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The Relevance of IL-1-Signaling in the Protection against Gram-Positive Bacteria

Previous studies performed using a model of group B streptococcus (GBS)-induced peritoneal inflammation indicate that the interleukin-1 receptor (IL-1R) family plays an important role in the innate host defense against this encapsulated Gram-positive bacteria. Since the role of IL-1-dependent signal...

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Autores principales: Midiri, Angelina, Mancuso, Giuseppe, Beninati, Concetta, Gerace, Elisabetta, Biondo, Carmelo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7911888/
https://www.ncbi.nlm.nih.gov/pubmed/33525468
http://dx.doi.org/10.3390/pathogens10020132
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author Midiri, Angelina
Mancuso, Giuseppe
Beninati, Concetta
Gerace, Elisabetta
Biondo, Carmelo
author_facet Midiri, Angelina
Mancuso, Giuseppe
Beninati, Concetta
Gerace, Elisabetta
Biondo, Carmelo
author_sort Midiri, Angelina
collection PubMed
description Previous studies performed using a model of group B streptococcus (GBS)-induced peritoneal inflammation indicate that the interleukin-1 receptor (IL-1R) family plays an important role in the innate host defense against this encapsulated Gram-positive bacteria. Since the role of IL-1-dependent signaling in peritoneal infections induced by other Gram-positive bacteria is unknown, in the present study we sought to investigate the contribution of IL-1R signaling in host defenses against Streptococcus pyogenes (group A streptococcus or GAS) or Staphylococcus aureus, two frequent and global human Gram-positive extracellular pathogens. We analyzed here the outcome of GAS or S. aureus infection in IL-1R-deficient mice. After inoculated intraperitoneal (i.p.) inoculation with group A Streptococcus or S. aureus, all the wild-type (WT) control mice survived the challenge, while, respectively, 63% or 50% of IL-1-defective mice died. Lethality was due to the ability of both bacterial species to replicate and disseminate to the target organs of IL-1R-deficient mice. Moreover, the experimental results indicate that IL-1 signaling promotes the production of leukocyte attractant chemokines CXCL-1 and CXCL-2 and recruitment of neutrophils to bacterial infection sites. Accordingly, the reduced neutrophil recruitment in IL-1R-deficient mice was linked with decreased production of neutrophil chemokines. Collectively, our findings indicate that IL-1 signaling, as previously showed in host defense against GBS, plays a fundamental role also in controlling the progression and outcome of GAS or S. aureus disease.
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spelling pubmed-79118882021-02-28 The Relevance of IL-1-Signaling in the Protection against Gram-Positive Bacteria Midiri, Angelina Mancuso, Giuseppe Beninati, Concetta Gerace, Elisabetta Biondo, Carmelo Pathogens Article Previous studies performed using a model of group B streptococcus (GBS)-induced peritoneal inflammation indicate that the interleukin-1 receptor (IL-1R) family plays an important role in the innate host defense against this encapsulated Gram-positive bacteria. Since the role of IL-1-dependent signaling in peritoneal infections induced by other Gram-positive bacteria is unknown, in the present study we sought to investigate the contribution of IL-1R signaling in host defenses against Streptococcus pyogenes (group A streptococcus or GAS) or Staphylococcus aureus, two frequent and global human Gram-positive extracellular pathogens. We analyzed here the outcome of GAS or S. aureus infection in IL-1R-deficient mice. After inoculated intraperitoneal (i.p.) inoculation with group A Streptococcus or S. aureus, all the wild-type (WT) control mice survived the challenge, while, respectively, 63% or 50% of IL-1-defective mice died. Lethality was due to the ability of both bacterial species to replicate and disseminate to the target organs of IL-1R-deficient mice. Moreover, the experimental results indicate that IL-1 signaling promotes the production of leukocyte attractant chemokines CXCL-1 and CXCL-2 and recruitment of neutrophils to bacterial infection sites. Accordingly, the reduced neutrophil recruitment in IL-1R-deficient mice was linked with decreased production of neutrophil chemokines. Collectively, our findings indicate that IL-1 signaling, as previously showed in host defense against GBS, plays a fundamental role also in controlling the progression and outcome of GAS or S. aureus disease. MDPI 2021-01-28 /pmc/articles/PMC7911888/ /pubmed/33525468 http://dx.doi.org/10.3390/pathogens10020132 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Midiri, Angelina
Mancuso, Giuseppe
Beninati, Concetta
Gerace, Elisabetta
Biondo, Carmelo
The Relevance of IL-1-Signaling in the Protection against Gram-Positive Bacteria
title The Relevance of IL-1-Signaling in the Protection against Gram-Positive Bacteria
title_full The Relevance of IL-1-Signaling in the Protection against Gram-Positive Bacteria
title_fullStr The Relevance of IL-1-Signaling in the Protection against Gram-Positive Bacteria
title_full_unstemmed The Relevance of IL-1-Signaling in the Protection against Gram-Positive Bacteria
title_short The Relevance of IL-1-Signaling in the Protection against Gram-Positive Bacteria
title_sort relevance of il-1-signaling in the protection against gram-positive bacteria
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7911888/
https://www.ncbi.nlm.nih.gov/pubmed/33525468
http://dx.doi.org/10.3390/pathogens10020132
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