Many seminars during the year will be delivered by the Purdue University Fort Wayne LDS Team on topics of interest to students, researchers, and local and global communities. The regular time of the seminars is Wednesday from 1:30pm to 2:30pm.

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Abstract

Mycobacterium tuberculosis (Mtb) infection is influenced by the innate immune response, in which macrophages contribute to bacterial containment but also provide an intracellular environment for bacterial survival and replication. Experimental evidence indicates that intracellular bacterial burden can affect infected-macrophage death, creating a feedback between bacterial accumulation, macrophage necrosis, bacterial release, and subsequent infection. In this talk, we present a within-host mathematical model that incorporates a saturating dependence of infected-macrophage necrosis on intracellular bacterial burden. We examine how this mechanism affects infection establishment, coexistence, bacterial burden, and local stability.

The analysis identifies distinct mechanisms governing bacterial invasion and persistent infection. While infection establishment is strongly influenced by the aggregate innate immune response, persistence depends on the interplay among intracellular bacterial burden, macrophage-mediated bacterial control, and infected-macrophage fate. In particular, numerical bifurcation analysis reveals two supercritical Hopf bifurcations as a parameter associated with macrophage-dependent intracellular bacterial control varies. These bifurcations delimit an interval in which stationary coexistence loses stability and stable periodic solutions emerge, before stability is recovered. This behavior is observed across three parameter families with substantially different oscillation periods. Overall, the results illustrate how different components of the innate immune response contribute to infection establishment and the dynamical regulation of persistent infection.

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Coming Soon!