Inflammatory Response of the Ascidian Ciona intestinalis

Abstract

The Ciona intestinalis inflammatory response to several irritants appears to be composed of a complex reaction set. The cellular reactions in the tunic involve hemocyte infiltration, hemocyte and epidermis activities, vacuolization, and cell disruption, while cell products can contribute to form capsule components and/or cause a tunic wound. In this response, the involvement of the pharynx, as the main immune-competent organ, has been disclosed by a lipopolysaccharide challenge that upregulates innate immunity genes and transcription activation genes. The pharynx responds through hemocyte recruitment into the pharynx vessels, enhancement of galectin-like lectins in the serum hemolymph, an alternative complement pathway, and phenoloxidase system activity. Upregulation involves genes for C-type lectins (CiCD94, CiMBL), galectins, cytokines (CiTNF?, IL17-like), phenoloxidase, FACIT-type IX-like collagen, and a transcription activator gene (CiCAP). The encoded proteins are components of distinct molecular families that support the evolution of several mechanisms, which generate sequence diversity in genes with immune functions. Clusters of similar genes or exons strengthen the concept that inflammatory factors are part of large molecular families originated by a process of divergent evolution from a common ancestor and in some cases of gene co-option during evolution.