Journal
JOURNAL OF MOLECULAR NEUROSCIENCE
Volume 62, Issue 2, Pages 163-180Publisher
HUMANA PRESS INC
DOI: 10.1007/s12031-017-0920-2
Keywords
Neisseria gonorrhoeae; Neisseria meningitidis; Snap23; Exocytosis; GluT4; SH-SY5Y cells
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Funding
- University Medicine Gottingen (UMG)
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Early maternal infections with Neisseria gonorrhoeae (NG) correlate to an increased lifetime schizophrenia risk for the offspring, which might be due to an immune-mediated mechanism. Here, we investigated the interactions of polyclonal antisera to NG (alpha-NG) with a first trimester prenatal brain multiprotein array, revealing among others the SNARE-complex protein Snap23 as a target antigen for alpha-NG. This interaction was confirmed by Western blot analysis with a recombinant Snap23 protein, whereas the closely related Snap25 failed to interact with alpha-NG. Furthermore, a polyclonal antiserum to the closely related bacterium Neisseria meningitidis (alpha-NM) failed to interact with both proteins. Functionally, in SH-SY5Y cells, alpha-NG pretreatment interfered with both insulin-induced vesicle recycling, as revealed by uptake of the fluorescent endocytosis marker FM1-43, and insulin-dependent membrane translocation of the glucose transporter GluT4. Similar effects could be observed for an antiserum raised directly to Snap23, whereas a serum to Snap25 failed to do so. In conclusion, Snap23 seems to be a possible immune target for anti-gonococcal antibodies, the interactions of which seem at least in vitro to interfere with vesicle-associated exocytosis. Whether these changes contribute to the correlation between maternal gonococcal infections and psychosis in vivo remains still to be clarified.
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