WorldCat Identities

Henriques-Normark, Birgitta

Overview
Works: 17 works in 17 publications in 1 language and 24 library holdings
Roles: Contributor, dgs, Other, Author
Publication Timeline
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Most widely held works by Birgitta Henriques-Normark
Small molecule inhibitors of the Yersinia type III secretion system impair the development of Chlamydia after entry into host cells by Sandra Muschiol( )

1 edition published in 2009 in English and held by 2 WorldCat member libraries worldwide

An individual-based network model to evaluate interventions for controlling pneumococcal transmission by Diana Karlsson( )

1 edition published in 2008 in English and held by 2 WorldCat member libraries worldwide

Prevalence of community-acquired bacteraemia in Guinea-Bissau: an observational study by Joakim Isendahl( )

1 edition published in 2014 in English and held by 2 WorldCat member libraries worldwide

Factor H binding proteins protect division septa on encapsulated Streptococcus pneumoniae against complement C3b deposition and amplification by Anuj Pathak( )

1 edition published in 2018 in English and held by 2 WorldCat member libraries worldwide

The influence of in vitro fitness defects on pneumococcal ability to colonize and to cause invasive disease by Jenny Fernebro( )

1 edition published in 2008 in English and held by 2 WorldCat member libraries worldwide

Pneumolysin binds to the mannose receptor C type 1 (MRC-1) leading to anti-inflammatory responses and enhanced pneumococcal survival by Karthik Subramanian( )

1 edition published in 2018 in English and held by 2 WorldCat member libraries worldwide

How Does Streptococcus pneumoniae Invade the Brain?( )

1 edition published in 2016 in English and held by 1 WorldCat member library worldwide

Abstract : Streptococcus pneumoniae (the pneumococcus) is the major cause of bacterial meningitis. The mechanisms by which pneumococci from the bloodstream penetrate the blood-brain barrier to reach the brain are not fully understood. Receptor-mediated adhesion of the bacteria to the brain endothelium is considered a key event leading to meningitis development. The aim of this review is to discuss recent advances and perspectives related to the interactions of S. pneumoniae with the blood-brain barrier during the events leading to meningitis. Altogether, the available data suggest that, by precisely defining the pathways and ligands by which S. pneumoniae adheres to specific receptors, it may be possible to interfere with the respective mechanisms and develop strategies to prevent or even cure pneumococcal meningitis. Trends: Streptococcus pneumoniae, the main causative agent of bacterial meningitis, penetrates the blood-brain barrier by binding to PECAM-1 and pIgR expressed by brain vascular endothelial cells. Overall, recent findings suggest that PECAM-1 and pIgR, together with platelet-activating factor receptor (PAFR), another receptor thought to be more involved in signaling rather than physical binding, might cooperate during adhesion of pneumococci to brain endothelial cells. The passage of S. pneumoniae across the blood-brain barrier is a crucial step for meningitis development. The knowledge of how S. pneumoniae penetrates the blood-brain barrier can be used to develop strategies aimed at interfering with the respective pathways in order to prevent the entry of the pathogen into the brain
Bacterial strain-dependency in secondary pneumococcal infection following influenza A virus infection elucidating underlying immune responses and long-term effects by Niharika Sharma( )

1 edition published in 2016 in English and held by 1 WorldCat member library worldwide

Analysis of IAV Replication and Co-infection Dynamics by a Versatile RNA Viral Genome Labeling Method by Dan Dou( )

1 edition published in 2017 in English and held by 1 WorldCat member library worldwide

Genome delivery to the proper cellular compartment for transcription and replication is a primary goal of viruses. However, methods for analyzing viral genome localization and differentiating genomes with high identity are lacking, making it difficult to investigate entry-related processes and co-examine heterogeneous RNA viral populations. Here, we present an RNA labeling approach for single-cell analysis of RNA viral replication and co-infection dynamics in situ, which uses the versatility of padlock probes. We applied this method to identify influenza A virus (IAV) infections in cells and lung tissue with single-nucleotide specificity and to classify entry and replication stages by gene segment localization. Extending the classification strategy to co-infections of IAVs with single-nucleotide variations, we found that the dependence on intracellular trafficking places a time restriction on secondary co-infections necessary for genome reassortment. Altogether, these data demonstrate how RNA viral genome labeling can help dissect entry and co-infections
THCz Small molecules with antimicrobial activity that block cell wall lipid intermediates by Elisabeth Reithuber( )

1 edition published in 2021 in English and held by 1 WorldCat member library worldwide

Emerging antibiotic resistance demands identification of novel antibacterial compound classes. A bacterial whole-cell screen based on pneumococcal autolysin-mediated lysis induction was developed to identify potential bacterial cell wall synthesis inhibitors. A hit class comprising a 1-amino substituted tetrahydrocarbazole (THCz) scaffold, containing two essential amine groups, displayed bactericidal activity against a broad range of gram-positive and selected gram-negative pathogens in the low micromolar range. Mode of action studies revealed that THCz inhibit cell envelope synthesis by targeting undecaprenyl pyrophosphate-containing lipid intermediates and thus simultaneously inhibit peptidoglycan, teichoic acid, and polysaccharide capsule biosynthesis. Resistance did not readily develop in vitro, and the ease of synthesizing and modifying these small molecules, as compared to natural lipid II-binding antibiotics, makes THCz promising scaffolds for development of cell wall-targeting antimicrobials
Immunomodulatory Effects of Pneumococcal Extracellular Vesicles on Cellular and Humoral Host Defenses by Mario Codemo( )

1 edition published in 2018 in English and held by 1 WorldCat member library worldwide

Gram-positive bacteria, including the major respiratory pathogen Streptococcus pneumoniae, were recently shown to produce extracellular vesicles (EVs) that likely originate from the plasma membrane and are released into the extracellular environment. EVs may function as cargo for many bacterial proteins, however, their involvement in cellular processes and their interactions with the innate immune system are poorly understood. Here, EVs from pneumococci were characterized and their immunomodulatory effects investigated. Pneumococcal EVs were protruding from the bacterial surface and released into the medium as 25 to 250 nm lipid stained vesicles containing a large number of cytosolic, membrane, and surface-associated proteins. The cytosolic pore-forming toxin pneumolysin was significantly enriched in EVs compared to a total bacterial lysate but was not required for EV formation. Pneumococcal EVs were internalized into A549 lung epithelial cells and human monocyte-derived dendritic cells and induced proinflammatory cytokine responses irrespective of pneumolysin content. EVs from encapsulated pneumococci were recognized by serum proteins, resulting in C3b deposition and formation of C5b-9 membrane attack complexes as well as factor H recruitment, depending on the presence of the choline binding protein PspC. Addition of EVs to human serum decreased opsonophagocytic killing of encapsulated pneumococci. Our data suggest that EVs may act in an immunomodulatory manner by allowing delivery of vesicle-associated proteins and other macromolecules into host cells. In addition, EVs expose targets for complement factors in serum, promoting pneumococcal evasion of humoral host defense. Importance: Streptococcus pneumoniae is a major contributor to morbidity and mortality worldwide, being the major cause of milder respiratory tract infections such as otitis and sinusitis and of severe infections such as community-acquired pneumonia, with or without septicemia, and meningitis. More knowledge is needed on how pneumococci interact with the host, deliver virulence factors, and activate immune defenses. Here we show that pneumococci form extracellular vesicles that emanate from the plasma membrane and contain virulence properties, including enrichment of pneumolysin. We found that pneumococcal vesicles can be internalized into epithelial and dendritic cells and bind complement proteins, thereby promoting pneumococcal evasion of complement-mediated opsonophagocytosis. They also induce pneumolysin-independent proinflammatory responses. We suggest that these vesicles can function as a mechanism for delivery of pneumococcal proteins and other immunomodulatory components into host cells and help pneumococci to avoid complement deposition and phagocytosis-mediated killing, thereby possibly contributing to the symptoms found in pneumococcal infections
The role of cell type specific MyD88 signalling in host defence against pulmonary S. pneumoniae infection by Markus Dudek( )

1 edition published in 2016 in English and held by 1 WorldCat member library worldwide

Bacterial strain-dependency in secondary pneumococcal infection following influenza A virus infection - elucidating underlying immune responses and long-term effects by Niharika Sharma( Book )

1 edition published in 2016 in English and held by 1 WorldCat member library worldwide

The Bactericidal Fatty Acid Mimetic 2CCA-1 Selectively Targets Pneumococcal Extracellular Polyunsaturated Fatty Acid Metabolism by Elisabeth Reithuber( )

1 edition published in 2020 in English and held by 1 WorldCat member library worldwide

Streptococcus pneumoniae, a major cause of pneumonia, sepsis, and meningitis worldwide, has the nasopharynges of small children as its main ecological niche. Depletion of pneumococci from this niche would reduce the disease burden and could be achieved using small molecules with narrow-spectrum antibacterial activity. We identified the alkylated dicyclohexyl carboxylic acid 2CCA-1 as a potent inducer of autolysin-mediated lysis of S. pneumoniae, while having low activity against Staphylococcus aureus. 2CCA-1-resistant strains were found to have inactivating mutations in fakB3, known to be required for uptake of host polyunsaturated fatty acids, as well as through inactivation of the transcriptional regulator gene fabT, vital for endogenous, de novo fatty acid synthesis regulation. Structure activity relationship exploration revealed that, besides the central dicyclohexyl group, the fatty acid-like structural features of 2CCA-1 were essential for its activity. The lysis-inducing activity of 2CCA-1 was considerably more potent than that of free fatty acids and required growing bacteria, suggesting that 2CCA-1 needs to be metabolized to exert its antimicrobial activity. Total lipid analysis of 2CCA-1 treated bacteria identified unique masses that were modeled to 2CCA-1 containing lysophosphatidic and phosphatidic acid in wild-type but not in fakB3 mutant bacteria. This suggests that 2CCA-1 is metabolized as a fatty acid via FakB3 and utilized as a phospholipid building block, leading to accumulation of toxic phospholipid species. Analysis of FabT-mediated fakB3 expression elucidates how the pneumococcus could ensure membrane homeostasis and concurrent economic use of host-derived fatty acids.IMPORTANCE Fatty acid biosynthesis is an attractive antibiotic target, as it affects the supply of membrane phospholipid building blocks. In Streptococcus pneumoniae, it is not sufficient to target only the endogenous fatty acid synthesis machinery, as uptake of host fatty acids may bypass this inhibition. Here, we describe a small-molecule compound, 2CCA-1, with potent bactericidal activity that upon interactions with the fatty acid binding protein FakB3, which is present in a limited number of Gram-positive species, becomes metabolized and incorporated as a toxic phospholipid species. Resistance to 2CCA-1 developed specifically in fakB3 and the regulatory gene fabT. These mutants reveal a regulatory connection between the extracellular polyunsaturated fatty acid metabolism and endogenous fatty acid synthesis in S. pneumoniae, which could ensure balance between efficient scavenging of host polyunsaturated fatty acids and membrane homeostasis. The data might be useful in the identification of narrow-spectrum treatment strategies to selectively target members of the Lactobacillales such as S. pneumoniae
Reply to Theilacker et al( )

1 edition published in 2017 in English and held by 1 WorldCat member library worldwide

Streptococcus pneumoniae : molecular epidemiology of isolates causing invasive disease and characterization of tolerance responses to lytic antibiotics by Birgitta Henriques Normark( Book )

1 edition published in 2000 in English and held by 1 WorldCat member library worldwide

 
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Alternative Names
Birgitta Henriques Normark professor/överläkare vid Karolinska Institutet

Birgitta Henriques-Normark researcher

Birgitta Henriques-Normark wetenschapper

Normark, Birgitta Henriques-

Languages
English (17)