Our research is focused on the mechanisms in innate immune inflammation in the lung, as seen in diseases such as ARDS or pneumonia. We concentrate on the neutrophil, as the first host defense cell that enters an inflamed region, and are particular interested in the role of chemokines in attracting this white blood cell into the inflammatory environment. We have generated several targeted strains of mice that lack particular chemokines, and they have taught us that the neutrophil-attracting chemokines are not all equivalent, that they may have unique functions in the organism.
Another theme that informs our work is the understanding that while inflammation in the lung or other organs may be local, it nonetheless has important systemic components that that regulate (among other things) neutrophil generation and mobilization from the marrow. These events are under the control of chemokines themselves as well as G-CSF, both of which may be regulated by IL-17A and F produced by lymphocytes of various lineages. A new direction is to deduce the importance of the gut and (perhaps) lung microbiomes in regulation of IL-17-producing lymphocytes, and the mechanisms by which this occurs.