Semen-Derived Enhancer of Viral Infection (SEVI) Binds Bacteria, Enhances Bacterial Phagocytosis by Macrophages, and Can Protect against Vaginal Infection by a Sexually Transmitted Bacterial Pathogen

Authors

David Easterhoff, University of Rochester Medical CenterFollow
Fernando Ontiveros, St. John Fisher UniversityFollow
Lauren R. Brooks, University of Rochester Medical CenterFollow
Yoel Kim, University of Rochester Medical Center
Brittany Ross, University of Rochester Medical CenterFollow
Jharon N. Silva, University of Rochester Medical CenterFollow
Joanna S. Olsen, University of Rochester Medical CenterFollow
Changyong Feng, University of Rochester Medical CenterFollow
Dwight J. Hardy, University of Rochester Medical CenterFollow
Paul M. Dunman, University of Rochester Medical Center
Stephen Dewhurst, University of Rochester Medical CenterFollow

Document Type

Article

Publication Date

6-2013

Abstract

The semen-derived enhancer of viral infection (SEVI) is a positively charged amyloid fibril that is derived from a self-assembling proteolytic cleavage fragment of prostatic acid phosphatase (PAP_248-286). SEVI efficiently facilitates HIV-1 infection in vitro, but its normal physiologic function remains unknown. In light of the fact that other amyloidogenic peptides have been shown to possess direct antibacterial activity, we investigated whether SEVI could inhibit bacterial growth. Neither SEVI fibrils nor the unassembled PAP_248-286 peptide had significant direct antibacterial activity in vitro. However, SEVI fibrils bound to both Gram-positive (Staphylococcus aureus) and Gram-negative (Escherichia coli and Neisseria gonorrhoeae) bacteria, in a charge-dependent fashion. Furthermore, SEVI fibrils but not the monomeric PAP_248-286 peptide promoted bacterial aggregation and enhanced the phagocytosis of bacteria by primary human macrophages. SEVI also enhanced binding of bacteria to macrophages and the subsequent release of bacterially induced proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin-6 [IL-6], and IL-1β). Finally, SEVI fibrils inhibited murine vaginal colonization with Neisseria gonorrhoeae. These findings demonstrate that SEVI has indirect antimicrobial activity and that this activity is dependent on both the cationic charge and the fibrillar nature of SEVI.

DOI

10.1128/AAC.02464-12

Comments

This article is also available through PubMed Central® (PMC): https://www.ncbi.nlm.nih.gov/pubmed/23507280

Publication Information

Easterhoff, David; Ontiveros, Fernando; Brooks, Lauren R.; Kim, Yoel; Ross, Brittany; Silva, Jharon N.; Olsen, Joanna S.; Feng, Changyong; Hardy, Dwight J.; Dunman, Paul M.; and Dewhurst, Stephen (2013). "Semen-Derived Enhancer of Viral Infection (SEVI) Binds Bacteria, Enhances Bacterial Phagocytosis by Macrophages, and Can Protect against Vaginal Infection by a Sexually Transmitted Bacterial Pathogen." Antimicrobial Agents and Chemotherapy 57.6, 2443-2450.

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