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Merck
  • Rapid GPR183-mediated recruitment of eosinophils to the lung after Mycobacterium tuberculosis infection.

Rapid GPR183-mediated recruitment of eosinophils to the lung after Mycobacterium tuberculosis infection.

Cell reports (2022-07-30)
Andrea C Bohrer, Ehydel Castro, Claire E Tocheny, Maike Assmann, Benjamin Schwarz, Eric Bohrnsen, Michelle A Makiya, Fanny Legrand, Kerry L Hilligan, Paul J Baker, Flor Torres-Juarez, Zhidong Hu, Hui Ma, Lin Wang, Liangfei Niu, Zilu Wen, Sang H Lee, Olena Kamenyeva, Keith D Kauffman, Michele Donato, Alan Sher, Daniel L Barber, Laura E Via, Thomas J Scriba, Purvesh Khatri, Yanzheng Song, Ka-Wing Wong, Catharine M Bosio, Amy D Klion, Katrin D Mayer-Barber
摘要

Influx of eosinophils into the lungs is typically associated with type II responses during allergy and fungal and parasitic infections. However, we previously reported that eosinophils accumulate in lung lesions during type I inflammatory responses to Mycobacterium tuberculosis (Mtb) in humans, macaques, and mice, in which they support host resistance. Here we show eosinophils migrate into the lungs of macaques and mice as early as one week after Mtb exposure. In mice this influx is CCR3 independent and instead requires cell-intrinsic expression of the oxysterol receptor GPR183, which is highly expressed on human and macaque eosinophils. Murine eosinophils interact directly with bacilli-laden alveolar macrophages, which upregulate the oxysterol-synthesizing enzyme Ch25h, and eosinophil recruitment is impaired in Ch25h-deficient mice. Our findings show that eosinophils are among the earliest cells from circulation to sense and respond to Mtb infection of alveolar macrophages and reveal a role for GPR183 in the migration of eosinophils into lung tissue.

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Sigma-Aldrich
白蛋白 来源于鸡蛋白, lyophilized powder, ≥98% (agarose gel electrophoresis)
Sigma-Aldrich
Anti-Eosinophil Peroxidase Antibody, clone AHE-1, ascites fluid, clone AHE-1, Chemicon®