Evidence map›Paper›PMID 33789094›Full record

ArticleCell reports2021

Streptococcus pyogenes upregulates arginine catabolism to exert its pathogenesis on the skin surface.

Yujiro Hirose, Masaya Yamaguchi, Tomoko Sumitomo, Masanobu Nakata, Tomoki Hanada, Daisuke Okuzaki, Daisuke Motooka, Yasushi Mori, Hiroshi Kawasaki, Alison Coady and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

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  20. Hydroquinine Inhibits the Growth of Multidrug-ResistantInternational journal of molecular sciences · 2023
    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

16 authors at 5 institutions in 2 countries.

Yujiro HiroseDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871, Japan; Department of Pediatrics, University of California at San Diego School of Medicine, La Jolla, CA 92093, USA. Electronic address: yujirohirose@dent.osaka-u.ac.jp.
Masaya YamaguchiDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871, Japan.
Tomoko SumitomoDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871, Japan.
Masanobu NakataDepartment of Oral Microbiology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima 890-8544, Japan.
Tomoki HanadaDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan.
Daisuke MotookaDepartment of Infection Metagenomics, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan.
Yasushi MoriDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871, Japan.
Hiroshi KawasakiDepartment of Dermatology, Keio University School of Medicine, Tokyo 160-8582, Japan; Immunology Data Integration Unit, RIKEN Medical Sciences Innovation Hub Program, Yokohama 230-0045, Japan; Laboratory for Skin Homeostasis, RIKEN Center for Integrative Medical Sciences, Yokohama 230-0045, Japan.
Alison CoadyDepartment of Pediatrics, University of California at San Diego School of Medicine, La Jolla, CA 92093, USA.
Satoshi UchiyamaDepartment of Pediatrics, University of California at San Diego School of Medicine, La Jolla, CA 92093, USA.
Masanobu HiraokaDepartment of Pediatrics, University of California at San Diego School of Medicine, La Jolla, CA 92093, USA; Department of Otorhinolaryngology-Head and Neck Surgery, Wakayama Medical University, Wakayama, Wakayama 641-8509, Japan.
Raymond H ZurichDepartment of Pediatrics, University of California at San Diego School of Medicine, La Jolla, CA 92093, USA.
Masayuki AmagaiDepartment of Dermatology, Keio University School of Medicine, Tokyo 160-8582, Japan; Laboratory for Skin Homeostasis, RIKEN Center for Integrative Medical Sciences, Yokohama 230-0045, Japan.
Victor NizetDepartment of Pediatrics, University of California at San Diego School of Medicine, La Jolla, CA 92093, USA; Skaggs School of Pharmaceutical Sciences, University of California at San Diego, La Jolla, CA 92093, USA.
Shigetada KawabataDepartment of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry, Suita, Osaka 565-0871, Japan. Electronic address: kawabata@dent.osaka-u.ac.jp.
The University of Osaka · JPUniversity of California San Diego · USKeio University · JPKagoshima University · JPWakayama Medical University · JP

Funding

Cathelicidin in Skin ImmunityR37AI052453 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard L Gallo, Victor Nizet · 2019 to 2026
$4.6M
GAS Switch from Colonizing Bacterium to Invasive PathogenR01AI077780 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NIZET, VICTOR · 2008 to 2019
$3.8M
C3-Dependent Intracellular Killing in Innate Immunity and Bacterial PathogenesisR01AI145325 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NIZET, VICTOR, RAFFATELLU, MANUELA · 2019 to 2023
$3.1M
Mechanisms of the M protein in group A Streptococcus virulenceR01AI096837 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GHOSH, PARTHO, NIZET, VICTOR · 2011 to 2015
$2.7M
Broad recognition of group A Streptococcus M proteinsR21AI140436 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GHOSH, PARTHO, NIZET, VICTOR · 2018 to 2019
$426k
NIAID NIH HHS R01 AI077780NIAID NIH HHS R01 AI096837NIAID NIH HHS R01 AI145325NIAID NIH HHS R21 AI140436NIAID NIH HHS R37 AI052453
6 · The paper itself

Abstract

The arginine deiminase (ADI) pathway has been found in many kinds of bacteria and functions to supplement energy production and provide protection against acid stress. The Streptococcus pyogenes ADI pathway is upregulated upon exposure to various environmental stresses, including glucose starvation. However, there are several unclear points about the advantages to the organism for upregulating arginine catabolism. We show that the ADI pathway contributes to bacterial viability and pathogenesis under low-glucose conditions. S. pyogenes changes global gene expression, including upregulation of virulence genes, by catabolizing arginine. In a murine model of epicutaneous infection, S. pyogenes uses the ADI pathway to augment its pathogenicity by increasing the expression of virulence genes, including those encoding the exotoxins. We also find that arginine from stratum-corneum-derived filaggrin is a key substrate for the ADI pathway. In summary, arginine is a nutrient source that promotes the pathogenicity of S. pyogenes on the skin.

Indexed as

AnimalsArginineBacterial ProteinsFilaggrin ProteinsGene Expression Regulation, BacterialHaCaT CellsHumansHydrolasesMaleMiceMice, Inbred C57BLMice, KnockoutMicrobial ViabilityPhosphorylationSkinStreptococcal InfectionsArgininearginine deiminaseBacterial ProteinsFilaggrin ProteinsHydrolasesargininearginine deiminase pathwaybacterial pathogenesisbacterial viabilityCovR phosphorylationfilaggringlucose starvationpyroptosisskin infectionStreptococcus pyogenes

Identifiers

PMID33789094
PMCPMC9214650
OpenAlexW3151075481

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.