# Alpha-bisabolol protects against neonatal asthma by suppressing airway inflammatory signaling

## TL;DR

Alpha-bisabolol reduces inflammation in neonatal asthma by suppressing key inflammatory signals in rat pups.

## Contribution

This study demonstrates that alpha-bisabolol pretreatment inhibits allergic airway inflammation in neonatal rats.

## Key findings

- Alpha-bisabolol pretreatment reduced mucous gland hypertrophy and eosinophil infiltration in rat pups.
- AB suppressed proinflammatory cytokines like IL-1β, IL-6, and IL-17 in allergic airway inflammation.
- Transcription of inflammatory genes such as cyclooxygenase-2 and toll-like receptor 4 was significantly inhibited by AB.

## Abstract

Objective: This study aimed to evaluate the anti-inflammatory effects of alpha-bisabolol (AB) in allergic airway inflammation-induced rat pups.

Methods: We evaluated the anti-adverse effects of AB against allergic airway inflammation-induced male Wistar rat pups, with four categorized groups including vehicle-controls (group 1), controls treated with 25 mg/kg of AB (group 2), allergic airway inflammation-induced cases (group 3), and cases treated with 25 mg/kg of AB before allergic airway inflammation induction (group 4). Lung histopathology, bronchoalveolar lavage fluid eosinophils, and several inflammatory markers were also examined in each group.

Results: AB significantly decreased mucous gland hypertrophy, eosinophil infiltration, and oxidative stress marker levels in the allergic airway inflammation-induced AB-pretreated rats. Moreover, AB pretreatment significantly reduced the levels of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-8, IL-17, monocyte chemoattractant protein-1, C-X-C chemokine receptor type 4 (CXCR4), and thymic stromal lymphopoietin, which were increased in allergic airway inflammation-induced cases. Furthermore, transcription of cyclooxygenase-2, tumor necrosis factor-α, CXCR4, toll-like receptor 4, Eotaxin-1, and regulated upon activation normal T cell expressed and secreted were significantly suppressed in allergic airway inflammation-induced AB-pretreated rats.

Conclusions: These results indicate that AB can protect against neonatal asthma by inhibiting acute or chronic inflammation induced during disease onset.