Grant: Travel Awards - Institute Community Support

RelB is a protein which is involved in controlling inflammation, a process that helps fight off infections. Although inflammation can be helpful in protecting ourselves from disease, excessive inflammation can also result in disease. Cigarette smoke has been known to cause excessive inflammation, increasing the risk for many diseases.The purpose of this project is to study the role of RelB in cigarette smoke-induced inflammation. RelB has been shown to play a protective role against inflammation in lung cells such that cells deficient of RelB responded more hashly to smoke treatments, releasing more inflammatory mediators. The protective role of RelB has not yet been established in a living animal model. Given the trend seen with cells lacking RelB, it was predicted that mice lacking RelB would also develop higher levels of inflammation in response to smoke in comparison to mice with RelB. Meanwhile normal mice that express RelB would be protected against the inflammatory effects of smoke to an extent. Surprisingly, this did not occur. Although mice lacking RelB naturally have high levels of inflammation smoke exposure did not result in even higher inflammation in the lungs. In fact, in the absence of RelB, smoke treated mice had lower levels of inflammatory cells in the airways than the untreated mice. This decrease in cell number was significantly pronounced in neutrophils, first responder inflammatory cells. When assessing the effect of other inflammatory lung inhalants present in the environment such as chlorine, ovalbumin (an allergy model), and LPS (an infection model) on these mice, it was found that levels of inflammation did not change in the absence of RelB after exposure to these toxicants. These results suggests that RelB may specifically regulate cigarette smoke inflammation and that it may do this by modulating the activity or survival of the body's first line of response: the neutrophils.