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. 2021 Jul 12;11:390. doi: 10.1038/s41398-021-01517-1

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Peripheral immune perturbation from IP LPS administration in the murine LPS Persistent Neuroinflammation model can mimic peripheral immune dysregulation similar to GWI that results in persistent neuroimmune bioactive serum that can modify the microglial pro-inflammatory response, long after the prototypical pro-inflammatory response in the serum has resolved. Inhibition of HMGB1 attenuates the persistent pro-inflammatory response in the brain and administration of recombinant HMGB1 can trigger neuroinflammation. Circulating HMGB1 is upregulated in the serum of Gulf War Veterans and in the bioactive serum of mice during the LPS-induced persistent neuroinflammation. Isolated microglia reveal a unique Persistent Pro-inflammatory Microglia transcriptome that is triggered in part by HMGB1, which may provide important insight into the persistent nature of neuroinflammation in GWI.