
Podcast with Yoram Vodovotz on inflammation and immune system
How collaboration arrises and why it fails · Prof. Dr. Paul F.M.J. Verschure
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Show Notes
What if inflammation is not a disease but a communication system , one that becomes pathological only when its own signaling cascades spiral beyond the control mechanisms that normally contain them? Immunologist Yoram Vodovotz reframes inflammation as the body's intermediate-timescale information network, connecting injury detection to healing response, and explains why understanding its failure requires thinking at the level of whole-organism control rather than individual molecules. Subscribe for more from the Convergent Science Network podcast series. Yoram Vodovotz joins Paul Verschure and Tony Prescott to trace inflammation from its origins in single-cell stress responses through multi-organ coordination to the neural regulation of immune function via the vagus nerve. At its core, inflammation is communication: molecular pathways that connect an initial insult to a coordinated response. The problem arises when these same communication molecules , cytokines, damage-associated molecular patterns, coagulation factors , cross thresholds and become causative agents of disease rather than mere markers. Vodovotz illustrates this with examples ranging from mosquitoes fighting malaria parasites using the same inflammatory pathways as their human hosts to the deadly positive feedback loop between coagulation and inflammation following traumatic injury. The conversation builds toward a systems-level understanding of how organs mount distinct inflammatory responses on different timescales, with gut and lung tissues maintaining high thresholds against constant environmental exposure while internal organs respond immediately to any bacterial signal. Vodovotz argues that predefined organ-specific response patterns, shaped by evolutionary pressures, interact with neural control circuits, particularly vagal pathways, that monitor and modulate inflammation across the whole organism. When genetic variability makes an individual overly sensitive or the threat exceeds containment capacity, the system fails and inflammation becomes the disease itself. Key topics include why inflammation may underlie all disease states, how autopoiesis and homeostatic self-maintenance connect to inflammatory control, the evidence for cross-organism transfer of inflammatory information between parasite vectors and hosts, why vagus nerve stimulation can outperform systemic drugs in treating inflammatory disease, and how computational models of organ-specific inflammatory dynamics could guide therapeutic intervention. Part of the Convergent Science Network podcast series from the BCBT Summer School.