# Trematode infection buffers heat stress in blue mussels Mytilus edulis: The role of heat shock proteins

## TL;DR

This study shows that trematode infection in blue mussels may help them survive heat stress by boosting heat shock proteins.

## Contribution

The study reveals a novel role of parasitism in enhancing thermal resilience through stress-induced heat shock protein upregulation.

## Key findings

- High trematode infection levels in mussels led to increased survival at 35°C despite no significant overall survival benefit.
- Heat shock proteins hsp24, hsp70, and hsp90 were upregulated with higher temperatures and infection levels.
- Parasite-induced upregulation of hsp90 suggests a potential tolerance mechanism through stress priming.

## Abstract

The influence of parasite infection on host thermal tolerance remains poorly understood. To address this, we investigated how infection with the trematode Himasthla elongata affects survival and heat shock protein expression in the blue mussel Mytilus edulis following repeated exposure to heat stress in a simulated intertidal environment.Two groups of mussels with experimentally induced low (55.3 ± 35.6 metacercariae per mussel) and high (148.6 ± 78.2 metacercariae per mussel) infection levels were exposed to air (31°C, 33°C or 35°C) for 2 h over 10 days to simulate a tidal cycle. Survival was assessed daily. In addition, the mRNA expression level of three heat shock genes (hsp24, hsp70 and hsp90) was assessed in mussels exposed to 17°C and 33°C for 2 h over a three‐day period. Dissection confirmed clear differences in infection levels between groups.Survival decreased significantly with increasing air temperature, but in the 35°C treatment, mussels with high infection levels exhibited a near‐significant increase in survival. Expression of hsp24, hsp70 and hsp90 increased with rising air temperatures, and high infection levels significantly upregulated hsp90.Although trematode infection did not significantly increase survival, our results suggest that trematode infection can protect against thermal stress by upregulating specific heat shock proteins in M. edulis. The hsp responses point to a parasite‐induced tolerance mechanism, potentially through stress priming or frontloading, and highlight an overlooked role of parasitism in mediating thermal resilience in intertidal ecosystems.

The influence of parasite infection on host thermal tolerance remains poorly understood. To address this, we investigated how infection with the trematode Himasthla elongata affects survival and heat shock protein expression in the blue mussel Mytilus edulis following repeated exposure to heat stress in a simulated intertidal environment.

Two groups of mussels with experimentally induced low (55.3 ± 35.6 metacercariae per mussel) and high (148.6 ± 78.2 metacercariae per mussel) infection levels were exposed to air (31°C, 33°C or 35°C) for 2 h over 10 days to simulate a tidal cycle. Survival was assessed daily. In addition, the mRNA expression level of three heat shock genes (hsp24, hsp70 and hsp90) was assessed in mussels exposed to 17°C and 33°C for 2 h over a three‐day period. Dissection confirmed clear differences in infection levels between groups.

Survival decreased significantly with increasing air temperature, but in the 35°C treatment, mussels with high infection levels exhibited a near‐significant increase in survival. Expression of hsp24, hsp70 and hsp90 increased with rising air temperatures, and high infection levels significantly upregulated hsp90.

Although trematode infection did not significantly increase survival, our results suggest that trematode infection can protect against thermal stress by upregulating specific heat shock proteins in M. edulis. The hsp responses point to a parasite‐induced tolerance mechanism, potentially through stress priming or frontloading, and highlight an overlooked role of parasitism in mediating thermal resilience in intertidal ecosystems.

The study shows that parasite infection changes heat shock protein expression and can increase heat tolerance in blue mussels. By separating parasite and temperature effects, the results suggest that infection may improve survival during heat stress, highlighting important parasite–host interactions for climate change resilience.