Rapid pathogen-specific recruitment of immune effector cells in the skin by secreted toxins.


Journal

Nature microbiology
ISSN: 2058-5276
Titre abrégé: Nat Microbiol
Pays: England
ID NLM: 101674869

Informations de publication

Date de publication:
01 2022
Historique:
received: 13 02 2020
accepted: 29 10 2021
pubmed: 8 12 2021
medline: 23 2 2022
entrez: 7 12 2021
Statut: ppublish

Résumé

Swift recruitment of phagocytic leucocytes is critical in preventing infection when bacteria breach through the protective layers of the skin. According to canonical models, this occurs via an indirect process that is initiated by contact of bacteria with resident skin cells and which is independent of the pathogenic potential of the invader. Here we describe a more rapid mechanism of leucocyte recruitment to the site of intrusion of the important skin pathogen Staphylococcus aureus that is based on direct recognition of specific bacterial toxins, the phenol-soluble modulins (PSMs), by circulating leucocytes. We used a combination of intravital imaging, ear infection and skin abscess models, and in vitro gene expression studies to demonstrate that this early recruitment was dependent on the transcription factor EGR1 and contributed to the prevention of infection. Our findings refine the classical notion of the non-specific and resident cell-dependent character of the innate immune response to bacterial infection by demonstrating a pathogen-specific high-alert mechanism involving direct recruitment of immune effector cells by secreted bacterial products.

Identifiants

pubmed: 34873293
doi: 10.1038/s41564-021-01012-9
pii: 10.1038/s41564-021-01012-9
pmc: PMC8732318
mid: NIHMS1752914
doi:

Substances chimiques

Bacterial Toxins 0
Virulence Factors 0
staphylococcal delta toxin 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

62-72

Subventions

Organisme : Intramural NIH HHS
ID : ZIA AI001171
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA AI001079
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA BC010725
Pays : United States
Organisme : Intramural NIH HHS
ID : Z01 AI000904
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA AI000904
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2021. This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.

Références

Grice, E. A. & Segre, J. A. The skin microbiome. Nat. Rev. Microbiol. 9, 244–253 (2011).
pubmed: 21407241 pmcid: 3535073 doi: 10.1038/nrmicro2537
Naik, S. et al. Commensal–dendritic-cell interaction specifies a unique protective skin immune sig. Nature 520, 104–108 (2015).
pubmed: 25539086 pmcid: 4667810 doi: 10.1038/nature14052
Klevens, R. M. et al. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA 298, 1763–1771 (2007).
pubmed: 17940231 doi: 10.1001/jama.298.15.1763
Moran, G. J. et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N. Engl. J. Med. 355, 666–674 (2006).
pubmed: 16914702 doi: 10.1056/NEJMoa055356
Kolaczkowska, E. & Kubes, P. Neutrophil recruitment and function in health and inflammation. Nat. Rev. Immunol. 13, 159–175 (2013).
pubmed: 23435331 doi: 10.1038/nri3399
Krishna, S. & Miller, L. S. Innate and adaptive immune responses against Staphylococcus aureus skin infections. Semin. Immunopathol. 34, 261–280 (2012).
pubmed: 22057887 doi: 10.1007/s00281-011-0292-6
Kumar, H., Kawai, T. & Akira, S. Pathogen recognition by the innate immune system. Int. Rev. Immunol. 30, 16–34 (2011).
pubmed: 21235323 doi: 10.3109/08830185.2010.529976
Sadik, C. D. & Luster, A. D. Lipid-cytokine-chemokine cascades orchestrate leukocyte recruitment in inflammation. J. Leukoc. Biol. 91, 207–215 (2012).
pubmed: 22058421 pmcid: 3290425 doi: 10.1189/jlb.0811402
Wang, R. et al. Identification of novel cytolytic peptides as key virulence determinants for community-associated MRSA. Nat. Med. 13, 1510–1514 (2007).
pubmed: 17994102 doi: 10.1038/nm1656
Surewaard, B. G. et al. Staphylococcal alpha-phenol soluble modulins contribute to neutrophil lysis after phagocytosis. Cell. Microbiol. 15, 1427–1437 (2013).
pubmed: 23470014 pmcid: 4784422 doi: 10.1111/cmi.12130
Cassat, J. E. et al. A secreted bacterial protease tailors the Staphylococcus aureus virulence repertoire to modulate bone remodeling during osteomyelitis. Cell Host Microbe 13, 759–772 (2013).
pubmed: 23768499 pmcid: 3721972 doi: 10.1016/j.chom.2013.05.003
Kobayashi, S. D. et al. Comparative analysis of USA300 virulence determinants in a rabbit model of skin and soft tissue infection. J. Infect. Dis. 204, 937–941 (2011).
pubmed: 21849291 pmcid: 3156927 doi: 10.1093/infdis/jir441
Nakagawa, S. et al. Staphylococcus aureus virulent PSMalpha peptides induce keratinocyte alarmin release to orchestrate IL-17-dependent skin inflammation. Cell Host Microbe 22, 667–677.e5 (2017).
pubmed: 29120744 pmcid: 5728420 doi: 10.1016/j.chom.2017.10.008
Weiss, E. et al. Formyl-peptide receptor 2 governs leukocyte influx in local Staphylococcus aureus infections. FASEB J. https://doi.org/10.1096/fj.201700441R (2017).
Kretschmer, D. et al. Human formyl peptide receptor 2 senses highly pathogenic Staphylococcus aureus. Cell Host Microbe 7, 463–473 (2010).
pubmed: 20542250 pmcid: 3417054 doi: 10.1016/j.chom.2010.05.012
Peschel, A. & Otto, M. Phenol-soluble modulins and staphylococcal infection. Nat. Rev. Microbiol. 11, 667–673 (2013).
pubmed: 24018382 pmcid: 4780437 doi: 10.1038/nrmicro3110
Cheung, G. Y., Joo, H. S., Chatterjee, S. S. & Otto, M. Phenol-soluble modulins–critical determinants of staphylococcal virulence. FEMS Microbiol. Rev. 38, 698–719 (2014).
pubmed: 24372362 doi: 10.1111/1574-6976.12057
Joo, H. S., Cheung, G. Y. & Otto, M. Antimicrobial activity of community-associated methicillin-resistant Staphylococcus aureus is caused by phenol-soluble modulin derivatives. J. Biol. Chem. 286, 8933–8940 (2011).
pubmed: 21278255 pmcid: 3059065 doi: 10.1074/jbc.M111.221382
Hanzelmann, D. et al. Toll-like receptor 2 activation depends on lipopeptide shedding by bacterial surfactants. Nat. Commun. 7, 12304 (2016).
pubmed: 27470911 pmcid: 4974576 doi: 10.1038/ncomms12304
Queck, S. Y. et al. RNAIII-independent target gene control by the agr quorum-sensing system: insight into the evolution of virulence regulation in Staphylococcus aureus. Mol. Cell 32, 150–158 (2008).
pubmed: 18851841 pmcid: 2575650 doi: 10.1016/j.molcel.2008.08.005
Cheung, G. Y. et al. Insight into structure–function relationship in phenol-soluble modulins using an alanine screen of the phenol-soluble modulin (PSM) alpha3 peptide. FASEB J. 28, 153–161 (2014).
pubmed: 24008753 pmcid: 3868839 doi: 10.1096/fj.13-232041
Cheung, G. Y. et al. Staphylococcus epidermidis strategies to avoid killing by human neutrophils. PLoS Pathog. 6, e1001133 (2010).
pubmed: 20949069 pmcid: 2951371 doi: 10.1371/journal.ppat.1001133
Prat, C., Bestebroer, J., de Haas, C. J., van Strijp, J. A. & van Kessel, K. P. A new staphylococcal anti-inflammatory protein that antagonizes the formyl peptide receptor-like 1. J. Immunol. 177, 8017–8026 (2006).
pubmed: 17114475 doi: 10.4049/jimmunol.177.11.8017
Brown, T. J., Rowe, J. M., Liu, J. W. & Shoyab, M. Regulation of IL-6 expression by oncostatin M. J. Immunol. 147, 2175–2180 (1991).
pubmed: 1918953 doi: 10.4049/jimmunol.147.7.2175
Schutyser, E., Struyf, S. & Van Damme, J. The CC chemokine CCL20 and its receptor CCR6. Cytokine Growth Factor Rev. 14, 409–426 (2003).
pubmed: 12948524 doi: 10.1016/S1359-6101(03)00049-2
Kobayashi, Y. The role of chemokines in neutrophil biology. Front. Biosci. 13, 2400–2407 (2008).
pubmed: 17981721 doi: 10.2741/2853
Bertheloot, D. & Latz, E. HMGB1, IL-1alpha, IL-33 and S100 proteins: dual-function alarmins. Cell. Mol. Immunol. 14, 43–64 (2017).
pubmed: 27569562 doi: 10.1038/cmi.2016.34
Greenblatt, M. B., Aliprantis, A., Hu, B. & Glimcher, L. H. Calcineurin regulates innate antifungal immunity in neutrophils. J. Exp. Med. 207, 923–931 (2010).
pubmed: 20421389 pmcid: 2867274 doi: 10.1084/jem.20092531
Abdel-Latif, M. M. et al. Helicobacter pylori activates the early growth response 1 protein in gastric epithelial cells. Infect. Immun. 72, 3549–3560 (2004).
pubmed: 15155664 pmcid: 415651 doi: 10.1128/IAI.72.6.3549-3560.2004
Cargnello, M. & Roux, P. P. Activation and function of the MAPKs and their substrates, the MAPK-activated protein kinases. Microbiol. Mol. Biol. Rev. 75, 50–83 (2011).
pubmed: 21372320 pmcid: 3063353 doi: 10.1128/MMBR.00031-10
Sundqvist, M. et al. Staphylococcus aureus-derived PSMalpha peptides activate neutrophil FPR2 but lack the ability to mediate beta-arrestin recruitment and chemotaxis. J. Immunol. https://doi.org/10.4049/jimmunol.1900871 (2019).
Migeotte, I., Communi, D. & Parmentier, M. Formyl peptide receptors: a promiscuous subfamily of G protein-coupled receptors controlling immune responses. Cytokine Growth Factor Rev. 17, 501–519 (2006).
pubmed: 17084101 doi: 10.1016/j.cytogfr.2006.09.009
Vuong, C. et al. Regulated expression of pathogen-associated molecular pattern molecules in Staphylococcus epidermidis: quorum-sensing determines pro-inflammatory capacity and production of phenol-soluble modulins. Cell. Microbiol. 6, 753–759 (2004).
pubmed: 15236642 doi: 10.1111/j.1462-5822.2004.00401.x
Panaro, M. A. & Mitolo, V. Cellular responses to FMLP challenging: a mini-review. Immunopharmacol. Immunotoxicol. 21, 397–419 (1999).
pubmed: 10466071 doi: 10.3109/08923979909007117
Keates, S., Keates, A. C., Nath, S., Peek, R. M. Jr. & Kelly, C. P. Transactivation of the epidermal growth factor receptor by cag+ Helicobacter pylori induces upregulation of the early growth response gene Egr-1 in gastric epithelial cells. Gut 54, 1363–1369 (2005).
pubmed: 15863471 pmcid: 1774684 doi: 10.1136/gut.2005.066977
de Grado, M., Rosenberger, C. M., Gauthier, A., Vallance, B. A. & Finlay, B. B. Enteropathogenic Escherichia coli infection induces expression of the early growth response factor by activating mitogen-activated protein kinase cascades in epithelial cells. Infect. Immun. 69, 6217–6224 (2001).
pubmed: 11553563 pmcid: 98754 doi: 10.1128/IAI.69.10.6217-6224.2001
Hannemann, S., Gao, B. & Galan, J. E. Salmonella modulation of host cell gene expression promotes its intracellular growth. PLoS Pathog. 9, e1003668 (2013).
pubmed: 24098123 pmcid: 3789771 doi: 10.1371/journal.ppat.1003668
de Klerk, N., Saroj, S. D., Wassing, G. M., Maudsdotter, L. & Jonsson, A. B. The host cell transcription factor EGR1 is induced by bacteria through the EGFR-ERK1/2 pathway. Front. Cell. Infect. Microbiol. 7, 16 (2017).
pubmed: 28180113 pmcid: 5264520 doi: 10.3389/fcimb.2017.00016
Xu, Z. et al. Bacterial peptidoglycan-induced tnf-alpha transcription is mediated through the transcription factors Egr-1, Elk-1, and NF-kappaB. J. Immunol. 167, 6975–6982 (2001).
pubmed: 11739517 doi: 10.4049/jimmunol.167.12.6975
Coleman, D. L., Bartiss, A. H., Sukhatme, V. P., Liu, J. & Rupprecht, H. D. Lipopolysaccharide induces Egr-1 mRNA and protein in murine peritoneal macrophages. J. Immunol. 149, 3045–3051 (1992).
pubmed: 1401930 doi: 10.4049/jimmunol.149.9.3045
Rautenberg, M., Joo, H. S., Otto, M. & Peschel, A. Neutrophil responses to staphylococcal pathogens and commensals via the formyl peptide receptor 2 relates to phenol-soluble modulin release and virulence. FASEB J. 25, 1254–1263 (2011).
pubmed: 21183593 pmcid: 3058707 doi: 10.1096/fj.10-175208
Chatterjee, S. S. et al. Essential Staphylococcus aureus toxin export system. Nat. Med. 19, 364–367 (2013).
pubmed: 23396209 pmcid: 3594369 doi: 10.1038/nm.3047
Dahlgren, C., Gabl, M., Holdfeldt, A., Winther, M. & Forsman, H. Basic characteristics of the neutrophil receptors that recognize formylated peptides, a danger-associated molecular pattern generated by bacteria and mitochondria. Biochem. Pharmacol. 114, 22–39 (2016).
pubmed: 27131862 doi: 10.1016/j.bcp.2016.04.014
Forsman, H. et al. Structural changes of the ligand and of the receptor alters the receptor preference for neutrophil activating peptides starting with a formylmethionyl group. Biochim. Biophys. Acta 1853, 192–200 (2015).
pubmed: 25447672 doi: 10.1016/j.bbamcr.2014.10.021
Qin, L. et al. Toxin mediates sepsis caused by methicillin-resistant Staphylococcus epidermidis. PLoS Pathog. 13, e1006153 (2017).
pubmed: 28151994 pmcid: 5289634 doi: 10.1371/journal.ppat.1006153
Schmittgen, T. D. & Livak, K. J. Analyzing real-time PCR data by the comparative C(T) method. Nat. Protoc. 3, 1101–1108 (2008).
pubmed: 18546601 doi: 10.1038/nprot.2008.73
Faust, N., Varas, F., Kelly, L. M., Heck, S. & Graf, T. Insertion of enhanced green fluorescent protein into the lysozyme gene creates mice with green fluorescent granulocytes and macrophages. Blood 96, 719–726 (2000).
pubmed: 10887140 doi: 10.1182/blood.V96.2.719
Kamenyeva, O. et al. Neutrophil recruitment to lymph nodes limits local humoral response to Staphylococcus aureus. PLoS Pathog. 11, e1004827 (2015).
pubmed: 25884622 pmcid: 4401519 doi: 10.1371/journal.ppat.1004827

Auteurs

Thuan H Nguyen (TH)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
University of Maryland School of Medicine, Baltimore, MD, USA.

Gordon Y C Cheung (GYC)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Kevin M Rigby (KM)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Pathogen-Host Cell Biology Section, Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.
miRagen Therapeutics, Inc., Boulder, CO, USA.

Olena Kamenyeva (O)

Biological Imaging Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Juraj Kabat (J)

Biological Imaging Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Daniel E Sturdevant (DE)

Genomics Unit, Research Technology Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.

Amer E Villaruz (AE)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Ryan Liu (R)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Pipat Piewngam (P)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Adeline R Porter (AR)

Pathogen-Host Cell Biology Section, Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.

Saba Firdous (S)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Chlamydia Pathogenesis Section, NIAID, Bethesda, MD, USA.

Janice Chiou (J)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Graduate School in Biomedical Science, Cedars Sinai Medical Center, Los Angeles, CA, USA.

Matthew D Park (MD)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Rachelle L Hunt (RL)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Microbial Pathogenesis Department, Yale University, New Haven, CT, USA.

Fawaz M F Almufarriji (FMF)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
School of Molecular and Cell Biology, University of Leeds, Leeds, UK.

Vee Y Tan (VY)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Tuberculosis Research Section, NIAID, Bethesda, MD, USA.

Titus K Asiamah (TK)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Joshua W McCausland (JW)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Johns Hopkins University, Baltimore, MD, USA.

Emilie L Fisher (EL)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Vanderbilt University, Nashville, TN, USA.

Anthony J Yeh (AJ)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
William Carey University College of Osteopathic Medicine, Hattiesburg, MS, USA.

Justin S Bae (JS)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Harvard University, Cambridge, MA, USA.

Scott D Kobayashi (SD)

Pathogen-Host Cell Biology Section, Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.

Ji Ming Wang (JM)

Laboratory of Cancer and Immunometabolism, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, USA.

Daniel L Barber (DL)

T-Lymphocyte Biology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Frank R DeLeo (FR)

Pathogen-Host Cell Biology Section, Laboratory of Bacteriology, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA.

Michael Otto (M)

Pathogen Molecular Genetics Section, Laboratory of Bacteriology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. motto@niaid.nih.gov.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH