Does cold activate the Drosophila melanogaster immune system?

Abstract

Cold exposure appears to activate aspects of the insect immune system; however, the functional significance of the relationship between cold and immunity is unclear. Insect success at low temperatures is shaped in part by interactions with biotic stressors, such as pathogens, thus it is important to understand how and why immunity might be activated by cold. Here we explore which components of the immune system are activated, and whether those components differ among different kinds of cold exposure. We exposed Drosophila melanogaster to both acute (2h, -2°C) and sustained (10h, -0.5°C) cold, and measured potential (antimicrobial peptide expression, phenoloxidase activity, haemocyte counts) and realised (survival of fungal infection, wound-induced melanisation, bacterial clearance) immunity following recovery. Acute cold increased circulating haemocyte concentration and the expression of Turandot-A and diptericin, but elicited a short-term decrease in the clearance of gram-positive bacteria. Sustained cold increased the expression of Turandot-A, with no effect on other measures of potential or realised immunity. We show that measures of potential immunity were up-regulated by cold, whereas realised immunity was either unaffected or down-regulated. Thus, we hypothesize that cold-activation of potential immunity in Drosophila may be a compensatory mechanism to maintain stable immune function during or after low temperature exposure.

Insect Immunity Varies Idiosyncratically During Overwintering

“…increased bacterial clearance after autumn. This increased immune activity in the spring could also represent a (potentially prophylactic) response to an increase in pathogen stress that may either act to increase immunocompetence overall, or compensate for any damage to, or trade-offs experienced by, the immune system (Salehipour-Shirazi et al, 2017). As temperatures increase, infection by new pathogens, or growth of pathogens overwintering in the insect, may increase (Harvell et al, 2002;Altizer et al, 2006), thereby initiating increased immune activity in response to, or in preparation for, increased pathogen stress (Sinclair et al, 2013).…”

“…Indeed, overwintering honeybees downregulate genes encoding antimicrobial peptides (Steinmann et al., ), and damselflies have reduced resistance to bacterial infections during the winter (Córdoba‐Aguilar et al., ). Conversely, both cold exposure and diapause induction can activate the immune system in some insects (Le Bourg et al., ; Ragland et al., ; Marshall and Sinclair, ), even in the absence of pathogen infection (Zhang et al., ; Xu and James, ), perhaps to compensate for trade‐offs or cold‐induced damage (Salehipour‐Shiraz et al., ). Because of the potential trade‐offs associated with increased immunity, this implies that increased immune activity (even if compensatory) may be an adaptive response to overwintering pathogen pressures (Sinclair et al., ).…”

Cold exposure causes cell death by depolarization-mediated Ca 2+ overload in a chill-susceptible insect

“…plants, mammals, and insects (28)(29)(30)(31)(32)(33)(34), in which it has been associated with either cell damage (28,33,34) or cold resistance (29)(30)(31)(32). However, while several authors have proposed that apoptotic mechanisms are involved in insect chill injury (24,32,(35)(36)(37), the hypothesized link between membrane potential (V m ) and cell injury has not been directly documented. Thus, while several findings imply a causal relationship between V m and the manifestation of chill injury, it remains to be shown that injury onset can be achieved by V m depolarization independent of changes in temperature and/or extracellular K + .…”

Sugar intake interacts with temperature to influence reproduction and immunity in adult Culex pipiens mosquitoes

“…For example, food-limited Manduca sexta enhance constitutive immune defences while decreasing investment in inducible immune defences (Adamo et al 2016). Further, this type of reconfiguration can also occur in response to thermal stress (Salehipour-Shirazi et al 2016).…”