Omalizumab could potentially inhibit eosinophil activation and infiltration into the local inflammatory site responsible for restoration of corticosteroid sensitivity through PP2A activation, according to data recently published in Biomedicines.
“Intranasal corticosteroids have limited effectiveness against [eosinophilic chronic rhinosinusitis] (ECRS). Topical corticosteroids that are administrated intranasally are not delivered to the inflammatory sites, such as the middle meatus, to which the ethmoid sinus opens due to functional–anatomical aspects,” Yokishi Kobayashi, MD, from the Airway Disease Section and Department of Otorhinolaryngology at Kansai Medical University, in Hirakata, Osaka 573-1010, Japan, and colleagues wrote. “Although intermittent oral corticosteroids are effective, they are not suitable for long-term administration owing to their adverse effects. Under such conditions, we have shown the usefulness of inhaled corticosteroid (ICS) exhalation through the nose (ETN) treatment for ECRS patients with bronchial asthma.”
The researchers evaluated 25 patients with ECRS and severe asthma who were refractory to conventional treatments and who received omalizumab between July 2015 and July 2019.
A total of 25 patients were responsive to omalizumab according to physician-assessed global evaluation of treatment effectiveness.
The levels of peripheral blood eosinophils and fractionated exhaled nitric oxide and of CCL4 and soluble CD69 among those who responded to treatment were reduced concomitantly with the restoration of corticosteroid sensitivity.
The study showed that omalizumab restored the eosinophil-peroxidase-mediated PP2A inactivation and steroid insensitivity in BEAS-2B.
Additionally, it was found that the local inflammation simulant model using BEAS-2B cells incubated with diluted serum from each patient confirmed omalizumab’s effects on restoration of corticosteroid sensitivity via PP2A activation, suggesting that omalizumab could be a promising therapeutic option for refractory eosinophilic airway inflammation with corticosteroid resistance.
“Taken together, omalizumab has the potential to inhibit eosinophil activation and infiltration into the local inflammatory site owing to restoration of corticosteroid sensitivity through PP2A activation,” the researchers concluded. “Omalizumab could be a promising therapeutic option in refractory eosinophilic airway inflammation with corticosteroid resistance.”
Disclosure: The authors report no relevant financial disclosures.
