Evidence map›Paper›PMID 34099635›Full record

ArticleCell death & disease2021

Effects of short-chain fatty acids in inhibiting HDAC and activating p38 MAPK are critical for promoting B10 cell generation and function.

Fagui Zou, Yi Qiu, Yilian Huang, Hang Zou, Xiao Cheng, Qingru Niu, Aoxiang Luo, Jianbo Sun

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
11.8field-weighted citation impact, top 1% of its field
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

85 citing papers in PubMed, 124 citations in OpenAlex.

  1. Review
  2. Review
  3. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
  4. Review
  5. Review
  6. Short-chain fatty acids.Nature metabolism · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
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  14. Review
  15. Article
  16. Review
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  19. Article
  20. International journal of molecular sciences · 2026
    Article

25 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 1 country.

Fagui ZouGuanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, 510055, China.
Yi QiuGuanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, 510055, China.ORCID http://orcid.org/0000-0002-3584-8154
Yilian HuangSchool of Nursing, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
Hang ZouGuanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, 510055, China.
Xiao ChengGuanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, 510055, China.
Qingru NiuGuanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, 510055, China.
Aoxiang LuoSchool of Nursing, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
Jianbo SunGuanghua School of Stomatology, Hospital of Stomatology, Sun Yat-Sen University, Guangzhou, 510055, China. sunjb3@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-8153-1847
Sun Yat-sen University · CNGuangdong Pharmaceutical University · CNStomatology Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31800006
6 · The paper itself

Abstract

B10 cells are regulatory B cells capable of producing IL-10 for maintaining immune homeostasis. Dysregulation of B10 cells occurs in autoimmune and inflammatory diseases. Modulation or adoptive transfer of B10 cells is a promising therapeutic strategy. The short-chain fatty acids (SCFAs), the metabolites of microbiota, play a critical role in maintaining immune homeostasis and are the potential drugs for the modulation of B10 cells. It is not clear whether and how SCFAs upregulate the frequency of B10 cells. Here, we found that SCFAs could promote murine and human B10 cell generation in vitro. Upregulation of B10 cells by butyrate or pentanoate was also observed in either healthy mice, mice with dextran sodium sulfate (DSS)-induced colitis, or mice with collagen-induced arthritis. Moreover, SCFA treatment could ameliorate clinical scores of colitis and arthritis. Adoptive transfer of B cells pretreated with butyrate showed more alleviation of DSS-induced colitis than those without butyrate. A further study demonstrates that SCFAs upregulate B10 cells in a manner dependent on their histone deacetylase (HDAC) inhibitory activity and independent of the G-protein-coupled receptor pathway. Transcriptomic analysis indicated that the MAPK signaling pathway was enriched in B10 cells treated with butyrate. A study with inhibitors of ERK, JNK, and p38 MAPK demonstrated that activating p38 MAPK by butyrate is critical for the upregulation of B10 cells. Moreover, HDAC inhibitor has similar effects on B10 cells. Our study sheds light on the mechanism underlying B10 cell differentiation and function and provides a potential therapeutic strategy with SCFAs and HDAC inhibitors for inflammation and autoimmune diseases.

Indexed as

AnimalsCell DifferentiationFatty Acids, VolatileHistone Deacetylase InhibitorsHumansMicep38 Mitogen-Activated Protein KinasesFatty Acids, VolatileHistone Deacetylase Inhibitorsp38 Mitogen-Activated Protein Kinases

Identifiers

PMID34099635
PMCPMC8184914
OpenAlexW3170349864

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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.