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Biomedical subjects

Christina Warrender

Publications and source records attributed to Christina Warrender.

2 recordsLinked to original sources

Modeling intercellular interactions in early Mycobacterium infection.

Infection with Mycobacterium tuberculosis (Mtb) is characterized by localized, roughly spherical lesions within which the pathogen interacts with host cells. Containment of the infection or progression of disease depends on the behavior of individual cells, which, in turn, depends on the local molecular environment and on contact with neighboring cells. Modeling can help us understand the nonlinear interactions that drive the overall dynamics in this system. Early events in infection are particularly important, as are spatial effects and inherently stochastic processes. We describe a model of early Mycobacterium infection using the CyCells simulator, which was designed to capture these effects. We relate CyCells simulations of the model to several experimental observations of individual components of the response to Mtb.

Computer Simulation↗

Homeostasis of peripheral immune effectors.

In this paper, we use both mathematical modeling and simulation to explore homeostasis of peripheral immune system effector cells, particularly alveolar macrophages. Our interest is in the distributed control mechanisms that allow such a population to maintain itself. We introduce a multi-purpose simulator designed to study individual cell responses to local molecular signals and their effects on population dynamics. We use the simulator to develop a model of growth factor regulation of macrophage proliferation and survival. We examine the effects of this form of regulation in the context of two competing hypotheses regarding the source of new alveolar macrophages. In one model, local cells divide to replenish the population; in the other, only cells migrating from circulation divide. We find that either scenario is plausible, although the influx-driven system is inherently more stable. The proliferation-driven system requires lower cell death and efflux rates than the influx-driven system.

Animals↗