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. Author manuscript; available in PMC: 2009 Jun 8.
Published in final edited form as: Cell Microbiol. 2008 Aug 5;10(11):2257–2270. doi: 10.1111/j.1462-5822.2008.01205.x

Fig. 1. Viable, exponentially-growing Opa- Gc do not induce the oxidative burst in PMNs.

Fig. 1

A. Absence of the oxidative burst in Gc-infected PMNs. Primary human PMNs were left uninfected, stimulated with PMA, or exposed to piliated, Opa- Gc of strains FA1090 (MOI 90) or MS11 (MOI 80). ROS production was measured as counts per sec of LDCL. B. Neither piliated nor nonpiliated Gc stimulate PMN oxidative metabolism. ROS production was measured in PMNs infected with MS11 Gc that were piliated (MOI 100) or constitutively nonpiliated due to deletion of the pilE pilin structural gene (MOI 94). C. Neither opsonized nor unopsonized Gc stimulate PMN oxidative metabolism. ROS production was measured in PMNs infected with unopsonized MS11 Gc (MOI 200) or bacteria opsonized in 10% autologous serum, either MS11 Gc (Gcops; MOI 130) or S. aureus (S. aureusops; MOI 40). D. PMNs bind and phagocytose unopsonized Gc. PMNs were infected with unopsonized FA1090 Gc at a MOI of 10 for 30 min. Intracellular and extracellular bacteria were discriminated from one another based on accessibility to a Gc-specific antibody before and after PMN permeabilization. Extracellular bacteria appear red/yellow; intracellular bacteria appear green. Scale bar = 10 µm.