Evaluating the mitochondrial activity and inflammatory state of dimethyl sulfoxide differentiated PLB-985 cells

Many factors negatively impact domesticated honeybee (Apis mellifera) health causing a global decrease in their population year after year with major losses occurring during winter, and the cause remains thus far unknown. Here, we monitored for 12 months North American colonies of honeybees enduring important temperature variations throughout the year, to assess the metabolism and immune system of honeybees of summer and winter individuals. Our results show that in flight muscle, mitochondrial respiration via complex I during winter is drastically reduced compared to summer. However, the capacity for succinate and glycerol-3-phosphate (G3P) oxidation by mitochondria is increased during winter, resulting in higher mitochondrial oxygen consumption when complex I substrates, succinate and G3P were assessed altogether. Pyruvate kinase, lactate dehydrogenase, aspartate aminotransferase, citrate synthase and malate dehydrogenase tend to have reduced activity levels in winter unlike hexokinase, NADH dehydrogenase and pyruvate dehydrogenase. Transcript abundance of highly important immunity proteins like Vitellogenin and Defensin-1 were also increased in winter bees, and a stronger phagocytic response as well as a better hemocyte viability was observed during winter. Thus, a reorganization of substrate utilization favoring succinate and G3P while negatively affecting complex I of the ETS is occurring during winter. We suggest that this might be due to complex I transitioning to a dormant conformation through post-translational modification. Winter bees also have an increased response for antibacterial elimination in honeybees. Overall, this study highlights previously unknown cellular mechanisms between summer and winter honeybees that further our knowledge about this important species.

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Functional platelet‐derived mitochondria induce the release of human neutrophil microvesicles

Léger

Soucy

Veilleux

et al. 2022

EMBO Reports

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Inflammation is an essential process of host defense against infections, illness, or tissue damage. Polymorphonuclear neutrophils (PMN) are among the first immune cells involved in acute inflammatory responses and are on the front line in the fight against bacterial infections. In the presence of bacterial fragments, PMN release inflammatory mediators, enzymes, and microvesicles in the extracellular milieu to recruit additional immune cells required to eliminate the pathogens. Recent evidence shows that platelets (PLTs), initially described for their role in coagulation, are involved in inflammatory responses. Furthermore, upon activation, PLT also release functional mitochondria (freeMitos) within their extracellular milieu. Mitochondria share characteristics with bacterial and mitochondrial damage‐associated molecular patterns, which are important contributors in sterile inflammation processes. Deep sequencing transcriptome analysis demonstrates that freeMitos increase the mitochondrial gene expression in PMN. However, freeMitos do not affect the mitochondrial‐dependent increase in oxygen consumption in PMN. Interestingly, freeMitos significantly induce the release of PMN‐derived microvesicles. This study provides new insight into the role of freeMitos in the context of sterile inflammation.

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Evaluating the mitochondrial activity and inflammatory state of dimethyl sulfoxide differentiated PLB-985 cells

Cited by 4 publications

References 69 publications

Caffeic acid phenethyl ester analogues as selective inhibitors of 12-lipoxygenase product biosynthesis in human platelets

Caffeic acid phenethyl ester analogues as selective inhibitors of 12-lipoxygenase product biosynthesis in human platelets

Overwintering in North American domesticated honeybees (Apis mellifera) causes mitochondrial reprogramming while enhancing cellular immunity

Functional platelet‐derived mitochondria induce the release of human neutrophil microvesicles

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