Evidence map›Paper›PMID 39370453›Full record

ArticleNPJ biofilms and microbiomes2024

Staphylococcus aureus SaeRS impairs macrophage immune functions through bacterial clumps formation in the early stage of infection.

Mingzhang Li, Boyong Wang, Jiani Chen, Luhui Jiang, Yawen Zhou, Geyong Guo, Feng Jiang, Yujie Hu, Changming Wang, Yi Yang and 4 more

Abstract read
In one paragraph

Article in NPJ biofilms and microbiomes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Review
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  13. Enhanced control of pathogenicApplied and environmental microbiology · 2025
    Article
  14. Article
  15. Review
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  19. Review
  20. LILRA5Frontiers in cellular and infection microbiology · 2025
    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

14 authors.

Mingzhang Li *Department of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China.
Boyong Wang *Department of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China.
Jiani Chen *Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Luhui JiangShanghai Jiao Tong University School of Medicine, Shanghai, PR China.ORCID http://orcid.org/0009-0005-9756-5685
Yawen ZhouShanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Geyong GuoDepartment of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China.
Feng JiangDepartment of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China.
Yujie HuDepartment of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China.
Changming WangDepartment of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China.
Yi YangDepartment of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China.
Jin TangDepartment of Clinical Laboratory, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China.
Pei HanDepartment of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China. hanpei_cn@163.com.
Jinlong YuDepartment of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China. yujinlong@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-5234-9285
Hao ShenDepartment of Orthopedics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, Shanghai, PR China. shenhao7212@shsmu.edu.cn.ORCID http://orcid.org/0009-0004-6766-6066

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Staphylococcus aureus (S. aureus) SaeRS two-component system (TCS) regulates over 20 virulence factors. While its impact on chronic infection has been thoroughly discussed, its role in the early stage of infection remains elusive. Since macrophages serve as the primary immune defenders at the onset of infection, this study investigates the influence of SaeRS on macrophage functions and elucidates the underlying mechanisms. Macrophage expression of inflammatory and chemotactic factors, phagocytosis, and bactericidal activity against S. aureus were assessed, along with the evaluation of cellular oxidative stress. SaeRS was found to impair macrophage function. Mechanistically, SaeRS inhibited NF-κB pathway activation via toll-like receptor 2 (TLR2). Its immune-modulating effect could partially be explained by the strengthened biofilm formation. More importantly, we found SaeRS compromised macrophage immune functions at early infection stages even prior to biofilm formation. These early immune evasion effects were dependent on bacterial clumping as cytokine secretion, phagocytosis, and bactericidal activity were repaired when clumping was inhibited. We speculate that the bacterial clumping-mediated antigen mask is responsible for SaeRS-mediated immune evasion at the early infection stage. In vivo, ΔsaeRS infection was cleared earlier, accompanied by early pro-inflammatory cytokines production, and increased tissue oxidative stress. Subsequently, macrophages transitioned to an anti-inflammatory state, thereby promoting tissue repair. In summary, our findings underscore the critical role of the SaeRS TCS in S. aureus pathogenicity, particularly during early infection, which is likely initiated by SaeRS-mediated bacterial clumping.

Indexed as

Bacterial ProteinsBiofilmsImmune EvasionMacrophagesPhagocytosisStaphylococcal InfectionsStaphylococcus aureusAnimalsCytokinesMiceNF-kappa BOxidative StressToll-Like Receptor 2Transcription FactorsVirulence FactorsBacterial ProteinsCytokinesNF-kappa BSaeR protein, Staphylococcus aureusToll-Like Receptor 2Transcription FactorsVirulence Factors

Identifiers

PMID39370453
PMCPMC11456606

What OpenQuestion holds

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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.