Microbial Hijacking of Complement–Toll-Like Receptor Crosstalk

Min Wang, Jennifer L. Krauss, Hisanori Domon, Kavita B. Hosur, Shuang Liang, Paola Magotti, Martha Triantafilou, Kathy Triantafilou, John D. Lambris, George Hajishengallis*

*To whom correspondence should be addressed. E-mail: g0haji01{at}louisville.edu

This PDF file includes:

• Table S1. Detection of P. gingivalis in blood and internal organs of wild-type and C5aR-deficient (C5ar^–/^–) mice after intraperitoneal infection.
• Fig. S1. C5a dose-dependently promotes the intracellular survival of P. gingivalis and the cAMP response.
• Fig. S2. C5a does not affect P. gingivalis phagocytosis.
• Fig. S3. Relative mRNA abundance of negative regulators of TLR signaling in P. gingivalis–stimulated macrophages in the absence or presence of C5a.
• Fig. S4. C5a inhibits nitric oxide production in a dose- and time-dependent way.
• Fig. S5. TLR2-dependent cAMP production by P. gingivalis.
• Fig. S6. Association of TLR2, C5aR, and CXCR4 with G_M1 (lipid raft marker) in P. gingivalis–stimulated macrophages.
• Fig. S7. Generation of C5a by P. gingivalis from heat-inactivated human serum.
• Fig. S8. Up-regulation of IL-6 production by C5a in P. gingivalis–stimulated macrophages.

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