Eosinophil chemokines eotaxin-1 and eotaxin-2 were significantly upregulated (false discovery rate [FDR] < 0.05) by approximately 2.1- and 1.4-fold in the asthma study and by 2.3- and 1.7-fold in the COPD study following benralizumab treatment.
Among elderly asthmatics, subjects with severe asthma had lower FEV1 (% predicted) value, but showed significantly higher serum levels of eotaxin-2 and TGF-β1, than those with non-severe asthma (<i>P</i> < 0.05 for each).
It was observed that lung interstitial macrophages derived from OVA-induced asthmatic mice expressed phenotypic markers associated with alternatively activated macrophages (M2), including cluster of differentiation-206, transglutaminase 2, arginase (Arg) 1 and chemokine ligand (CCL)17/CCL22/CCL24 secretion.
We previously suggested that Eo2+179T>C and Eo2+275C>T of the eotaxin-2, and Eo3+2497T>G of the eotaxin-3 were significantly associated with susceptibility to asthma.
In conclusion, the susceptibility of patients with asthma to high eotaxin-2 production may be due to genetic effects of the CCL24+1272A--> G polymorphism, ht2 and ht6 haplotypes.
We previously suggested that Eo2+179T>C and Eo2 +275C>T of the eotaxin-2, and Eo3 +2497T>G of the eotaxin-3 were significantly associated with susceptibility to asthma.
We found that EoB179T > C (P = 0.0001), EoB275C > T (P = 0.018) of the eotaxin-2 and EoA2497T > G (P = 0.003) of the eotaxin-3 were significantly associated with the susceptibility of asthma.