Adaptation and conservation of CL-10/11 in avian lungs: implications for their role in pulmonary innate immune protection

The common avian origin of many zoonotic infections and epidemics warrants investigation into the mechanism of respiratory surface protection in reservoir species such as birds. Our recent molecular investigations on the evolution and pulmonary expression of an ancient family of proteins, the C-type lectins, have revealed unique molecular adaptations in the surfactant proteins avian SP-A1 (aSP-A1), aSP-A2 and aSP-C coupled with the loss of surfactant protein-D (SP-D) in the avian lineage. As surfactant proteins are members of the collectin family, a subgroup of the C-type lectins, an in silico search for related non-surfactant collectin proteins (Collectin-10 (CL-10) and Collectin-11 (CL-11)) in the NCBI genome database was conducted to understand their evolution in the avian lineage. In addition, both CL-10 and CL-11 gene expression in the lungs and other organs of zebra finches and turkeys was confirmed by PCR. These PCR-confirmed zebra finch and turkey CL-10 and CL-11 sequences were compared with sequenced and in silico-predicted vertebrate homologues to develop a phylogenetic tree. Compared with avian surfactant proteins, CL-10 and CL-11 are highly conserved among vertebrates, suggesting a critical role in development and innate immune protection. The conservation of CL-11 EPN and collagen domain motifs may compensate to some extent for the loss of SP-D in the avian lineage.This article is part of the theme issue 'The biology of the avian respiratory system'.