Background: Both acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP) show prominent eosinophilia in lung tissue; however, they differ in clinical course and pathological findings. Thus far, there have been some reports discussing the clinicopathological differences of AEP and CEP, however, biological approaches defining their differences were few. Objective: Interleukin-33 (IL-33) is a new cytokine known as inducer of Th2 cytokine and it potently enhances increase of eosinophils. We focused on IL-33 and compared its levels as well as Th2 cytokines in AEP and CEP. Methods: IL-33, Th2 cytokines (IL-4, IL-5) and IgE were measured in serum from healthy controls (n=8), and patients with AEP (n=3) and CEP (n=12) at admission. IL-33, IL-4, and IL-5 in bronchoalveolar lavage fluid (BALF) were also measured from patients with AEP (n=3), and CEP (n=8). Results: Serum IL-33 was dramatically elevated in patients with AEP (1684.1±1025.8 pg/ml), but not in controls (64.7±112.8 pg/ml) and CEP (143.9±200.4 pg/ml). In BALF analysis, IL-33 was under detectable levels in controls and CEP; by contrast, it was prominently elevated in AEP (394.7±318.8 pg/ml). Further, IL-4 and IL-5 were also significantly elevated in AEP, and levels of serum IL-33 was positively correlated with serum IL-4 and IL-5, and BALF IL-33 was also positively correlated with BALF IL-5. Conclusion: Our results suggested that IL-33 is a key molecule triggering the eosinophilia in AEP. This is the first report to establish the impact of IL-33 in eosinophilic pneumonia and to demonstrate the biological differences between AEP and CEP through IL-33 level.
Mato et al. (Thu,) studied this question.