Group B streptococci continue to be a significant cause of morbidity and mortality in human neonates and other immunocompromised hosts. Although great strides have been made in understanding the mechanisms of host defense against these organisms, we still do not understand a great deal about the pathogenesis of this most fulminant of bacterial infections. We wish to concentrate on three aspects of the pathogenesis of, and immunity to group B streptococcal infection that we feel have exciting potential. First, we will seek to determine exactly what role fibronectin (FN) has in promoting epithelial cell adherence to group B streptococci. In addition, we will determine how FN enhances the opsonic activity of polyclonal and monoclonal antibody. Second, we will determine if the profound neutropenia and marrow granulocyte store depletion commonly observed in human and experimental animal group B disease is the result of decreased production of leukocyte mobilizing factors, such as C3e, derived from the complement system. Lastly, we will determine if group B streptococci or their soluble products affect vascular endothelial cell-neutrophil interactions and, thus, contribute to the pathogenesis of the lung damage in this serious and often overwhelming bacterial infection.
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