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. 2023 Dec 9;14:8161. doi: 10.1038/s41467-023-43937-1

Fig. 5. PZA’s anti-inflammatory effects are PARP1-dependent.

Fig. 5

a Schematic overview. Male and female PARP1-null (PARP1−/−) or 129S1 (WT) mice were aerosols infected with the PZA-resistant M.tb H37Rv ∆pncA (A146V) mutant (implantation: 54 ± 5 CFU). Starting one month after infection, half of the mice were administered PZA (150 mg/kg) 5 days/week for 2 months before lung bacterial burden and cyto-/chemokine levels (Luminex multiplex assay) were determined. n = 9 (PZA-treated WT) or 10 (all other groups). b, c Bacterial burden (b) and cytokine/chemokine concentrations (c) in untreated (−) or PZA-treated (+) mice at the end of treatment. d Change in cyto-/chemokine levels in PZA-treated mice relative to the levels in untreated mice of the same strain. Values below 1 indicate levels that are lower in the lungs of PZA-treated than untreated mice. Each symbol represents an individual mouse, with mean ± SEM indicated. Statistical differences between groups were determined by two-way ANOVA with Šidák’s multiple comparisons test. p Values for all relevant comparisons are indicated in the figure. PZA reduced lung cyto- and chemokine levels in WT but not in PARP1−/− mice and independently of bacterial burden. Source data are provided as a Source Data file.