Neutrophil S100A9 supports M2 macrophage niche formation in granulomas
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA684150 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13238661_1.fastq.gz | Fastqsanger.gz | |||
| SRR13238661_2.fastq.gz | Fastqsanger.gz | |||
| SRR13238662_1.fastq.gz | Fastqsanger.gz | |||
| SRR13238662_2.fastq.gz | Fastqsanger.gz | |||
| SRR13238663_1.fastq.gz | Fastqsanger.gz |
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Project description:Mycobacterium infection gives rise to granulomas predominantly composed of inflammatory M1-like macrophages, with bacteria-permissive M2 macrophages also detected in deep granulomas. Our histological analysis of Mycobacterium bovis bacillus Calmette-Guerin-elicited granulomas in guinea pigs revealed that S100A9-expressing neutrophils bordered a unique M2 niche within the inner circle of concentrically multilayered granulomas. We evaluated the effect of S100A9 on macrophage M2 polarization based on guinea pig studies. S100A9-deficient mouse neutrophils abrogated M2 polarization, which was critically dependent on COX-2 signaling in neutrophils. Mechanistic evidence suggested that nuclear S100A9 interacts with C/EBPβ, which cooperatively activates the Cox-2 promoter and amplifies prostaglandin E2 production, followed by M2 polarization in proximal macrophages. Because the M2 populations in guinea pig granulomas were abolished via treatment with celecoxib, a selective COX-2 inhibitor, we propose the S100A9/Cox-2 axis as a major pathway driving M2 niche formation in granulomas.
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