Asthma is a common chronic inflammatory disease in the airways. It was thought to be caused by the combination of environment and genetic factors. Previous studies have suggested that cell immunity played a vital role in regulating the airway hyper reactivity (AHR) and inflammation. Fei Xu of the First Affiliated Hospital of Nanchang University in China developed a mouse model for asthma by expressing the human IL10 and TGFB1 genes to explore the possible interaction between these two during asthma progression.

The transgenic mice exhibited enhanced expression of IL10 and TGFB1. During the ovalbumin challenge, transgenic mice displayed a 1.9-fold higher MCh50 score than wildtype counterparts. Meanwhile, a three-fold decrease of cell counts in bronchoalveolar lavage fluid (BALF) was also recorded. These results suggested that IL10 and TGFB1 cooperatively protected the respiratory system in response to antigenic stimulus.

To study the behaviors of these two genes, the team quantified the expression of downstream genes in both IL10 and TGFB1 signaling. The examined genes in IL10 signaling were significantly repressed, especially IL5. Meanwhile, most genes were not altered in TGFB1 signaling.

These evidences proved that the activation of IL10 and TGFB1 protected the host from ovalbumin-induced asthma, possibly through IL10 signaling. This study shed some light on the modulations these two genes and related networks to asthma progression.

For more on this study, read the article in Transgenic Research.