Neutrophilic asthma is connected to more than half of the asthma cases that are not caused by eosinophils. Furthermore, neutrophilic airway inflammation is related to severe asthma and asthma that resists steroid treatment.
Interleukin 17 (IL-17) is an inflammatory molecule produced by Th17 helper T cells. It is connected with airway inflammation, hyperresponsiveness, and remodeling caused by asthma.
IL-17 is countered by ligustrazine, a bioactive compound found in fermented cacao beans, natto, and the Chinese medicinal herb Szechuan lovage (Ligusticum wallichi). In a standard asthma mouse model, ligustrazine can reduce IL-17 production and improve asthma symptoms.
Researchers from Shandong University (SU) studied the effects of ligustrazine on airway inflammation and levels of IL-17 and its opposite number, IL-10, in neutrophilic asthma mice. They also looked at the mechanism by which ligustrazine affects inflammation of the airways. (Related: Holistic treatments for asthma in children: TCM found to be effective at reducing attacks, hospitalizations.)
In their experiment, the researchers constructed a mouse model with four groups of randomly selected animals. The control group was composed of healthy mice, while neutrophilic asthma was induced in the animals of the other three groups.
The neutrophilic asthma group did not receive any treatment. The ligustrazine group was injected with 80 milligrams per kilogram (mg/kg) of the natural compound. The dexamethasone group was treated with 0.5 mg/kg injection of the aforementioned corticosteroid, a common treatment for asthma.
The treatment lasted for two weeks. Twenty-four hours after the last challenge, all animals underwent the bronchoprovocation test by inhaling metacholine aerosol, a substance that tests the reactivity of the lungs.
After sacrificing the mice, researchers collected bronchoalveolar lavage fluid for analysis. They measured the total number of while blood cells and performed differential counts of neutrophils and eosophils.
They also analyzed the levels of IL-17 and IL-10 present in the lavage fluid. The former cytokine triggers inflammation in asthma and other diseases and disorders, while the latter inhibits it.
Last but not least, they examined the lung tissue for pathological changes caused by the induction of neutrophilic asthma. They also looked for changes wrought by treating the mice with either ligustrazine or dexamethasone.
The SU researchers reported that the airways of the neutrophilic asthmatic mice were much more responsive than those in the animals of the control group. However, the ligustrazine and dexamethasone groups showed much lower airway reactivity.
Furthermore, the neutrophil and eosinophil counts in the two treated groups were lower than in the untreated asthmatic group. The mice treated with natural ligustrazine had much lower counts than the animals treated with the corticosteroid.
Examination of the lung tissue of neutrophilic asthmatic mice revealed a significant amount of inflammatory cells from around the broncheoles and blood vessels of the lungs.
The two treatment groups showed significant improvement of their airways. Again, the ligustrazine-treated mice were better off than their dexamethasone-treated counterparts.
Asthmatic mice showed much higher levels of inflammation-causing IL-17 and lower levels of IL-10. The treatments were able to reduce the IL-17 levels while improving the amount of IL-10 present. The changes were greater in the ligustrazine-treated mice.
The researchers concluded that ligustrazine could improve the airway inflammation of mice with neutrophilic asthma. Ligustrazine lowered the levels of an inflammatory cytokine while also improving an anti-inflammatory cytokine.
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