Molecular pathogenesis of the hyaluronic acid capsule of Pasteurella multocida

2020 ◽  
Vol 149 ◽  
pp. 104380
Author(s):  
Lijun Guan ◽  
Lin Zhang ◽  
Yun Xue ◽  
Jinqian Yang ◽  
Zhanqin Zhao
2016 ◽  
Vol 84 (5) ◽  
pp. 1361-1370 ◽  
Author(s):  
Marianne Mégroz ◽  
Oded Kleifeld ◽  
Amy Wright ◽  
David Powell ◽  
Paul Harrison ◽  
...  

The Gram-negative bacteriumPasteurella multocidais the causative agent of a number of economically important animal diseases, including avian fowl cholera. NumerousP. multocidavirulence factors have been identified, including capsule, lipopolysaccharide (LPS), and filamentous hemagglutinin, but little is known about how the expression of these virulence factors is regulated. Hfq is an RNA-binding protein that facilitates riboregulation via interaction with small noncoding RNA (sRNA) molecules and their mRNA targets. Here, we show that aP. multocidahfqmutant produces significantly less hyaluronic acid capsule during all growth phases and displays reducedin vivofitness. Transcriptional and proteomic analyses of thehfqmutant during mid-exponential-phase growth revealed altered transcript levels for 128 genes and altered protein levels for 78 proteins. Further proteomic analyses of thehfqmutant during the early exponential growth phase identified 106 proteins that were produced at altered levels. Both the transcript and protein levels for genes/proteins involved in capsule biosynthesis were reduced in thehfqmutant, as were the levels of the filamentous hemagglutinin protein PfhB2 and its secretion partner LspB2. In contrast, there were increased expression levels of three LPS biosynthesis genes, encoding proteins involved in phosphocholine and phosphoethanolamine addition to LPS, suggesting that these genes are negatively regulated by Hfq-dependent mechanisms. Taken together, these data provide the first evidence that Hfq plays a crucial role in regulating the global expression ofP. multocidagenes, including the regulation of keyP. multocidavirulence factors, capsule, LPS, and filamentous hemagglutinin.


1957 ◽  
Vol 106 (3) ◽  
pp. 365-384 ◽  
Author(s):  
Richard M. Krause

The host ranges of bacteriophages for group A, types 1, 6, 12, and 25 and group C streptococci have been determined. The findings indicate that the susceptibility to these phages is primarily a group-specific phenomenon, although it is modified by several factors such as the hyaluronic acid capsule, lysogeny, and possibly the presence of surface proteins. Phage antibody studies indicate that while the group A phages are antigenically related, they are distinct from the group C phage. This is in agreement with the observation that group A phages are not specific for their homologous streptococcal types. The purified group C carbohydrate inactivates group C phage but not the group A phages, thus suggesting that the carbohydrate, a component of the cell wall, may serve as the phage receptor site. It has not been possible to inactivate the group A phages with group A carbohydrate. Phage lysis of groups A and C streptococci is accompanied by fragmentation of the cell wall since the C carbohydrate has been identified serologically and chemically in the supernate of centrifuged lysates. The immediate lysis of groups A and C hemolytic streptococci and their isolated cell walls by an accesory heat-labile lytic factor in fresh group C lysates is also described.


1991 ◽  
Vol 88 (19) ◽  
pp. 8317-8321 ◽  
Author(s):  
M. R. Wessels ◽  
A. E. Moses ◽  
J. B. Goldberg ◽  
T. J. DiCesare

mBio ◽  
2016 ◽  
Vol 7 (3) ◽  
Author(s):  
Vincent A. Fischetti ◽  
James B. Dale

ABSTRACT The ability to hide in the animal kingdom is essential for survival; the same is true for bacteria . Streptococcus pyogenes is considered one of the more successful stealth bacteria in its production of a hyaluronic acid capsule that is chemically identical to the hyaluronic acid lining human joints. It has also acquired the capacity to enter eukaryotic cells to avoid the onslaught of the host’s immune defenses, as well as drugs. From this intracellular vantage point, it may remain dormant from days to weeks, only to cause disease again at a later time, perhaps causing a relapse in a drug-treated patient. We now learn that it is able to enter macrophages as well, enabling the Streptococcus to use this “Trojan horse” approach to be transported to distant sites in the body.


1959 ◽  
Vol 110 (4) ◽  
pp. 617-628 ◽  
Author(s):  
Marie Judith Foley ◽  
W. Barry Wood

A quantitative study of the combined antiphagocytic effects of the M protein and the hyaluronic acid capsules of four strains of Group A streptococci revealed the following facts relating to their intraperitoneal virulence in mice and rats: 1. The most virulent strain, S23M (matt), produced both a large hyaluronic acid capsule and a full complement of M protein, the combined effects of which rendered the organism highly resistant to surface phagocytosis. 2. The slightly less virulent strain, T14/46 (matt virulent) was somewhat more susceptible to surface phagocytosis owing to the fact that its smaller capsule was less antiphagocytic than that of the S23M organism. 3. The glossy variant of the S23 strain (S23G), which ranked third in virulence, was still more susceptible to surface phagocytosis because of its lack of detectable M substance. Its large hyaluronic acid capsule, however, was capable of protecting it against phagocytosis on glass. 4. The least virulent strain, T14 (matt avirulent), was the most susceptible of all to phagocytosis. Though it possessed both M substance and capsule, which together prevented its phagocytosis on glass, each of them was shown to be quantitatively and functionally deficient as compared to Strain S23M. The differences in phagocytability, which appear to be directly related to the pathogenicity of the organisms, could be adequately demonstrated in vitro only by phagocytic tests designed to measure surface phagocytosis in the absence of opsonins. This fact is in keeping with the observation, previously reported, that surface phagocytosis plays a critical role in the defense of the host, particularly during the earliest stages of experimental streptococcal infections. Its possible relation to suppuration during the later stages of infection is also discussed.


mBio ◽  
2015 ◽  
Vol 6 (4) ◽  
Author(s):  
Claire E. Turner ◽  
James Abbott ◽  
Theresa Lamagni ◽  
Matthew T. G. Holden ◽  
Sophia David ◽  
...  

ABSTRACTGroup AStreptococcus(GAS) genotypeemm89 is increasingly recognized as a leading cause of disease worldwide, yet factors that underlie the success of thisemmtype are unknown. Surveillance identified a sustained nationwide increase inemm89 invasive GAS disease in the United Kingdom, prompting longitudinal investigation of this genotype. Whole-genome sequencing revealed a recent dramatic shift in theemm89 population with the emergence of a new clade that increased to dominance over previousemm89 variants. Temporal analysis indicated that the clade arose in the early 1990s but abruptly increased in prevalence in 2008, coinciding with an increased incidence ofemm89 infections. Although standard variable typing regions (emmsubtype,teetype,softype, and multilocus sequence typing [MLST]) remained unchanged, uniquely the emergent clade had undergone six distinct regions of homologous recombination across the genome compared to the rest of the sequencedemm89 population. Two of these regions affected known virulence factors, the hyaluronic acid capsule and the toxins NADase and streptolysin O. Unexpectedly, and in contrast to the rest of the sequencedemm89 population, the emergent clade-associated strains were genetically acapsular, rendering them unable to produce the hyaluronic acid capsule. The emergent clade-associated strains had also acquired an NADase/streptolysin O locus nearly identical to that found inemm12 and modernemm1 strains but different from the rest of the sequencedemm89 population. The emergent clade-associated strains had enhanced expression of NADase and streptolysin O. The genome remodeling in the new clade variant and the resultant altered phenotype appear to have conferred a selective advantage over otheremm89 variants and may explain the changes observed inemm89 GAS epidemiology.IMPORTANCESudden upsurges or epidemic waves are common features of group A streptococcal disease. Although the mechanisms behind such changes are largely unknown, they are often associated with an expansion of a single genotype within the population. Using whole-genome sequencing, we investigated a nationwide increase in invasive disease caused by the genotypeemm89 in the United Kingdom. We identified a new clade variant that had recently emerged in theemm89 population after having undergone several core genomic recombination-related changes, two of which affected known virulence factors. An unusual finding of the new variant was the loss of the hyaluronic acid capsule, previously thought to be essential for causing invasive disease. A further genomic adaptation in the NADase/streptolysin O locus resulted in enhanced production of these toxins. Recombination-related genome remodeling is clearly an important mechanism in group AStreptococcusthat can give rise to more successful and potentially more pathogenic variants.


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