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. 2020 Oct 12;117(43):26936–26945. doi: 10.1073/pnas.2012379117

Fig. 3.

Fig. 3.

Engineered peptide mast-MO triggers immune cell migration and represses inflammation pathways in vivo. (A) Schematic of different interactions displayed by mastoparan peptides on the surface of biological membranes leading to internalization into the cell and subsequent immunomodulatory effects. (B) Mast-MO (10 mg kg−1) triggered leukocyte recruitment to the E. coli ATCC8739 infection site to levels comparable to the positive control TGA, (C) release over time (48 h) of IL-12, and (D) TNF-α into the peritoneal cavity of mice. Cytokines monitored in mice for 24 h after infection with (E) E. coli ATCC8739 and (F) S. aureus ATCC29213. Cytokine release (i.e., IFN-γ, IL-6, IL-10, IL-12p70, and TNF-α) into the peritoneal cavity of C57BL/6 mice was detected and quantified 24 h after infection with E. coli ATCC8739 and S. aureus ATCC29213. In all experiments, mice were treated with 10 mg kg−1 of mastoparan-MO and 5 mg kg−1 of mastoparan-L. PBS and imipenem (10 mg kg−1) were used as negative and positive controls, respectively. Data were expressed as mean ± SD. Statistical analysis was performed using Bonferroni test. *P < 0.1, ***P < 0.001 as significant compared to the control.