Table 1: Effects of PPARγ ligands in mouse OVA models of allergic airways disease.

StrainLigandInflammationRemodelingAHRMechanismReferences

Balb/CCGZ IL-4, IL-5, IL-6, IL-13
eosinophils
mucus
collagen
wall thickness
GATA-3[25, 94]
Balb/CCGZ IFNγ, IL-2, IL-4
eosinophils
mucusN.D.[100]
Balb/CCGZ eosinophils ASM thickness [95]
Balb/CCGZ RGZ eosinophilsN.D. IL-10[99]
Balb/CRGZ PGZ IL-4, IL-5, IL-13, ECP
eosinophils
PTEN
IL-10
[27, 47]
Balb/CGI 262570 eosinophilsN.D.[92]

C57Bl/6RGZ PGZ IL-4, IL-5, IL-13,
VEGF, eotaxin, RANTES
eosinophils
IL-17 via NF 𝜅 B[93, 97]
C57Bl/6RGZ eosinophils mucus
wall thickness
[98]

ASM: airway smooth muscle; CGZ: ciglitazone; ECP: eosinophil cationic protein; IL: interleukin; N.D.: not determined; PGZ: pioglitazone; PTEN: phosphatase and tensin homologue deleted on chromosome ten; RANTES: regulated upon activation, normal T-cell expressed, and secreted; RGZ: rosiglitazone; VEGF: vascular endothelial growth factor.