Evidence map›Paper›PMID 35810689›Full record

ArticleJournal of autoimmunity2022

Staphylococcus aureus peptidoglycan (PGN) induces pathogenic autoantibody production via autoreactive B cell receptor clonal selection, implications in systemic lupus erythematosus.

Wangbin Ning, Da Cheng, Philip H Howe, Chuanxiu Bian, Diane L Kamen, Zhenwu Luo, Xiaoyu Fu, Elizabeth Ogunrinde, Liuqing Yang, Xu Wang and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of autoimmunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Systemic translocation ofJournal of virology · 2026
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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

17 authors at 3 institutions in 2 countries.

Wangbin NingDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA; Department of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Da ChengDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA; Department of Infectious Disease, Xiangya Hospital, Central South University, Changsha, China.
Philip H HoweDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, SC, USA.
Chuanxiu BianDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA.
Diane L KamenDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, 114 Doughty Street, Strom Thurmond Research Building Room 416, Charleston, SC, 29403, USA.
Zhenwu LuoDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA.
Xiaoyu FuDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA; Department of Infectious Disease, Xiangya Hospital, Central South University, Changsha, China.
Elizabeth OgunrindeDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA.
Liuqing YangDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA; The Third People's Hospital of Shenzhen, Guangdong, China.
Xu WangDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA; Department of Urology, Capital Medical University Affiliated XuanWu Hospital, Beijing, China.
Quan-Zhen LiDepartment of Immunology and Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Jim OatesDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, 114 Doughty Street, Strom Thurmond Research Building Room 416, Charleston, SC, 29403, USA; Ralph H. Johnson VA Medical Center, Charleston, SC, USA.
Weiru ZhangDepartment of Rheumatology and Immunology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
David WhiteDepartment of Otolaryngology, Medical University of South Carolina, Charleston, SC, USA.
Zhuang WanDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA.
Gary S GilkesonDivision of Rheumatology and Immunology, Department of Medicine, Medical University of South Carolina, 114 Doughty Street, Strom Thurmond Research Building Room 416, Charleston, SC, 29403, USA; Ralph H. Johnson VA Medical Center, Charleston, SC, USA. Electronic address: gilkeson@musc.edu.
Wei JiangDepartment of Microbiology and Immunology, Medical University of South Carolina, 173 Ashley Avenue, BSB208D, Charleston, SC, 29425, USA; Ralph H. Johnson VA Medical Center, Charleston, SC, USA; Division of Infectious Diseases, Department of Medicine, Medical University of South Carolina, Charleston, SC, USA. Electronic address: jianw@musc.edu.
Medical University of South Carolina · USCentral South University · CNThe University of Texas Southwestern Medical Center · US

Funding

South Carolina Clinical & Translational Research Institute (SCTR)UL1TR001450 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T., FLUME, PATRICK A · 2015 to 2024
$41.1M
SOUTH CAROLINA CLINICAL & TRANSLATIONAL RESEARCH INSTITUTE (SCTR)UL1RR029882 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2009 to 2011
$10.1M
Resource CoreP30AR072582 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAMES C OATES · 2017 to 2026
$8.5M
Patient Resource CoreP60AR062755 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI GILKESON, GARY S · 2012 to 2016
$5.8M
Training Grant in Inflammatory and Fibrosing DiseasesT32AR050958 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DIANE L KAMEN · 2005 to 2026
$4.2M
Environmental Determinants of Lupus among African AmericansK24AR068406 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KAMEN, DIANE L · 2016 to 2020
$862k
Sex Differences in Gut Permeability; Impact on AutoimmunityI01CX001211 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI GILKESON, GARY S · 2015 to 2022
–
CSRD VA I01 CX001211NCATS NIH HHS UL1 TR001450NCRR NIH HHS UL1 RR029882NIAMS NIH HHS K24 AR068406NIAMS NIH HHS P30 AR072582NIAMS NIH HHS P60 AR062755NIAMS NIH HHS T32 AR050958
6 · The paper itself

Abstract

objectivesThere is an intricate interplay between the microbiome and the immune response impacting development of normal immunity and autoimmunity. However, we do not fully understand how the microbiome affects production of natural-like and pathogenic autoantibodies. Peptidoglycan (PGN) is a component of the bacterial cell wall which is highly antigenic. PGNs from different bacteria can differ in their immune regulatory activities.

methodsC57BL/6 and MRL/lpr mice were intraperitoneally injected with saline or PGN from Staphylococcus aureus or Bacillus subtilis. Spleen anti-double-stranded DNA (dsDNA) IgG + B cells were sorted for B-cell receptor sequencing. Serum autoantibody levels and kidney damage were analyzed. Further, the association between plasma S. aureus translocation and systemic lupus erythematosus (SLE) pathogenesis was assessed in women.

resultsAdministration of B. subtilis PGN induced natural-like anti-dsDNA autoantibodies (e.g., IgM, short lived IgG response, and no tissue damage), whereas S. aureus PGN induced pathogenic anti-dsDNA autoantibodies (e.g., prolonged IgG production, low IgM, autoantibody-mediated kidney damage) in C57BL/6 and/or MRL/lpr mice. However, serum total IgG did not differ. S. aureus PGN induced antibodies with reduced clonality and greater hypermutation of IGHV3-74 in splenic anti-dsDNA IgG + B cells from C57BL/6 mice. Further, S. aureus PGN promoted IgG class switch recombination via toll-like receptor 2. Plasma S. aureus DNA levels were increased in women with SLE versus control women and correlated with levels of lupus-related autoantibodies and renal involvement.

conclusionsS. aureus PGN induces pathogenic autoantibody production, whereas B. subtilis PGN drives production of natural nonpathogenic autoantibodies.

Indexed as

Lupus Erythematosus, SystemicStaphylococcus aureusAnimalsAntibodies, AntinuclearAutoantibodiesCell WallDNAFemaleHumansImmunoglobulin GImmunoglobulin MMiceMice, Inbred C57BLMice, Inbred MRL lprPeptidoglycanReceptors, Antigen, B-CellAntibodies, Antinuclearanti-dsDNA autoantibodyAutoantibodiesDNAImmunoglobulin GImmunoglobulin MPeptidoglycanReceptors, Antigen, B-CellAutoantibodyClass switch recombinationPeptidoglycanStaphylococcus aureusSystemic lupus erythematosus

Identifiers

PMID35810689
PMCPMC9397544
OpenAlexW4284887846

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 Socratic graph.