Excessive inflammation caused by unregulated inflammatory processes ca
n lead to disease. One example of this is seen in acute lung injury in
which an individual is unable to regulate an inflammatory response in
the lungs, with the net effect of self-induced tissue injury and loss
of organ function. The acute-phase reactant, C-reactive protein, inhi
bits acute lung injury in animal models and, in this regard, acts as a
major anti-inflammatory agent. Therefore, understanding the mechanism
by which C-reactive protein elicits this inhibitory effect may provid
e important information about the design of therapeutic agents for the
prevention or treatment of inflammation-mediated tissue injury and re
sultant loss of organ function.