Pulmonary parenchyma becomes a self-organized dissipative structure in lung cancers and pulmonary inflammatory diseases.

Far-from-equilibrium thermodynamics were studied in patients with either lung cancer or pulmonary inflammatory diseases. Histological and mechanical activities were due to myofibroblasts. A study on isolated lung fragments treated with the Huxley formalism showed that mechanical abnormalities were similar in both groups: maximum velocity, isometric tension, maximum efficiency, force of non-muscle (NM) myosin crossbridge (CB), time stroke (ts), rate constants for CB detachment, and catalytic constant. Only maximum myosin ATPase activity, myosin content, and CB attachment constant were higher in inflammatory processes than in cancers. Contractile samples were open systems. In each group, β-catenin, NMIIA and B myosins were present. Thermodynamic force (TFo) and flow (TFl) did not show any significant difference between the two groups of patients. In both groups, TFo varied nonlinearly with TFl. This showed that these two systems behaved far-from-equilibrium. Entropy production rate was equal to the TFo × TFl product and did not show any significant statistical difference between the two groups. Excess entropy production was negative in both groups which showed that they were self-organized. In conclusion, the two groups of patients evolved towards self-organized dissipative structures driven by TGF-β1, which created a tissue capable of contractility thanks to myofibroblasts generated by inflammation.