FPR1 and infection: This may occur in a tissue infection milieu where neutrophils are subjected to numerous innate signals, such as integrin stimulation from Yptb binding, and LPS and fMLP shed from Yptb. While it is tempting to speculate that YopH prevents phagocytosis in tissue infection as has been observed in isolated phagocytes [39], internalized ΔyopH was recovered in infected tissues at levels comparable to WT-Yptb [36], suggesting that YopH does not contribute significantly to anti-phagocytosis activities of Yptb in this model of Yptb tissue infection.