutrient disorder across all age groups, affecting nearly one quarter of the global population. Iron deficiency triggers nutritional immunity, a host defense mechanism that withholds and redistributes iron, contributing
Franziska Roth‐Walter   +19 more
wiley   +1 more source

Polypropylene Nanoplastic Exposure to Respiratory Epithelial Barrier‐On‐Chip and Interfacial Interactions With Human Serum Albumin

open access: yesAllergy, EarlyView.
Exposure to 305 nm PP NPs significantly disrupts the airway barrier‐on‐chip, reducing TEER, suppressing ZO‐1/ACE2 expression, and triggering ROS‐mediated apoptosis. In biological media, PP NPs exhibit a biphasic adsorption pattern, leading to the formation of a protein corona that increases their size to 364 nm.
Omur Sert   +9 more
wiley   +1 more source

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