The β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages.

S. agalactiae (group B streptococci, GBS) is a major microbial pathogen in human neonates and causes invasive infections in pregnant women and immunocompromised individuals. The S. agalactiae β-hemolysin is regarded as an important virulence factor for the development of invasive disease. To examine...

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Autores principales: Anubha Sagar, Carolin Klemm, Lara Hartjes, Stefanie Mauerer, Ger van Zandbergen, Barbara Spellerberg
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Publicado: Public Library of Science (PLoS) 2013
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spelling oai:doaj.org-article:522c63ff856b4d928d25722ee3d977d62021-11-18T07:50:39ZThe β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages.1932-620310.1371/journal.pone.0060160https://doaj.org/article/522c63ff856b4d928d25722ee3d977d62013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23593170/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203S. agalactiae (group B streptococci, GBS) is a major microbial pathogen in human neonates and causes invasive infections in pregnant women and immunocompromised individuals. The S. agalactiae β-hemolysin is regarded as an important virulence factor for the development of invasive disease. To examine the role of β-hemolysin in the interaction with professional phagocytes, the THP-1 monocytic cell line and human granulocytes were infected with a serotype Ia S. agalactiae wild type strain and its isogenic nonhemolytic mutant. We could show that the nonhemolytic mutants were able to survive in significantly higher numbers than the hemolytic wild type strain, in THP-1 macrophage-like cells and in assays with human granulocytes. Intracellular bacterial multiplication, however, could not be observed. The hemolytic wild type strain stimulated a significantly higher release of Tumor Necrosis Factor-α than the nonhemolytic mutant in THP-1 cells, while similar levels of the chemokine Interleukin-8 were induced. In order to investigate bacterial mediators of IL-8 release in this setting, purified cell wall preparations from both strains were tested and found to exert a potent proinflammatory stimulus on THP-1 cells. In conclusion, our results indicate that the β-hemolysin has a strong influence on the intracellular survival of S. agalactiae and that a tightly controlled regulation of β-hemolysin expression is required for the successful establishment of S. agalactiae in different host niches.Anubha SagarCarolin KlemmLara HartjesStefanie MauererGer van ZandbergenBarbara SpellerbergPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 4, p e60160 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Anubha Sagar
Carolin Klemm
Lara Hartjes
Stefanie Mauerer
Ger van Zandbergen
Barbara Spellerberg
The β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages.
description S. agalactiae (group B streptococci, GBS) is a major microbial pathogen in human neonates and causes invasive infections in pregnant women and immunocompromised individuals. The S. agalactiae β-hemolysin is regarded as an important virulence factor for the development of invasive disease. To examine the role of β-hemolysin in the interaction with professional phagocytes, the THP-1 monocytic cell line and human granulocytes were infected with a serotype Ia S. agalactiae wild type strain and its isogenic nonhemolytic mutant. We could show that the nonhemolytic mutants were able to survive in significantly higher numbers than the hemolytic wild type strain, in THP-1 macrophage-like cells and in assays with human granulocytes. Intracellular bacterial multiplication, however, could not be observed. The hemolytic wild type strain stimulated a significantly higher release of Tumor Necrosis Factor-α than the nonhemolytic mutant in THP-1 cells, while similar levels of the chemokine Interleukin-8 were induced. In order to investigate bacterial mediators of IL-8 release in this setting, purified cell wall preparations from both strains were tested and found to exert a potent proinflammatory stimulus on THP-1 cells. In conclusion, our results indicate that the β-hemolysin has a strong influence on the intracellular survival of S. agalactiae and that a tightly controlled regulation of β-hemolysin expression is required for the successful establishment of S. agalactiae in different host niches.
format article
author Anubha Sagar
Carolin Klemm
Lara Hartjes
Stefanie Mauerer
Ger van Zandbergen
Barbara Spellerberg
author_facet Anubha Sagar
Carolin Klemm
Lara Hartjes
Stefanie Mauerer
Ger van Zandbergen
Barbara Spellerberg
author_sort Anubha Sagar
title The β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages.
title_short The β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages.
title_full The β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages.
title_fullStr The β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages.
title_full_unstemmed The β-hemolysin and intracellular survival of Streptococcus agalactiae in human macrophages.
title_sort β-hemolysin and intracellular survival of streptococcus agalactiae in human macrophages.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/522c63ff856b4d928d25722ee3d977d6
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