Research Interests of the Laboratory: The main focus of our laboratory is the regulation of the inflammatory response. An in vivo model of acute lung injury induced by the intrapulmonary deposition of IgG immune complexes in rats has been developed. The role of various adhesion molecules (e.g. ICAM-1, VCAM-1), cytokines (e.g. TNFa), chemokines (e.g. MIP-2, CINC), anti-inflammatory interleukins (e.g. IL-10, IL-13), complement factors (e.g. C5a), and endogenous protease inhibitors (e.g. TIMP-2 and SLPI) are studied in this model as well as in vitro. A second area of research is sepsis. Major features of sepsis are the systemic responses (e.g. failing blood pressure, etc.) and the susceptibility to intrapulmonary infection. In an effort to understand this process, rats develop sepsis by cecal ligation/puncture and are then evaluated for increased susceptibility to injury after a direct pulmonary insult (airway instillation lipopolysaccharide or IgG immnue complex deposition). We find that adhesion molecules, cytokines, and especially the complement factor C5a contribute to the enhanced lung injury in the state of sepsis. In addition, we study some of the signaling molecules such as MAP-kinases and the transcription factor NF-kB involved in the inflammatory response. Our laboratory routinely uses some of the standard cellular and molecular biological techniques such as cloning, RT-PCR, Southern, Western and Northern blot analysis, ELISA, chemotaxis, antibody production, bacterial and mammalian expression of proteins, transfections etc.   Projects Under Study: Principal Investigator, “Lung Immunopathology” (Training Grant) HL07517 06/01/96 - 05/31/06 Principal Investigator, “Inflammatory Cells and Lung Injury” NIH/NHLBI PO1-HL31963 03/01/99 - 02/29/04 Principal Investigator; “Lung Injury by Oxygen Metabolites (MERIT) RO1- GM29507 NIH/NIGMS, 07/01/01 - 06/30/05 Principal Investigator, “Protective Effects of Anti-C5a in Sepsis,” NIH/NIGMS RO1- GM61656, 01/01/02 - 05/31/07