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. 2024 Mar 19;15(4):e00303-24. doi: 10.1128/mbio.00303-24

Fig 1.

Fig 1

A defect in cell-autonomous immunity correlates with a transient increase in C. trachomatis burden in the female genital tract of pan-Irgm−/− mice. (A) MEFs were primed overnight with 100 U/mL IFNγ prior to infection with C. trachomatis elementary bodies (EBs) at a multiplicity of infection (MOI) of 1:1. DNA was harvested from the infected cells at 24 hpi and bacterial burden was quantified using quantitative real-time polymerase chain reaction (qPCR). Graphs represent the proportion of bacterial burden in IFNγ-primed vs. unprimed cells. Data points represent MEFs derived from separate embryos (n = 4 separate MEF lines). Statistical significance was determined using one-way analysis of variance (ANOVA). (B) Mice were infected transcervically with 5 × 106 C. trachomatis EBs, and female genital tracts were harvested at the indicated timepoints or (C) harvested at 3 dpi and then segmented. DNA was extracted from the harvested organ, and bacterial burden was quantified using qPCR. Each data point represents one mouse. Data in B represent pooled data from one experiment including all timepoints and one additional experiment for 3 dpi and 10 dpi timepoints: 4 hpi n = 4 mice; 1 dpi wild-type n = 7, pan-Irgm−/− n = 9; 3 dpi wild-type n = 3, pan-Irgm−/− n = 5; 6 dpi n = 4; and 10 dpi wild-type n = 7, pan-Irgm−/− n = 5. Data in C represent one experiment (n = 4 mice). Statistical significance was determined using t-test (B, C); *P < 0.05, ***P < 0.0005, and ****P < 0.00005; ns, not significant.