Biology subjects

Myerscough, M. R.

Publications and source records attributed to Myerscough, M. R..

3 recordsLinked to original sources

bioRxiv2020

Poor hive thermoregulation produces an Allee effect and leads to colony collapse

In recent years the honey bee industry has bee experiencing increased loss of hives. The accumulation of multiple stressors on a hive potentially drives hive loss in various ways, including winter loss and colony collapse disorder. One of these stressors is the breakdown of thermoregulation inside the hive. For pupae to develop correctly into healthy adult bees, the temperature within the hive must be regulated by the hive bees to within a narrow range that ensures optimal development. Suboptimal development in adults affects their brain and flight muscles so bees becomes inefficient foragers with shorter life spans. We model the effect of thermoregulation on hive health using a system of delay differential equations that gives insights into how varying hive temperatures have an effect on the survival of the colony. We show that thermoregulatory stress has the capacity to drive colony loss in the model via a saddle-node bifurcation with an associated Allee effect.

ecology↗

bioRxiv2019

Efferocytosis perpetuates substance accumulation inside macrophage populations

In both cells and animals, cannibalism can transfer harmful substances from the consumed to the consumer. Macrophages are immune cells that consume their own dead via a process called cannibalistic efferocytosis. Macrophages that contain harmful substances are found at sites of chronic inflammation, yet the role of cannibalism in this context remains unexplored. Here we take mathematical and experimental approaches to study the relationship between cannibalistic efferocytosis and substance accumulation in macrophages. Through mathematical modelling, we deduce that substances which transfer between individuals through cannibalism will concentrate inside the population via a coalescence process. This prediction was confirmed for macrophage populations inside a closed system. We used image analysis of whole slide photomicrographs to measure both latex microbead and neutral lipid accumulation inside murine bone marrow-derived macrophages (104 - 105 cells) following their stimulation into an inflammatory state ex vivo. While the total number of phagocytosed beads remained constant, cell death reduced cell numbers and efferocytosis concentrated the beads among the surviving macrophages. Since lipids are also conserved during efferocytosis, these cells accumulated lipid derived from the membranes of dead and consumed macrophages (becoming macrophage foam cells). Consequently, enhanced macrophage cell death increased the rate and extent foam cell formation. Our results demonstrate that cannibalistic efferocytosis perpetuates exogenous (e.g. beads) and endogenous (e.g. lipids) substance accumulation inside macrophage populations. As such, cannibalism has similar detrimental consequences in both cells and animals.

immunology↗

bioRxiv2019

A lipid-structured model for macrophage populations in atherosclerotic plaques

Atherosclerosis is a chronic inflammatory disease driven by the accumulation of pro-inflammatory, lipid-loaded macrophages at sites inside artery walls. These accumulations lead to the development of atherosclerotic plaques. The rupture of plaques that contain lipid-rich necrotic cores can trigger heart attacks and strokes via occlusion of blood vessels. We construct and analyse a system of partial integro-differential equations that model lipid accumulation by macrophages, including generating apoptotic cells and a necrotic core. The model includes the following cell behaviours: recruitment of macrophages into the plaque; macrophage ingestion of low density lipoproteins LDL and of apoptotic cells and necrotic material; lipid offloading to high density lipoproteins (HDL); macrophage emigration; and macrophage apoptosis and necrosis of apoptotic cells. With this model, we study how changes in parameters predict the characteristic features of plaque pathology. In particular, we find the qualitative form of lipid distribution across the macrophage population and show that high lipid loads can occur in the absence of LDL ingestion. We also demonstrate the importance of macrophage emigration in the model in mitigating and resolving inflammation and plaque lipid accumulation. ContributionsO_LIHZF: conceptualisation, formal analysis, investigation, methodology, visualisation, writing-- original draft preparation, writing--review and editing. C_LIO_LIHMB: conceptualisation, funding acquisition, methodology, project administration, resources, supervision, writing--review and editing. C_LIO_LIMRM: conceptualisation, funding acquisition, methodology, project administration, resources, supervision, writing--original draft, writing--review and editing. C_LI

immunology↗