Airway Inflammation and Cellular Stress in Noneosinophilic Atopic Asthma: Recommendation


Airway Inflammation and Cellular Stress in Noneosinophilic Atopic Asthma: RecommendationToward this result, Douwes et al have supported the hypothesis that nonatopic asthma derives from the activation of innate immunity, which triggers the neutrophilic response. Still, Simpson et al recruited mainly atopic asthmatic patients and were still able to identify a significant percentage of neutrophilic subjects. Therefore, the relationship between nona-topic asthma and neutrophilia is not yet clear. there
It is important to notice that by defining sputum neutrophilia at neutrophil percentages of > 65.3% or > 61%, respectively, Green et al and Simpson et al included a large number of asthmatic patients in the neutrophilic subgroup. However, Belda et al analyzed sputum samples from a large cohort of healthy subjects and set the upper normal limit for neutrophil percentages at 77.7%, according to which neutrophilic NEA is less frequent than what these authors showed.
Having found no difference in neutrophil numbers between patients with EA and those with NEA, no difference was also found in the levels of neutrophilic markers, such as MPO and IL-8. Gibson et al2 also reported similar MPO levels in NEA and EA patients, but increased IL-8 levels in NEA patients.
However, in that study NEA patients showed increased numbers of neutrophils. Despite low eosinophil numbers in NEA patients, no difference was found in ECP or GM-CSF levels compared to EA patients. GM-CSF has been designated as the main cytokine enhancing the survival of eosinophils in the asthmatic airways, but it affects multiple leukocyte lineages and has much broader functional activities. ECP is an eosinophil degranulation product; however, there have been re-ports from patients with noneosinophilic airway disease, such as COPD, of increased ECP levels. Previous studies have shown a close correlation between total cell count and ECP levels, as well as between the severity of airflow limitation and ECP levels. It is possible that the few eosinophils that are present in the airways of NEA patients are highly degranulated due to an increase in the presence of degranulating agents. There is also evidence that other types of cells except eosinophils, like neutrophils, contain ECP. Therefore, our finding of similar ECP levels in NEA and EA patients might be associated with the similar neutrophil counts in the two groups of asthma patients.