scholarly journals Attachment of capsular polysaccharide to the cell wall of Streptococcus pneumoniae type 2 is required for invasive disease

2006 ◽  
Vol 103 (22) ◽  
pp. 8505-8510 ◽  
Author(s):  
J. K. Morona ◽  
R. Morona ◽  
J. C. Paton
Keyword(s):  
Cell Wall ◽  
Streptococcus Pneumoniae ◽  
Capsular Polysaccharide ◽  
Invasive Disease

scholarly journals Monoclonal antibodies against protease-sensitive pneumococcal antigens can protect mice from fatal infection with Streptococcus pneumoniae.

1984 ◽  
Vol 160 (2) ◽  
pp. 386-397 ◽  
Author(s):  
L S McDaniel ◽  
G Scott ◽  
J F Kearney ◽  
D E Briles
Keyword(s):  
Cell Wall ◽  
Monoclonal Antibodies ◽  
Streptococcus Pneumoniae ◽  
Capsular Polysaccharide ◽  
Minimum Amount ◽  
Binding Studies ◽  
Fatal Infection ◽  
Rough Strain ◽  
Type 3

Monoclonal antibodies were raised against surface determinants of Streptococcus pneumoniae by hyperimmunizing X-linked immunodeficient (xid) CBA/N mice with the heat-killed rough strain R36A. 17 hybridomas produced antibody that bound intact R36A and did not cross-react with phosphocholine, an antigen common in the cell wall of all S. pneumoniae. The antibody produced by at least two of these hybridomas, Xi64 (IgM) and Xi126 (IgG2b), could protect mice from a lethal intravenous challenge of type 3 S. pneumoniae strains WU2 and A66 and of the type 2 strain D39. The minimum amount of antibody required to protect xid mice from 100 WU2 was 4.5 micrograms/mouse for Xi64 and 2.6 micrograms/mouse for Xi126,. Free phosphocholine, C-polysaccharide, and type 3 capsular polysaccharide all failed to inhibit the binding of Xi64 or Xi126 to R36A. These antibodies appeared to bind surface polypeptides, since treatment of R36A with either pepsin or trypsin, or of R36A lysate with trypsin, effectively eliminated the ability of Xi64 and Xi126 to bind antigens in these preparations. Binding studies indicated that these two antibodies recognized different epitopes that were expressed on several but not all serotypes of pneumococci.

DiiA is a novel dimorphic cell wall protein of Streptococcus pneumoniae involved in invasive disease

2016 ◽  
Vol 73 (1) ◽  
pp. 71-81 ◽  
Author(s):  
María S. Escolano-Martínez ◽  
Arnau Domenech ◽  
José Yuste ◽  
María I. Cercenado ◽  
Carmen Ardanuy ◽  
...  
Keyword(s):  
Cell Wall ◽  
Streptococcus Pneumoniae ◽  
Invasive Disease ◽  
Cell Wall Protein

Structural studies of the capsular polysaccharide from streptococcus pneumoniae type 2, a reinvestigation

1988 ◽  
Vol 182 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Per-Erik Jansson ◽  
Bengt Lindberg ◽  
Mats Andersson ◽  
Ulf Lindquist ◽  
Jørgen Henrichsen
Keyword(s):  
Streptococcus Pneumoniae ◽  
Capsular Polysaccharide ◽  
Structural Studies

scholarly journals Intranasal Immunization of Mice with a Mixture of the Pneumococcal Proteins PsaA and PspA Is Highly Protective against Nasopharyngeal Carriage of Streptococcus pneumoniae

2000 ◽  
Vol 68 (2) ◽  
pp. 796-800 ◽  
Author(s):  
David E. Briles ◽  
Eddie Ades ◽  
James C. Paton ◽  
Jacquelyn S. Sampson ◽  
George M. Carlone ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Capsular Polysaccharide ◽  
Herd Immunity ◽  
Invasive Disease ◽  
Mucosal Vaccine ◽  
Nasopharyngeal Carriage ◽  
Intranasal Immunization ◽  
Protein Conjugates

ABSTRACT Acquisition of pneumococci is generally from carriers rather than from infected individuals. Therefore, to induce herd immunity againstStreptococcus pneumoniae it will be necessary to elicit protection against carriage. Capsular polysaccharide-protein conjugates, PspA, and PsaA are known to elicit some protection against nasopharyngeal carriage of pneumococci but do not always completely eliminate carriage. In this study, we observed that PsaA elicited better protection than did PspA against carriage. Pneumolysin elicited no protection against carriage. Immunization with a mixture of PsaA and PspA elicited the best protection against carriage. These results indicate that PspA and PsaA may be useful for the elicitation of herd immunity in humans. As PspA and pneumolysin are known to elicit immunity to bacteremia and pneumonia, their inclusion in a mucosal vaccine may enable such a vaccine to prevent invasive disease as well as carriage.

scholarly journals Degradation Products of the Extracellular Pathogen Streptococcus pneumoniae Access the Cytosol via Its Pore-Forming Toxin

mBio ◽  
2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Jamie K. Lemon ◽  
Jeffrey N. Weiser
Keyword(s):  
Cell Wall ◽  
Streptococcus Pneumoniae ◽  
Capsular Polysaccharide ◽  
Mapk Signaling ◽  
Innate Immune ◽  
Host Cells ◽  
Content Type ◽  
Cell Wall Components ◽  
Immune Detection ◽  
Wall Components

ABSTRACT Streptococcus pneumoniaeis a leading pathogen with an extracellular lifestyle; however, it is detected by cytosolic surveillance systems of macrophages. The innate immune response that follows cytosolic sensing of cell wall components results in recruitment of additional macrophages, which subsequently clear colonizing organisms from host airways. In this study, we monitored cytosolic access by following the transit of the abundant bacterial surface component capsular polysaccharide, which is linked to the cell wall. Confocal and electron microscopy visually characterized the location of cell wall components in murine macrophages outside membrane-bound organelles. Quantification of capsular polysaccharide through cellular fractionation demonstrated that cytosolic access of bacterial cell wall components is dependent on phagocytosis, bacterial sensitivity to the host’s degradative enzyme lysozyme, and release of the pore-forming toxin pneumolysin. Activation of p38 mitogen-activated protein kinase (MAPK) signaling is important for limiting access to the cytosol; however, ultimately, these are catastrophic events for both the bacteria and the macrophage, which undergoes cell death. Our results show how expression of a pore-forming toxin ensures the death of phagocytes that take up the organism, although cytosolic sensing results in innate immune detection that eventually allows for successful host defense. These findings provide an example of how cytosolic access applies to an extracellular microbe and contributes to its pathogenesis.IMPORTANCE Streptococcus pneumoniae(the pneumococcus) is a bacterial pathogen that is a leading cause of pneumonia. Pneumococcal disease is preceded by colonization of the nasopharynx, which lasts several weeks before being cleared by the host’s immune system. Although S. pneumoniae is an extracellular microbe, intracellular detection of pneumococcal components is critical for bacterial clearance. In this study, we show that following bacterial uptake and degradation by phagocytes, pneumococcal products access the host cell cytosol via its pore-forming toxin. This phenomenon of cytosolic access results in phagocyte death and may serve to combat the host cells responsible for clearing the organism. Our results provide an example of how intracellular access and subsequent immune detection occurs during infection with an extracellular pathogen.

scholarly journals Sequence Elements Upstream of the Core Promoter Are Necessary for Full Transcription of the Capsule Gene Operon in Streptococcus pneumoniae Strain D39

2015 ◽  
Vol 83 (5) ◽  
pp. 1957-1972 ◽  
Author(s):  
Zhensong Wen ◽  
Odeniel Sertil ◽  
Yongxin Cheng ◽  
Shanshan Zhang ◽  
Xue Liu ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Capsular Polysaccharide ◽  
Core Promoter ◽  
Virulent Strain ◽  
Bacterial Pathogen ◽  
Content Type ◽  
The Core ◽  
Sequence Elements ◽  
Almost All

Streptococcus pneumoniaeis a major bacterial pathogen in humans. Its polysaccharide capsule is a key virulence factor that promotes bacterial evasion of human phagocytic killing. WhileS. pneumoniaeproduces at least 94 antigenically different types of capsule, the genes for biosynthesis of almost all capsular types are arranged in the same locus. The transcription of the capsular polysaccharide (cps) locus is not well understood. This study determined the transcriptional features of thecpslocus in the type 2 virulent strain D39. The initial analysis revealed that thecpsgenes are cotranscribed from a major transcription start site at the −25 nucleotide (G) upstream ofcps2A, the first gene in the locus. Using unmarked chromosomal truncations and a luciferase-based transcriptional reporter, we showed that the full transcription of thecpsgenes not only depends on the core promoter immediately upstream ofcps2A, but also requires additional elements upstream of the core promoter, particularly a 59-bp sequence immediately upstream of the core promoter. Unmarked deletions of these promoter elements in the D39 genome also led to significant reduction in CPS production and virulence in mice. Lastly, commoncpsgene (cps2ABCD) mutants did not show significant abnormality incpstranscription, although they produced significantly less CPS, indicating that the CpsABCD proteins are involved in the encapsulation ofS. pneumoniaein a posttranscriptional manner. This study has yielded important information on the transcriptional characteristics of thecpslocus inS. pneumoniae.

scholarly journals The Core Promoter of the Capsule Operon of Streptococcus pneumoniae Is Necessary for Colonization and Invasive Disease

2013 ◽  
Vol 82 (2) ◽  
pp. 694-705 ◽  
Author(s):  
Mara G. Shainheit ◽  
Matthew Mulé ◽  
Andrew Camilli
Keyword(s):  
Transcriptional Regulation ◽  
Streptococcus Pneumoniae ◽  
Capsular Polysaccharide ◽  
Core Promoter ◽  
Invasive Disease ◽  
Fine Tuning ◽  
Anatomical Site ◽  
Content Type ◽  
The Core

ABSTRACTStreptococcus pneumoniaeis a commensal of the human nasopharynx but can cause invasive diseases, including otitis media, pneumonia, sepsis, and meningitis. The capsular polysaccharide (capsule) is a critical virulence factor required for both asymptomatic colonization and invasive disease, yet the expression level is different in each anatomical site. During colonization, reduced levels of capsule promote binding to the host epithelium and biofilm formation, while during systemic infection, increased capsule is required to evade opsonophagocytosis. How this regulation of capsule expression occurs is incompletely understood. To investigate the contribution of transcriptional regulation on capsule level in the serotype 4 strain TIGR4, we constructed two mutants harboring a constitutive promoter that was either comparably weaker (Pcat) or stronger (PtRNAGlu) than the wild-type (WT) capsule promoter, Pcps. Mild reductions incpsAandcpsEtranscript levels in the Pcatpromoter mutant resulted in a 2-fold reduction in total amounts of capsule and in avirulence in murine models of lung and blood infection. Additionally, the PtRNAGlumutant revealed that, despite expressing enhanced levels ofcpsAandcpsEand possessing levels of capsule comparable to those of WT TIGR4, it was still significantly attenuated in all testedin vivoniches. Further analysis using chimeric promoter mutants revealed that the WT −10 and −35 boxes are required for optimal nasopharyngeal colonization and virulence. These data support the hypothesis that dynamic transcriptional regulation of the capsule operon is required and that the core promoter region plays a central role in fine-tuning levels of capsule to promote colonization and invasive disease.

scholarly journals Evaluation of the Specificity of Pneumococcal Polysaccharide Enzyme-Linked Immunosorbent Assay and the Effect of Serum Adsorption Based on Standard Pneumococcal Serogroup- or Serotype-Specific Rabbit Antisera

2009 ◽  
Vol 16 (9) ◽  
pp. 1279-1284 ◽  
Author(s):  
Hans-Christian Slotved ◽  
Christina Guttmann ◽  
Charlotte Demuth Pedersen ◽  
Jasper Neergaard Jacobsen ◽  
Karen Angeliki Krogfelt
Keyword(s):  
Cell Wall ◽  
Streptococcus Pneumoniae ◽  
Human Serum ◽  
Immunosorbent Assay ◽  
Capsular Polysaccharide ◽  
Enzyme Linked Immunosorbent Assay ◽  
Capsular Polysaccharides ◽  
Who Guidelines ◽  
Specific Antibodies ◽  
Specific Rabbit

ABSTRACT Worldwide, Streptococcus pneumoniae (pneumococcus) is a major cause of morbidity and mortality, especially in infants and elderly people. Pneumococcal capsular polysaccharides are well characterized, and more than 90 different serotypes have been identified. Serotype-specific antibodies against the capsular polysaccharide are produced during infection. Detection of antibodies against pneumococci by enzyme-linked immunosorbent assay (ELISA) is performed according to WHO guidelines, using antigens provided by ATCC. However, testing the ELISA for specificity is challenging due to the difficulty in obtaining human naïve serum with pneumococcal antibodies as well as human serum with antibodies against a single serotype. The application of well-defined serotype-specific sera produced in animals to evaluate the specificity of the ATCC antigens and the effect of adsorption with cell wall and 22F polysaccharides has not been performed before, to our knowledge. In this study, the specificity of ATCC antigens (serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F) was tested by using commercial serotype-, serogroup-, and pool-specific pneumococcal rabbit antisera.

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