Biology subjects

Bajgar, A.

Publications and source records attributed to Bajgar, A..

3 recordsLinked to original sources

bioRxiv2026

Photoperiod induces sex-specific immune priming in Pyrrhocoris apterus

Seasonal variation in day length provides a reliable cue that allows insects to anticipate upcoming environmental challenges. Here, we demonstrate that photoperiod induces pronounced, sex-specific immune priming in the linden bug Pyrrhocoris apterus. Females exposed to short-day, diapause-inducing conditions exhibited broadly enhanced immune activity compared with long-day females, whereas immune parameters in males were largely unaffected by photoperiod. Short-day females showed increased immune cell abundance, elevated expression of immune-related genes, enhanced humoral immune activity, and increased resistance to bacterial infection. Importantly, photoperiod-induced immune priming depended on a functional m-cryptochrome gene, linking seasonal immune regulation to the photoperiodic timer. Consistent with laboratory results, females collected under natural short-day conditions also displayed enhanced immune parameters despite increased environmental variability. Together, our findings identify photoperiod as a key regulator of immune preparedness in female insects and reveal a sex-specific anticipatory immune strategy associated with seasonal timing.

physiology↗

bioRxiv2023

Metabolism of glucose and trehalose by cyclic pentose phosphate pathway is essential for effective immune response in Drosophila

Activation of immune cells requires the remodeling of cell metabolism in order to support immune function. We study these metabolic changes through the infection of Drosophila larvae by parasitoid wasp. Neutralization of the parasitoid egg involves the differentiation of lamellocytes, which encapsulate the egg. A melanization cascade is initiated, producing toxic molecules to destroy the egg; meanwhile the capsule created also protects the host from the toxic reaction. We combine transcriptomics and metabolomics, including 13C-labeled glucose and trehalose tracing, as well as genetic manipulation of sugar metabolism to study changes in metabolism, specifically in Drosophila hemocytes. We found that hemocytes increase the expression of several carbohydrate transporters, and accordingly uptake of sugar during infection. These carbohydrates are metabolized by increased glycolysis, associated with lactate production, and cyclic pentose phosphate pathway (PPP), in which glucose-6-phosphate is re-oxidized to maximize NADPH production. Oxidative PPP is required for lamellocyte differentiation and resistance, as is systemic trehalose metabolism. In addition, fully differentiated lamellocytes use a cytoplasmic form of trehalase to cleave trehalose to glucose, within the cell, to fuel cyclic PPP. Intracellular trehalose metabolism is not required for resistance, but may be associated with host protection from its own toxic response. Thus, our results suggest that sugar metabolism within immune cells, and specifically in cyclic PPP, may be important for not only fighting infection, but also for protecting the host from its own immune response and ensuring sufficient fitness of the survivor.

immunology↗

bioRxiv2020

Macrophage-derived insulin/IGF antagonist ImpL2 regulates systemic metabolism for mounting an effective acute immune response in Drosophila

In response to invading pathogens, macrophages metabolically polarize towards Hif1-induced aerobic glycolysis, requiring increased supply of nutrients. Here, we show that in order to obtain sufficient resources, Drosophila macrophages release the insulin/IGF antagonist ImpL2, whose expression is regulated by Hif1. ImpL2 remotely induces the release of lipids and carbohydrates from adipose tissue by reducing insulin signaling, followed by increased nutrient accumulation in activated immune cells. ImpL2 thus translates the metabolic requirements of immune cells into a systemic metabolic switch. Although these ImpL2 effects are essential during the acute immune response to streptococcal infection, they become maladaptive upon chronic infection by an intracellular pathogen. The relevance of our model to mammalian immunometabolism is demonstrated by the increased expression of the ImpL2 homolog IGFBP7 in human macrophages exposed to Streptococcus.

immunology↗