Cargando…
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...
Autores principales: | , , , , |
---|---|
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 |
_version_ | 1783656447671795712 |
---|---|
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. |
format | Online Article Text |
id | pubmed-7911888 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
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 |
work_keys_str_mv | AT midiriangelina therelevanceofil1signalingintheprotectionagainstgrampositivebacteria AT mancusogiuseppe therelevanceofil1signalingintheprotectionagainstgrampositivebacteria AT beninaticoncetta therelevanceofil1signalingintheprotectionagainstgrampositivebacteria AT geraceelisabetta therelevanceofil1signalingintheprotectionagainstgrampositivebacteria AT biondocarmelo therelevanceofil1signalingintheprotectionagainstgrampositivebacteria AT midiriangelina relevanceofil1signalingintheprotectionagainstgrampositivebacteria AT mancusogiuseppe relevanceofil1signalingintheprotectionagainstgrampositivebacteria AT beninaticoncetta relevanceofil1signalingintheprotectionagainstgrampositivebacteria AT geraceelisabetta relevanceofil1signalingintheprotectionagainstgrampositivebacteria AT biondocarmelo relevanceofil1signalingintheprotectionagainstgrampositivebacteria |