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Divisions of 1 Pulmonary and
Critical Care Medicine, and 2 Bone
Marrow Transplantation,
We reported that
allogeneic T cells given to irradiated mice at the time of marrow
transplantation stimulated tumor necrosis factor
(TNF)-
, interferon (IFN)-
, and nitric oxide
(· NO) production in the lung, and the addition of
cyclophosphamide (known to stimulate superoxide production) favored the
generation of a nitrating species. Although keratinocyte growth factor
(KGF) prevents experimental lung injury by promoting epithelial repair,
its effects on the production of inflammatory mediators has not been
studied. KGF given before transplantation inhibited the T cell-induced
increase in bronchoalveolar lavage fluid protein, TNF-, IFN-, and
nitrite levels measured on day 7 after
transplantation without modifying cellular infiltration or
proinflammatory cytokines and inducible · NO synthase mRNA.
KGF also suppressed · NO production by alveolar macrophages
obtained from mice injected with T cells. In contrast, the same
schedule of KGF failed to prevent permeability edema or suppress
TNF-, IFN-, and · NO production in mice injected with
both T cells and cyclophosphamide. Because only epithelial cells
respond to KGF, these data are consistent with the production of an
epithelial cell-derived mediator capable of downregulating macrophage
function. However, the presence of a nitrating agent impairs
KGF-derived responses.
nitric oxide; peroxynitrite; idiopathic pneumonia syndrome; polymerase chain reaction; proinflammatory cytokines
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