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. Author manuscript; available in PMC: 2018 Feb 26.
Published in final edited form as: Cell Rep. 2018 Feb 13;22(7):1787–1797. doi: 10.1016/j.celrep.2018.01.016

Figure 7. Model for Evasion of the Phagocyte Respiratory Burst by Typhoidal Salmonella Serovars.

Figure 7

(A) The polysaccharide chains of the Vi antigen shield underlying surface structures from IgM binding.

(B) Restoration of the fepE pseudogene (ΨfepE) in S. Typhi results in production of very long O antigen chains that rival the Vi antigen in length, thereby elevating IgM binding to the bacterial surface.

(C) Deletion of the capsule biosynthesis genes in the S. Typhi tviB-vexE mutant exposes the short and long O antigen chains, thereby resulting in IgM binding.

(D) The very long O antigen chains of S. Paratyphi A contain the O2 antigen, which does not bind natural IgM, thereby shielding underlying surface structures.

(E) The short and long O antigen chains present in an S. Paratyphi A fepE mutant do not bind IgM, but are too short to prevent IgM binding to other surface antigens. Ag, antigens; CM, plasma membrane; L, long O antigen chains; OM, outer membrane; S, short O antigen chains; Vi, Vi antigen; VL, very long O antigen chains.