Communications biology · 2024
An immune-adrenergic pathway induces lethal levels of platelet-activating factor in mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Tanaka Shuto, Kawakita Masataka, Yasui Hikaru, Sudo Koichi, Itoh Fumie, Sasaki Masato, Shibata Nobuyuki, Hara Hiromitsu, Iwakura Yoichiro, Hashidate-Yoshida Tomomi, Shindou Hideo, Shimizu Takao, Oyama Taiki, Matsunaga Himawari, Takahara Kazuhiko
Аннотация
Acute immune responses with excess production of cytokines, lipid/chemical mediators, or coagulation factors, often result in lethal damage. In addition, the innate immune system utilizes multiple types of receptors that recognize neurotransmitters as well as pathogen-associated molecular patterns, making immune responses complex and clinically unpredictable. We here report an innate immune and adrenergic link inducing lethal levels of platelet-activating factor. Injecting mice with toll-like receptor (TLR) 4 ligand lipopolysaccharide (LPS), cell wall N-glycans of Candida albicans, and the α2-adrenergic receptor (α2-AR) agonist medetomidine induces lethal damage. Knocking out the C-type lectin Dectin-2 prevents the lethal damage. In spleen, large amounts of platelet-activating factor (PAF) are detected, and knocking out lysophospholipid acyltransferase 9 (LPLAT9/LPCAT2), which encodes an enzyme that converts inactive lyso-PAF to active PAF, protects mice from the lethal damage. These results reveal a linkage/crosstalk between the nervous and the immune system, possibly inducing lethal levels of PAF.