Computed C3b opsonization per cell if factor H can be acquired on the cell surface of the pathogen.

Upper panels, distributions of opsonization for different C. albicans concentrations. Microbial cell densities for subfigures (I)-(V) can be seen from the corresponding points in the lower panel (see also text). The dotted vertical line in each subfigure represents the mean value of the optimal threshold interval to distinguish the two signals. Lower panel, mean opsonization on host and pathogen surfaces as functions of pathogen concentration, double logarithmic plot. Erythrocyte counts used are indicated by the light blue shaded area (mean 4.64 ⋅ 1012 erythrocytes per litre, low: 1st percentile, high: 99th percentile, see S1 Fig). C3b opsonization is similar to the case where no FH can be aquired up to a C. albicans density of approx. 5 ⋅ 1011 (i.e., erythrocytes are still 10 times more abundant). Beyond this point crypsis is successful with low opsonization in general. If the pathogen concentration increases even more, competition for factor H dominates and opsonization of both species increases with higher opsonization of host cells until the point where the inflow of C3 is not sufficient to maintain opsonization and C3b decreases again, notably faster for pathogen cells. Separability of the two signals for macrophages is only possible for low pathogen densities. At high pathogen load, the host C3b distribution is similar to the pathogen’s C3b distribution at low pathogen load (subfigures (I) and (V)).