SEVI fibrils are induced by bacterial surface molecules and exert antimicrobial activity against ESKAPE pathogens
Abstract
IntroductionSemen-derived enhancer of viral infection (SEVI) is an amyloid fibril formed from PAP248-286, a fragment of prostatic acid phosphatase naturally occuring in seminal plasma. Beyond its role in HIV transmission, SEVI may contribute to innate immunity. Since many amyloids display antimicrobial effects, we investigated its antibacterial activity against ESKAPE pathogens and urogenital bacteria.MethodsWe evaluated SEVI’s antibacterial activity in radial diffusion and survival assays against Pseudomonas aeruginosa, Klebsiella quasipneumoniae, Escherichia coli, Acinetobacter baumannii, Streptococcus agalactiae, Listeria monocytogenes, Staphylococcus aureus, and Enterococcus faecium. The role of fibril structure was examined using epigallocatechin gallate, while lipopolysaccharide and lipoteichoic acid induced fibril formation was evaluated kinetically. Mechanisms were investigated through electron microscopy, membrane-disruption assays, and analysis of intracellular polyphosphate granules.ResultsSEVI exhibited direct, dose-dependent antibacterial activity against most ESKAPE pathogens, at concentrations estimated to occur in seminal plasma. Lipopolysaccharides and lipoteichoic acid induced SEVI fibril formation, whereas epigallocatechin gallate abolished antibacterial activity, indicating that fibrils are required. Electron microscopy showed limited membrane disruption and intracellular polyphosphate granule accumulation in some P. aeruginosa cells, suggesting bacterial stress.DiscussionSEVI may have a physiological antimicrobial function in addition to its role in HIV transmission. Its activity against urogenital pathogens suggests a potential contribution to vaginal mucosal innate immunity. The dependence on fibril structure and induction by bacterial surface molecules imply that bacteria may promote formation of an antimicrobial SEVI conformation. Limited membrane damage and polyphosphate granule accumulation suggest that SEVI acts partly through intracellular stress responses rather than extensive membrane lysis. Further studies should clarify its molecular mechanism and in vivo relevance.
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BibTeX
@article{vogel2026sevi,
title = {{SEVI fibrils are induced by bacterial surface molecules and exert antimicrobial activity against ESKAPE pathogens}},
author = {Verena Vogel and Lia-Raluca Olari and Richard Bauer and Sandra Burczyk and Fiona Witz and Emely Walker and Nourice Jaber and Stefanie Mauerer and Ulrich Rupp and Ulrich Stifel and Annalena Kuhn and Julia Zinngrebe and Clarissa Read and Pamela Fischer-Posovszky and Thunchanok Thummaraj and Jasmina Gačanin and Jan Münch and Barbara Spellerberg},
journal = {Frontiers in Immunology},
year = {2026},
month = nov,
doi = {10.3389/fimmu.2026.1906582},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1906582},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - SEVI fibrils are induced by bacterial surface molecules and exert antimicrobial activity against ESKAPE pathogens
AU - Verena Vogel
AU - Lia-Raluca Olari
AU - Richard Bauer
AU - Sandra Burczyk
AU - Fiona Witz
AU - Emely Walker
AU - Nourice Jaber
AU - Stefanie Mauerer
AU - Ulrich Rupp
AU - Ulrich Stifel
AU - Annalena Kuhn
AU - Julia Zinngrebe
AU - Clarissa Read
AU - Pamela Fischer-Posovszky
AU - Thunchanok Thummaraj
AU - Jasmina Gačanin
AU - Jan Münch
AU - Barbara Spellerberg
PY - 2026
DA - 2026/11/06
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1906582
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1906582
AB - IntroductionSemen-derived enhancer of viral infection (SEVI) is an amyloid fibril formed from PAP248-286, a fragment of prostatic acid phosphatase naturally occuring in seminal plasma. Beyond its role in HIV transmission, SEVI may contribute to innate immunity. Since many amyloids display antimicrobial effects, we investigated its antibacterial activity against ESKAPE pathogens and urogenital bacteria.MethodsWe evaluated SEVI’s antibacterial activity in radial diffusion and survival assays against Pseudomonas aeruginosa, Klebsiella quasipneumoniae, Escherichia coli, Acinetobacter baumannii, Streptococcus agalactiae, Listeria monocytogenes, Staphylococcus aureus, and Enterococcus faecium. The role of fibril structure was examined using epigallocatechin gallate, while lipopolysaccharide and lipoteichoic acid induced fibril formation was evaluated kinetically. Mechanisms were investigated through electron microscopy, membrane-disruption assays, and analysis of intracellular polyphosphate granules.ResultsSEVI exhibited direct, dose-dependent antibacterial activity against most ESKAPE pathogens, at concentrations estimated to occur in seminal plasma. Lipopolysaccharides and lipoteichoic acid induced SEVI fibril formation, whereas epigallocatechin gallate abolished antibacterial activity, indicating that fibrils are required. Electron microscopy showed limited membrane disruption and intracellular polyphosphate granule accumulation in some P. aeruginosa cells, suggesting bacterial stress.DiscussionSEVI may have a physiological antimicrobial function in addition to its role in HIV transmission. Its activity against urogenital pathogens suggests a potential contribution to vaginal mucosal innate immunity. The dependence on fibril structure and induction by bacterial surface molecules imply that bacteria may promote formation of an antimicrobial SEVI conformation. Limited membrane damage and polyphosphate granule accumulation suggest that SEVI acts partly through intracellular stress responses rather than extensive membrane lysis. Further studies should clarify its molecular mechanism and in vivo relevance.
SN - 1664-3224
ER -