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Allergic inflammation is a general host-defense mechanism for dealing with perceived foreign invaders. Although most effort has been directed toward understanding how this response gets turned on, how it gets turned off again when no longer needed is just as important to an organism's survival. We postulate that the control of the allergic inflammatory response is achieved via frequency modulation whereby a sequence of self-resolving events is repetitively invoked only so long as Ag is present. This leads to the notion of a unitary inflammatory event that we argue has formal similarity to the skeletal muscle twitch, albeit manifest over a much longer time scale. To test the plausibility of this hypothesis, we created an agent-based computational model of the allergic inflammatory response in the lungs. Continual stimulation of the model results in cycles of tissue damage and repair interspersed with periods of nonresponsiveness indicative of a refractory period. These findings are consistent with the inflammatory twitch hypothesis and the notion that the allergic inflammatory response is controlled via frequency modulation. We speculate that chronic inflammatory diseases may represent a failure of the inflammatory twitch to resolve toward baseline.

The Inflammatory Twitch as a General Strategy for Controlling the Host Response