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