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. Author manuscript; available in PMC: 2017 Jan 1.
Published in final edited form as: J Immunol. 2015 Nov 23;196(1):428–436. doi: 10.4049/jimmunol.1501688

Figure 7. Working model illustrating that LPS and TRPV4 signal cooperate to alter macrophage phenotypic change leading to enhanced clearance of infection and resolution of lung injury.

Figure 7

Our data suggest that TRPV4 is sensitized by extracellular matrix stiffness in the range of inflamed/fibrotic lung. Interaction between the LPS signal and the matrix stiff signal through TRPV4 promote increased TRPV4 channel activity and macrophage phenotypic change leading to increased clearance of bacteria and resolution of infection-associated lung injury.