AI Article Synopsis
- Eosinophils typically respond to allergies and infections, but new research shows they also accumulate in the lungs during type I responses to Mycobacterium tuberculosis (Mtb).
- Eosinophils start migrating into the lungs just one week after Mtb exposure in both macaques and mice, highlighting their quick response.
- The migration of eosinophils is linked to the oxysterol receptor GPR183 rather than CCR3 and involves interactions with infected macrophages, suggesting a crucial role for eosinophils in early Mtb infections.
Article Abstract
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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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9460869 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2022.111144 | DOI Listing |
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