Heat shock affects host-pathogen interaction in Galleria mellonella infected with Bacillus thuringiensis

- Galleria mellonella exposed to short-term heat shock is more resistant to infection.
- Higher expression of defense genes is observed in shocked animals.
- Hemolymph of heat-shocked animals shows enhanced antimicrobial activity.
- Defense peptides of shocked insects are more resistant to bacterial proteases.

We report that Galleria mellonella larvae exposed to heat shock was more resistant to infection with entomopathogenic bacteria Bacillus thuringiensis. The insects were exposed to a temperature of 40 °C for 30 min directly before injection of vegetative bacterial cells. It appeared that the kinetics of the immune response was affected in heat-shocked animals. The infection-induced antimicrobial activity of larval hemolymph was stronger in shocked animals in comparison to the non-shocked ones. Hemolymph proteins of molecular weight below 10 kDa, corresponding to the size of antimicrobial peptides, were responsible for this activity. Furthermore, the transcription level of genes encoding antimicrobial peptides: cecropin, gallerimycin, and galiomycin was increased in the fat bodies of insects exposed to heat shock before infection. On the contrary, the heat-shock treatment did not enhance expression of the metalloproteinase inhibitor-IMPI in the infected animals. The difference in the amount of antimicrobial peptides and, consequently, in the defense activity of insect hemolymph, persisted after the action of bacterial metalloproteinases, which are well-known virulence factors. Furthermore, peptides with antimicrobial activity in the hemolymph of infected larvae pre-exposed to heat shock appeared to be more resistant to proteolytic degradation both in vitro and in vivo. Our results point to the mechanism of cross-protection of thermal stress toward innate immune response.