Fig. 4

Dysbiosis clustering of CI patients and the pathogenic microbiome in wounded skin of CI patients. A PCoA plots showing beta diversity metrics in dry, moist, sebaceous, and wounded CI skin, colored according to CI type. B CI microbiome dysbiosis clusters and distribution of P1-P5 in each skin region, including Dry, Sebaceous (Seb), Moist, and Wounded were determined by principal co-ordinate analysis in panel A (PC1/commensal, PC2/pathogenic). Specifically, the sample composition for the Dry, Seb, and Moist areas encompassed 7 Healthy, 3 TTD, 1 ARC, 2 SLS, 8 HI, 3 LI, 15 IV, and 4 EI samples. Meanwhile, the sample composition for the Wound area consisted of 1 Healthy, 2 TTD, 1 SLS, 6 HI, 3 LI, 9 IV, and 2 EI samples. C (top) Dynamic changes in abundance of S. aureus and S. epidermis communities in non-wounded (blue) and wounded (red) skin from representative CI patients (IV, EI, TTD, LI, HI, SLS) compared with healthy controls. (bottom) Heatmap diagram showing each CI group compared to healthy controls, and each group compared to each other, using two-way ANOVA analysis. Results of each bar are expressed as mean ± SEM standard error. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001. D, E After wounding CI patients and healthy controls with 5 mm punch biopsy, healing time, measured as the change in percent wound area over 7 days, was delayed for the 4 CI dysbiosis clusters P2-P5 compared to healthy P1 controls in the absence of antibiotics (D), but in the presence of β-lactam antibiotics healing time improved to levels comparable to healthy controls in (E). F, G Measurement of relative colonies of Staphylococcus aureus (F) or Staphylococcus epidermidis (G) across the 5 dysbiosis clusters in wounded skin over 36 h