Evidence map›Paper›PMID 41299657›Full record

ArticleRespiratory research2025

Glucocorticoid-mediated suppression of the CCL2-CCR2 axis drives monocyte dysfunction in severe pneumonia among immunocompromised hosts.

Zhongshu Kuang, Yue Luo, Yao Chen, Yilin Yang, Chen Chen, Feixiang Xu, Yumei Chen, Yannan Zhou, Yongqi Shen, Li Yuan and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Zhongshu Kuang *Department of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Yue Luo *Department of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Yao Chen *Department of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Yilin YangDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Chen ChenDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Feixiang XuDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Yumei ChenDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Yannan ZhouDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Yongqi ShenDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Li YuanDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Hua SuInstitutes of Biomedical Sciences, Zhongshan Hospital, Liver Cancer Institute, Fudan University, Shanghai, China.
Chaoyang TongDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China. tong.chaoyang@zs-hospital.sh.cn.
Zhenju SongDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China. song.zhenju@zs-hospital.sh.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmunocompromised hosts (ICHs) face elevated risks of severe respiratory infections and mortality. Glucocorticoids, commonly used to treat underlying conditions in ICHs, may further impair immune defenses, but the underlying mechanisms remain unclear.

methodsRetrospective analysis of peripheral blood immune cell profiles was conducted in pneumonia patients with ICHs. Prospective immunophenotyping of PBMCs by Cytek flow cytometry was performed to compare immune cell subsets in survivors versus deceased patients. To explore glucocorticoid effects on ICH immune mechanisms, we used a murine model of severe pneumonia (MRL/lpr mice) and an in vitro ICH infection mimic model. Glucocorticoid effects on immune cell populations and function were examined in these models.

resultsFocusing on key immune cells, we observed that ICH patients with severe pneumonia exhibit a reduction in classical monocyte subsets. Mechanistically, glucocorticoids downregulated CCL2 expression in the lung via GR/STAT3, thereby inhibiting the PA-LPS/TLR4/PI3K/AKT/STAT signaling pathway and diminishing pulmonary CCL2 and Ly6C+CCR2+ monocyte levels. Importantly, exogenous recombinant CCL2 administration restored monocyte function, reduced lung injury, and enhanced survival.

conclusionThese findings uncovered a critical immunosuppressive mechanism by which glucocorticoids, via GR/STAT3-mediated suppression of the CCL2-CCR2 axis, impair monocyte-driven antibacterial responses in severe pneumonia, highlighting the need for targeted immunomodulation in ICH patients.

Indexed as

Chemokine CCL2GlucocorticoidsImmunocompromised HostMonocytesPneumoniaReceptors, CCR2Severity of Illness IndexAnimalsFemaleHumansMaleMiceRetrospective StudiesSignal TransductionCCL2 protein, humanCCR2 protein, humanCcr2 protein, mouseChemokine CCL2GlucocorticoidsReceptors, CCR2CCL2-CCR2 axisGlucocorticoidsImmunocompromised hostsMonocyte dysfunctionSevere pneumonia

Identifiers

PMID41299657
PMCPMC12751247

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.