Suppression of intestinal immunity through silencing of TCTP by RNAi in transgenic silkworm, Bombyx mori

• BmTCTP RNAi silkworms were constructed successfully by transgenic technique.
• The gut AMP from BmTCTP RNAi silkworm wasn't induced after oral microbial challenge.
• Survival rates of BmTCTP RNAi silkworm larvae decreased upon bacterial infection.
• BmTCTP RNAi affected dynamics of ERK phosphorylation in silkworm midgut.

Intestinal immune response is a front line of host defense. The host factors that participate in intestinal immunity response remain largely unknown. We recently reported that Translationally Controlled Tumor Protein (BmTCTP) was obtained by constructing a phage display cDNA library of the silkworm midgut and carrying out high throughput screening of pathogen binding molecules. To further address the function of BmTCTP in silkworm intestinal immunity, transgenic RNAi silkworms were constructed by microinjection piggBac plasmid to Dazao embryos. The antimicrobial capacity of transgenic silkworm decreased since the expression of gut antimicrobial peptide from transgenic silkworm was not sufficiently induced during oral microbial challenge. Moreover, dynamic ERK phosphorylation from transgenic silkworm midgut was disrupted. Taken together, the innate immunity of intestinal was suppressed through disruption of dynamic ERK phosphorylation after oral microbial infection as a result of RNAi-mediated knockdown of midgut TCTP in transgenic silkworm.