Neutrophil S100A9 supports M2 macrophage niche formation in granulomas

被引:2
|
作者
Mizutani, Tatsuaki [1 ]
Ano, Toshiaki
Tsuruyama, Yuya
Mizuta, Satoshi
Takemoto, Keiko [1 ]
Ouchi, Yuki
Morita, Daisuke
Kitano, Satsuki [2 ]
Miyachi, Hitoshi [2 ]
Tsuruyama, Tatsuaki [3 ]
Fujiwara, Nagatoshi [4 ]
Sugita, Masahiko
机构
[1] Kyoto Univ, Inst Life & Med Sci, Lab Cell Regulat, Kyoto, Japan
[2] Kyoto Univ, Grad Sch Biostudies, Lab Cell Regulat, Mol Network, Kyoto, Japan
[3] Nagasaki Univ, Ctr Bioinformat & Mol Med, Grad Sch Biomed Sci, Nagasaki, Japan
[4] Kyoto Univ, Inst Life & Med Sci, Lab Immune Regulat, Kyoto, Japan
基金
日本学术振兴会;
关键词
ALTERNATIVE ACTIVATION; INFLAMMATION; DIFFERENTIATION; EXPRESSION; MRP14; POLARIZATION; PATHWAY; DISEASE; GROWTH;
D O I
10.1016/j.isci.2023.106081
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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/EBP beta, 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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页数:24
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