CXCL14 Protects against Polymicrobial Sepsis by Enhancing Antibacterial Functions of Macrophages

Lai, Xiaofei; Ding, Hao; Yu, Renlin; Bai, Haobo; Liu, Yi; Cao, Ju

doi:10.1165/rcmb.2022-0249oc

Cited by 8 publications

(3 citation statements)

References 40 publications

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“…Effective and rapid bacterial clearance is a fundamental determinant of outcomes in sepsis ( 28 , 29 ). Therefore, we examined the effects of BMP9 treatment on bacterial burdens.…”

Section: Resultsmentioning

confidence: 99%

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Bone morphogenetic protein 9 is a candidate prognostic biomarker and host-directed therapy target for sepsis

Bai,

Lu,

et al. 2024

Sci. Transl. Med.

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Defining next-generation immune therapeutics for the treatment of sepsis will involve biomarker-based therapeutic decision-making. Bone morphogenetic protein 9 (BMP9) is a cytokine in the transforming growth factor–β superfamily. Here, circulating BMP9 concentrations were quantified in two independent cohorts of patients with sepsis. Decreased concentrations of serum BMP9 were observed in the patients with sepsis at the time of admission as compared with healthy controls. Concentrations of BMP9 at the time of admission were also associated with 28-day mortality, because patients with sepsis at a higher risk of death had lower BMP9 concentrations. The mechanism driving the contribution of BMP9 to host immunity was further investigated using in vivo murine sepsis models and in vitro cell models. We found that BMP9 treatment improved outcome in mice with experimental sepsis. BMP9-treated mice exhibited increased macrophage influx into the peritoneal cavity and more efficient bacterial clearance than untreated mice. In vitro, BMP9 promoted macrophage recruitment, phagocytosis, and subsequent bacterial killing. We further found that deletion of the type 1 BMP receptor ALK1 in macrophages abolished BMP9-mediated protection against polymicrobial sepsis in vivo. Further experiments indicated that the regulation of macrophage activation by the BMP9-ALK1 axis was mainly mediated through the suppressor of mother against decapentaplegic 1/5 signaling pathway. Together, these results suggest that BMP9 can both serve as a biomarker for patient stratification with an independent prognostic value and be developed as a host-directed therapy for sepsis.

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“…Effective and rapid bacterial clearance is a fundamental determinant of outcomes in sepsis ( 28 , 29 ). Therefore, we examined the effects of BMP9 treatment on bacterial burdens.…”

Section: Resultsmentioning

confidence: 99%

“…Because macrophages are the primary effector cells for bacterial clearance during sepsis ( 28 , 31 , 32 ), we tested whether BMP9 modulates intrinsic antibacterial functions of macrophages. BMP9 treatment significantly ( P < 0.01) enhanced phagocytosis of Escherichia coli by macrophages (Fig.…”

Section: Resultsmentioning

confidence: 99%

Bone morphogenetic protein 9 is a candidate prognostic biomarker and host-directed therapy target for sepsis

Bai,

Lu,

et al. 2024

Sci. Transl. Med.

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“…[ 34 ] Expression of Foxp1 is inhibited in placental tissue of PE patients, while Foxp1 inhibits the expression of GNG7 and promotes the expression of the mTOR pathway. [ 35 ] Another study in sheep also showed that the activation of the mTOR pathway is essential for the vasculogenesis and angiogenesis involved in placental development. [ 36 ] It has been reported that the downregulation of mTOR pathway has a strong correlation with the development of PE.…”

Section: Introductionmentioning

confidence: 99%

ATL1 inhibits the proliferation and invasion of trophoblast cells via inhibition of the mTOR signaling pathway

Zhang

Feng

Wang

et al. 2022

J Biochem & Molecular Tox

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Pre‐eclampsia (PE) is a major cause of hypertension in maternal and fetal. Atlastin‐1 (ATL1), one regulator of endoplasmic reticulum (ER) morphology, participates in tubular ER formation and protein synthesis. The objective of this study is to investigate the role and molecular mechanism of ATL1 in PE. GEO databases showed that ATL1 was upregulated in PE patients. Our data also found that ATL1 was highly expressed in PE placental tissues. The cell viability, proliferation, migration, and invasion of HTR‐8/SVneo cells increased/decreased after the downregulation/upregulation of ATL1. The mTOR pathway is the downstream pathway of ATL1. The levels of p‐p70S6K and p‐mTOR were increased/decreased after the downregulation/upregulation of ATL1. Moreover, rapamycin, an inhibitor of mTOR pathway, reversed the promotive effect of siATL1 on proliferation, migration, and invasion in HTR‐8/SVneo cells. In conclusion, ATL1 inhibits the proliferation and invasion of trophoblast cells via the inhibition of the mTOR signaling pathway in HTR‐8/SVneo cells.

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Fibroblast-derived CXCL14 aggravates crystalline silica–induced pulmonary fibrosis by mediating polarization and recruitment of interstitial macrophages

You,

Yuan,

Min

et al. 2023

Journal of Hazardous Materials

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CXCL14 Protects against Polymicrobial Sepsis by Enhancing Antibacterial Functions of Macrophages

Cited by 8 publications

References 40 publications

Bone morphogenetic protein 9 is a candidate prognostic biomarker and host-directed therapy target for sepsis

Bone morphogenetic protein 9 is a candidate prognostic biomarker and host-directed therapy target for sepsis

ATL1 inhibits the proliferation and invasion of trophoblast cells via inhibition of the mTOR signaling pathway

Fibroblast-derived CXCL14 aggravates crystalline silica–induced pulmonary fibrosis by mediating polarization and recruitment of interstitial macrophages

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