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NF-kB is a major transcription factor mediating inflammatory response. Inresponse to pro-inflammatory stimulus, it exhibits characteristic response -- apulse followed by noisy oscillations in concentrations of considerably smalleramplitude. NF-kB is an important mediator of cellular communication, as it isboth activated by and upregulates production of cytokines, signals used bywhite blood cells to find the source of inflammation. While the oscillatorydynamics of NF-$\kappa$B has been extensively investigated both experimentallyand theoretically, the role of the noise and the lower secondary amplitude hasnot been addressed.  We use a cellular automaton model to address these issues in the context ofspatially distributed communicating cells. We find that noisy secondaryoscillations stabilize concentric wave patterns, thus improving signal quality.Furthermore, both lower secondary amplitude as well as noise in the oscillationperiod might be working against chronic inflammation, the state ofself-sustained and stimulus-independent excitations.  Our findings suggest that the characteristic irregular secondary oscillationsof lower amplitude are not accidental. On the contrary, they might have evolvedto increase robustness of the inflammatory response and the system's ability toreturn to pre-stimulated state.

Noisy NFkB oscillations stabilize and sensitize cytokine signaling in space