Dynamic capsule restructuring by the main pneumococcal autolysin LytA in response to the epithelium

Kietzman, Colin C.; Gao, Geli; Mann, Beth; Myers, Lance; Tuomanen, Elaine

doi:10.1038/ncomms10859

Cited by 79 publications

(94 citation statements)

References 57 publications

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“…Cps A appears to act as a transcriptional activator of polysaccharide production but is not necessary for encapsulation 24. Unencapsulated pneumococcal strains evolve through either downregulation of the capsule or loss of the capsular biosynthesis locus 30. Non-typeable isolates of S. pneumoniae have been reported increasingly following vaccination and one earlier study found them to represent 28% of pneumococcal isolates, although the sample size of pneumococcal isolates was small (59 isolates) similar to that of our work 31.…”

Section: Discussionsupporting

confidence: 66%

Phenotypic and molecular study of pneumococci causing respiratory tract infections

Alnimr

Farhat

2017

SMJ

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Objectives:To study serotype distribution and antimicrobial resistance to beta-lactams and macrolides in pneumococci causing respiratory diseases after the introduction of the 13-valent pneumococcal conjugate vaccine in Saudi Arabia.Methods:This is a hospital-based and a cross-sectional prospective surveillance study conducted at King Fahad Hospital of the University, AlKhobar, Kingdom of Saudi Arabia, in which respiratory pneumococcal isolates collected between 2012 and 2014 were serotyped by multiplex sequential polymerase chain reaction (PCR) and Pneumotest-Latex. Resistance genes to beta-lactams and macrolides were detected by multiplex PCR.Results:The most common serotypes encountered were 11A, 19A, 17F, 23F, 3, and 19F, representing 64% of the typeable strains. Interestingly, 24% of the 94 isolates were not typeable and 18% were negative for the housekeeping gene cpsA. Among the 53 typeable pneumococci isolates, 36 (67.9%) carried genes encoding resistance to both penicillin and macrolides, 9 (17%) were penicillin-monoresistant, 3 (5.6%) were macrolide-monoresistant, and 5 (9.4%) were designated non-resistant. The high rate of resistance genes did not significantly differ according to serotype (p=0.76). Similarly, non-typeable pneumococci (cpsA+ and cpsA-) had high rates of resistance to both penicillin (62.5%) and macrolides (47%).Conclusion:These data highlight the emergence of a previously rare capsular type, 11A (mean patient age, 29 years; p=0.001). Moreover, the high percentage of non-typeable isolates shows the emergence of possible atypical pneumococcal serotypes not covered by available vaccines.

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Section: Discussionsupporting

confidence: 66%

Phenotypic and molecular study of pneumococci causing respiratory tract infections

Alnimr

Farhat

2017

SMJ

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“…The central region of IgG-binding sites in M proteins appear to be contradictory to its role as an immune evasion mechanism, since a direct contact with the host's immunoglobulins is abrogated. However, capsule expression is a very dynamic process and can vary depending on environmental and stress conditions, such as nutrient availability or antibiotic treatments (Hammerschmidt et al, 2005; Willenborg et al, 2011; Haas and Grenier, 2016; Kietzman et al, 2016). Under nutrient-rich conditions, capsule expression is highly upregulated which is consistent with numerous studies characterizing the bacterial capsule as the main virulence factor of streptococci in the blood (Wu et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

SCM, the M Protein of Streptococcus canis Binds Immunoglobulin G

Bergmann

Eichhorn

Kohler

et al. 2017

Front. Cell. Infect. Microbiol.

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The M protein of Streptococcus canis (SCM) is a virulence factor and serves as a surface-associated receptor with a particular affinity for mini-plasminogen, a cleavage product of the broad-spectrum serine protease plasmin. Here, we report that SCM has an additional high-affinity immunoglobulin G (IgG) binding activity. The ability of a particular S. canis isolate to bind to IgG significantly correlates with a scm-positive phenotype, suggesting a dominant role of SCM as an IgG receptor. Subsequent heterologous expression of SCM in non-IgG binding S. gordonii and Western Blot analysis with purified recombinant SCM proteins confirmed its IgG receptor function. As expected for a zoonotic agent, the SCM-IgG interaction is species-unspecific, with a particular affinity of SCM for IgGs derived from human, cats, dogs, horses, mice, and rabbits, but not from cows and goats. Similar to other streptococcal IgG-binding proteins, the interaction between SCM and IgG occurs via the conserved Fc domain and is, therefore, non-opsonic. Interestingly, the interaction between SCM and IgG-Fc on the bacterial surface specifically prevents opsonization by C1q, which might constitute another anti-phagocytic mechanism of SCM. Extensive binding analyses with a variety of different truncated SCM fragments defined a region of 52 amino acids located in the central part of the mature SCM protein which is important for IgG binding. This binding region is highly conserved among SCM proteins derived from different S. canis isolates but differs significantly from IgG-Fc receptors of S. pyogenes and S. dysgalactiae sub. equisimilis, respectively. In summary, we present an additional role of SCM in the pathogen-host interaction of S. canis. The detailed analysis of the SCM-IgG interaction should contribute to a better understanding of the complex roles of M proteins in streptococcal pathogenesis.

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“…However, pneumococci markedly reduce capsule thickness when in close contact with epithelial cells and during the invasion process 123 . This process of capsule shedding has recently been shown to depend on the major pneumococcal autolysin LytA and is triggered by exposure to cationic antimicrobial peptides that are released by the host cells 124 .…”

Section: Invasive Pneumococcal Diseasementioning

confidence: 99%

Streptococcus pneumoniae: transmission, colonization and invasion

2018

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Streptococcus pneumoniae as a complex relationship with its obligate human host. On the one hand, the pneumococci are highly adapted commensals, and their main reservoir on the mucosal surface of the upper airways of carriers enables transmission. On the other hand, they can cause severe disease when bacterial and host factors allow them to invade essentially sterile sites, such as the middle ear spaces, lungs, bloodstream and meninges. Transmission, colonization and invasion depend on the remarkable ability of S. pneumoniae to evade or take advantage of the host inflammatory and immune responses. The different stages of pneumococcal carriage and disease have been investigated in detail in animal models and, more recently, in experimental human infection. Furthermore, widespread vaccination and the resulting immune pressure have shed light on pneumococcal population dynamics and pathogenesis. Here, we review the mechanistic insights provided by these studies on the multiple and varied interactions of the pneumococcus and its host.

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Dynamic capsule restructuring by the main pneumococcal autolysin LytA in response to the epithelium

Cited by 79 publications

References 57 publications

Phenotypic and molecular study of pneumococci causing respiratory tract infections

Phenotypic and molecular study of pneumococci causing respiratory tract infections

SCM, the M Protein of Streptococcus canis Binds Immunoglobulin G

Streptococcus pneumoniae: transmission, colonization and invasion

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