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. 2018 Apr 25;9:862. doi: 10.3389/fimmu.2018.00862

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Copyright © 2018 Chu, Zhou, Jiang, Chen, Guo, Zhang, Chu and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Staphylococcus aureus phenol-soluble modulins (PSMs) α1–α3 inhibit HMGB1-induced inflammatory response. (A) THP-1 cells were transfected with a NF-κB-dependent luciferase reporter. The luciferase activity of THP-1 cells was measured after stimulated with 1.0 µg/mL recombinant HMGB1 or S. aureus PSMs (PSMα1, 5 µg/mL; PSMα2, 5 µg/mL; PSMα3, 0.5 µg/mL, PSMα4, 5 µg/mL; PSMβ1, 10 µg/mL; PSMβ2, 10 µg/mL; δ-toxin, 2 µg/mL). (B) The NF-κB activity of THP-1 cells challenged with HMGB1 in the presence and absence of S. aureus PSMs as prior described. The values for medium treated cells were arbitrarily expressed as 1.0. (C) THP-1 cells were stimulated for 12 h with 1.0 µg/mL recombinant HMGB1 or S. aureus PSMs as prior described. The expression of human TNF-α and IL-6 was assessed by RT-PCR. (D) The expression of human TNF-α and IL-6 in THP-1 cells challenged with HMGB1 in the presence and absence of S. aureus PSMs as prior described. (E) THP-1 cells were stimulated with 1.0 µg/mL recombinant HMGB1 or S. aureus PSMs as prior described for 24 h. Supernatants were analyzed for human TNF-α and IL-6 by enzyme-linked immunosorbent assay. (F) The levels of human TNF-α and IL-6 in the supernatants of THP-1 cells challenged with HMGB1 in the presence and absence of S. aureus PSMs. Data shown are mean ± SEM (n = 5). Significance was calculated by Student’s t-test. ***p < 0.001.

Staphylococcus aureus phenol-soluble modulins (PSMs) α1–α3 inhibit HMGB1-induced inflammatory response. (A) THP-1 cells were transfected with a NF-κB-dependent luciferase reporter. The luciferase activity of THP-1 cells was measured after stimulated with 1.0 µg/mL recombinant HMGB1 or S. aureus PSMs (PSMα1, 5 µg/mL; PSMα2, 5 µg/mL; PSMα3, 0.5 µg/mL, PSMα4, 5 µg/mL; PSMβ1, 10 µg/mL; PSMβ2, 10 µg/mL; δ-toxin, 2 µg/mL). (B) The NF-κB activity of THP-1 cells challenged with HMGB1 in the presence and absence of S. aureus PSMs as prior described. The values for medium treated cells were arbitrarily expressed as 1.0. (C) THP-1 cells were stimulated for 12 h with 1.0 µg/mL recombinant HMGB1 or S. aureus PSMs as prior described. The expression of human TNF-α and IL-6 was assessed by RT-PCR. (D) The expression of human TNF-α and IL-6 in THP-1 cells challenged with HMGB1 in the presence and absence of S. aureus PSMs as prior described. (E) THP-1 cells were stimulated with 1.0 µg/mL recombinant HMGB1 or S. aureus PSMs as prior described for 24 h. Supernatants were analyzed for human TNF-α and IL-6 by enzyme-linked immunosorbent assay. (F) The levels of human TNF-α and IL-6 in the supernatants of THP-1 cells challenged with HMGB1 in the presence and absence of S. aureus PSMs. Data shown are mean ± SEM (n = 5). Significance was calculated by Student’s t-test. ***p < 0.001.