A group led by Dr. You-Yang Zhou at the University of Illinois College
of Medicine, Chicago, IL have discovered that caveolin-1 modulation of
endothelial nitric oxide synthase (eNOS) activity regulates innate
immunity and inflammation-induced lung injury. They present these
findings in the May 2010 issue of The American Journal of Pathology.
The innate immune system defends the body against infection in a
non-specific manner. Nitric oxide, an antimicrobial agent, and eNOS, an
enzyme that produces nitric oxide, play a key role in innate immunity
and inflammation, as does caveolin-1, a protein involved in cell
signaling. An interaction between caveolin-1 and eNOS is thought to be
involved in this process.
To determine the respective roles of caveolin-1 and eNOS in innate
immunity and inflammation, Mirza et al generated mice that lacked
expression of both caveolin-1 and eNOS. They show that eNOS activation
inhibited the immune system in caveolin-1-deficient mice, resulting in a
decrease in the levels of proinflammatory molecules and improved
survival when compared with mice deficient in both caveolin-1 and eNOS.
In addition, eNOS activation in caveolin-1-deficient mice protected
against inflammation-induced lung injury. The interaction between
caveolin-1 and eNOS may therefore represent a new therapeutic target for
inflammation and lung injury.
Dr. Zhou’s group "present the first genetic evidence of the
physiological significance of [caveolin-1] modulation of eNOS activity
in regulating [innate immune] signaling. …[They] show that [caveolin-1]
modulation of eNOS activity is a key regulator of innate immunity and
inflammatory lung injury."
Source : American Journal of Pathology