@article{4b08a328fe174c88ba17f97db02be7e8,
title = "Monocytes maintain central nervous system homeostasis following helminth-induced inflammation",
abstract = "Neuroimmune interactions are crucial for regulating immunity and inflammation. Recent studies have revealed that the central nervous system (CNS) senses peripheral inflammation and responds by releasing molecules that limit immune cell activation, thereby promoting tolerance and tissue integrity. However, the extent to which this is a bidirectional process, and whether peripheral immune cells also promote tolerance mechanisms in the CNS remains poorly defined. Here we report that helminth-induced type 2 inflammation promotes monocyte responses in the brain that are required to inhibit excessive microglial activation and host death. Mechanistically, infection-induced monocytes express YM1 that is sufficient to inhibit tumor necrosis factor production from activated microglia. Importantly, neuroprotective monocytes persist in the brain, and infected mice are protected from subsequent lipopolysaccharide-induced neuroinflammation months after infection-induced inflammation has resolved. These studies demonstrate that infiltrating monocytes promote CNS homeostasis in response to inflammation in the periphery and demonstrate that a peripheral infection can alter the immunologic landscape of the host brain.",
keywords = "helminth, innate immune cells, monocyte, neuroimmune cross-talk",
author = "Jianya Peng and Sy, {Chandler B.} and Ponessa, {John J.} and Lemenze, {Alexander D.} and Hernandez, {Christina M.} and Inclan-Rico, {Juan M.} and Arman Sawhney and Federman, {Hannah G.} and Krupa Chavan and Vanessa Espinosa and Kotenko, {Sergei V.} and Amariliz Rivera and Siracusa, {Mark C.}",
note = "Funding Information: We thank members of the Center for Immunity and Inflammation for discussions and critical reading, the New Jersey Medical School (NJMS) Flow Cytometry and Immunology Core Laboratory for technical assistance, the NJMS Histology Core, and the NJMS Genomics Research Laboratory for bioinformatics assistance. This work was supported by NIH (RO1 AI169769 to A.R.; R01 AI123224 and R01 AI131634 to M.C.S.). C.B.S. is supported by T32 Grant T32 AI125185; J.J.P. is supported by T32 Grant T32 AI125185; and C.M.H. is supported by RO1 AI131634-02W1. Funding Information: ACKNOWLEDGMENTS. We thank members of the Center for Immunity and Inflammation for discussions and critical reading, the New Jersey Medical School (NJMS) Flow Cytometry and Immunology Core Laboratory for technical assistance, the NJMS Histology Core, and the NJMS Genomics Research Laboratory for bioinformatics assistance. This work was supported by NIH (RO1 AI169769 to A.R.; R01 AI123224 and R01 AI131634 to M.C.S.). C.B.S. is supported by T32 Grant T32 AI125185; J.J.P. is supported by T32 Grant T32 AI125185; and C.M.H. is supported by RO1 AI131634-02W1. Publisher Copyright: Copyright {\textcopyright} 2022 the Author(s). Published by PNAS.",
year = "2022",
month = sep,
day = "13",
doi = "https://doi.org/10.1073/pnas.2201645119",
language = "American English",
volume = "119",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "37",
}