inhibit local inflammatory responses to Actinetobacter baumannii Pneumonia (a Gram-negative pathogen that is often resistant to many antibiotics), and may thereby actually facilitate, rather than inhibit, bacterial survival and outgrowth [8]. Here we report for the first time that SAA (specifically SAA1/2 and to a smaller extent SAA3) is greatly induced in the bladder wall and, to a lesser extent, the urothelium in response to UPEC instilled into the urinary tract via catheterization. As seen by immunofluorescence microscopy, infection with UPEC resulted in high levels of cytoplasmic SAA in comparison to the more subdued, primarily nuclear expression pattern of SAA in uninfected urothelial cells (see Fig. 1). Heightened levels of SAA expression within the bladder wall versus the urothelium suggest that infiltrating immune effector cells and resident host cells within this compartment are primary contributors to SAA production during a UTI. 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