pathogenicity island
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Pathogens ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 72
Author(s):  
Mamadou Thiam ◽  
Astrid Lissette Barreto Sánchez ◽  
Jin Zhang ◽  
Jie Wen ◽  
Guiping Zhao ◽  
...  

Salmonella causes significant economic loss to the poultry industry and represents a real threat to human health. The region of difference 21 (ROD21) pathogenicity island removal is a genetic mechanism by which Salmonellaenteritidis (SE) invades the intestinal epithelium and induces systemic infection in mice. The heterophil/lymphocyte (H/L) ratio reflects the chicken’s robustness and immune system status. The H/L ratio is considered a disease resistance trait, and it could be used as a marker for selecting Salmonella resistance in live chickens. However, the association of the H/L ratio with Salmonella resistance and the inflammatory response remains to be elucidated. Moreover, the kinetics of ROD21 excision in the intestine and immune organs of chickens is unknown. Therefore, this study aimed to investigate the bacterial load, the ROD21 excision, the IL-1β, IL-8, and INF-γ blood serum concentration kinetics, and the association with the H/L ratio in chicken at 1, 3, 7, and 21 days post-SE infection. The results showed a significant correlation between the H/L ratio and the bacterial load in the ileum and caecum at 7 dpi. The ROD21 pathogenicity island absolute and relative excision in the caecum were positively correlated at 1 dpi but negatively correlated at 7 dpi with the H/L ratio. However, in the liver, we found the opposite tendency. The association of the H/L ratio with IL-1β, IL-8, and INF-γ blood serum concentrations showed that a low H/L ratio is correlated with increased IL-1β and INF-γ at 21 dpi. This study confirmed that the H/L ratio is associated with robustness and Salmonella-resistance in chicken. The methodology used in this study can separate individuals into susceptible and resistant and can help in the selection and breeding of Salmonella-resistant chickens.


mBio ◽  
2022 ◽  
Author(s):  
George L. Katumba ◽  
Hung Tran ◽  
Jeffrey P. Henderson

Interactions between bacteria and transition metal ions play an important role in encounters between humans and bacteria. Siderophore systems have long been prominent mediators of these interactions.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Katelyn Knuff-Janzen ◽  
Antonio Serapio-Palacios ◽  
James McCoy ◽  
Zakhar Krekhno ◽  
Kyung-Mee Moon ◽  
...  

AbstractIntracellular pathogens need to establish an intracellular replicative niche to promote survival and replication within the hostile environment inside the host cell. Salmonella enterica serovar Typhimurium (S. Typhimurium) initiates formation of the unique Salmonella-containing vacuole and an extensive network of Salmonella-induced tubules in order to survive and thrive within host cells. At least six effectors secreted by the type III secretion system encoded within Salmonella pathogenicity island-2 (SPI-2), namely SifA, SopD2, PipB2, SteA, SseJ, and SseF, purportedly manipulate host cell intracellular trafficking and establish the intracellular replicative niche for S. Typhimurium. The phenotypes of these effectors are both subtle and complex, complicating elucidation of the mechanism underpinning host cell manipulation by S. Typhimurium. In this work we used stable isotope labeling of amino acids in cell culture (SILAC) and a S. Typhimurium mutant that secretes increased amounts of effectors to identify cognate effector binding partners during infection. Using this method, we identified the host protein annexin A2 (AnxA2) as a binding partner for both SopD2 and PipB2 and were able to confirm its binding to SopD2 and PipB2 by reciprocal pull down, although there was a low level of non-specific binding of SopD2-2HA and PipB2-2HA to the Ni-Sepharose beads present. We further showed that knockdown of AnxA2 altered the intracellular positioning of the Salmonella containing vacuole (SCV). This suggests that AnxA2 plays a role in the subcellular positioning of the SCV which could potentially be mediated through protein–protein interactions with either SopD2 or PipB2. This demonstrates the value of studying effector interactions using proteomic techniques and natural effector delivery during infection rather than transfection.


2021 ◽  
Vol 12 ◽  
Author(s):  
Marta A. Lages ◽  
Manuel L. Lemos ◽  
Miguel Balado

The high-pathogenicity island irp-HPI is widespread among Vibrionaceae encoding the piscibactin siderophore system. The expression of piscibactin genes in the fish pathogen Vibrio anguillarum is favored by low temperatures. However, information about the regulatory mechanism behind irp-HPI gene expression is scarce. In this work, in-frame deletion mutants of V. anguillarum defective in the putative regulators AraC1 and AraC2, encoded by irp-HPI, and in the global regulators H-NS and ToxRS, were constructed and their effect on irp-HPI gene expression was analyzed at 15 and 25°C. The results proved that only AraC1 (renamed as PbtA) is required for the expression of piscibactin biosynthesis and transport genes. PbtA inactivation led to an inability to grow under iron restriction, a loss of the outer membrane piscibactin transporter FrpA, and a significant decrease in virulence for fish. Inactivation of the global repressor H-NS, which is involved in silencing of horizontally acquired genes, also resulted in a lower transcriptional activity of the frpA promoter. Deletion of toxR-S, however, did not have a relevant effect on the expression of the irp-HPI genes. Therefore, while irp-HPI would not be part of the ToxR regulon, H-NS must exert an indirect effect on piscibactin gene expression. Thus, the temperature-dependent expression of the piscibactin-encoding pathogenicity island described in V. anguillarum is the result of the combined effect of the AraC-like transcriptional activator PbtA, harbored in the island, and other not yet defined regulator(s) encoded by the genome. Furthermore, different expression patterns were detected within different irp-HPI evolutionary lineages, which supports a long-term evolution of the irp-HPI genomic island within Vibrionaceae. The mechanism that modulates piscibactin gene expression could also be involved in global regulation of virulence factors in response to temperature changes.


2021 ◽  
Vol 70 (4) ◽  
pp. 65-72
Author(s):  
Evgenia V. Kuleshevich ◽  
Yury Y. Ilyasov ◽  
Dmitry S. Linnik ◽  
Anastasia A. Malchenkova ◽  
Olga N. Arzhanova ◽  
...  

Group B streptococci, or Streptococcus agalactiae, are the major cause of severe diseases in newborns and adults. The PAI-A and PAI-A1 pathogenicity islands containing the sspB1 and sspB1a genes, respectively, were found among group B streptococci mobile genetic elements. The presence of sspB genes correlates with urogenital tract infections. The aim of this study was to determine the frequency of group B streptococci strains with the PAI-A and PAI-A1 pathogenicity islands, circulating in Moscow, in comparison with strains from St. Petersburg. The sspB1 gene, and hence the PAI-A pathogenicity island, was not found in the genomes of strains from Moscow. The frequency of the sspB1a gene and the PAI-A1 pathogenicity island in the genomes of clinical strains was three times higher than in the genomes of colonizing strains. Thus, it can be assumed that the genes of the sspB family are more specific of group B streptococci colonizing pregnant women and newborns.


Author(s):  
Andreas F. Haag ◽  
Magdalena Podkowik ◽  
Rodrigo Ibarra-Chávez ◽  
Francisca Gallego del Sol ◽  
Geeta Ram ◽  
...  

2021 ◽  
Author(s):  
Laura Miguel-Romero ◽  
Mohammed Alqasmi ◽  
Julio Bacarizo ◽  
Jason A. Tan ◽  
Richard J. Cogdell ◽  
...  

ABSTRACTMobile genetic elements (MGEs) control their life cycles by the expression of a master repressor, whose function must be disabled to allow the spread of these elements in nature. Here we describe an unprecedented repression-derepression mechanism involved in the transfer of the Staphylococcus aureus pathogenicity islands (SaPIs). Contrary to the classical phage and SaPI repressors, which are dimers, the SaPI1 repressor StlSaPI1 presents a unique tetrameric conformation, never seen before. Importantly, not just one but two tetramers are required for SaPI1 repression, which increases the novelty of the system. To derepress SaPI1, the phage-encoded protein Sri binds to and induces a conformational change in the DNA binding domains of StlSaPI1, preventing the binding of the repressor to its cognate StlSaPI1 sites. Finally, our findings demonstrate that this system is not exclusive to SaPI1 but widespread in nature. Overall, our results characterise a novel repression-induction system involved in the transfer of MGE-encoded virulence factors in nature.SignificanceWhile most repressors controlling the transfer of mobile genetic elements are dimers, we demonstrate here that the Staphylococcal pathogenicity island 1 (SaPI1) is repressed by two tetramers, which have a novel structural fold in their body that has never been seen before in other proteins. Moreover, by solving the structure of the SaPI1 repressor in complex with its inducing protein Sri, we have demonstrated that Sri forces the SaPI1 repressor to adopt a conformation that is incompatible with DNA binding, explaining how SaPI1 is induced. Finally, our results demonstrate that this repression system is not exclusive of the SaPIs but widespread in nature. Our studies provide important insights understanding how SaPIs spread in nature.


2021 ◽  
Vol 12 ◽  
Author(s):  
Beth A. Bachert ◽  
Joshua B. Richardson ◽  
Kevin D. Mlynek ◽  
Christopher P. Klimko ◽  
Ronald G. Toothman ◽  
...  

Francisella tularensis is one of several biothreat agents for which a licensed vaccine is needed to protect against this pathogen. To aid in the development of a vaccine protective against pneumonic tularemia, we generated and characterized a panel of F. tularensis isolates that can be used as challenge strains to assess vaccine efficacy. Our panel consists of both historical and contemporary isolates derived from clinical and environmental sources, including human, tick, and rabbit isolates. Whole genome sequencing was performed to assess the genetic diversity in comparison to the reference genome F. tularensis Schu S4. Average nucleotide identity analysis showed >99% genomic similarity across the strains in our panel, and pan-genome analysis revealed a core genome of 1,707 genes, and an accessory genome of 233 genes. Three of the strains in our panel, FRAN254 (tick-derived), FRAN255 (a type B strain), and FRAN256 (a human isolate) exhibited variation from the other strains. Moreover, we identified several unique mutations within the Francisella Pathogenicity Island across multiple strains in our panel, revealing unexpected diversity in this region. Notably, FRAN031 (Scherm) completely lacked the second pathogenicity island but retained virulence in mice. In contrast, FRAN037 (Coll) was attenuated in a murine pneumonic tularemia model and had mutations in pdpB and iglA which likely led to attenuation. All of the strains, except FRAN037, retained full virulence, indicating their effectiveness as challenge strains for future vaccine testing. Overall, we provide a well-characterized panel of virulent F. tularensis strains that can be utilized in ongoing efforts to develop an effective vaccine against pneumonic tularemia to ensure protection is achieved across a range F. tularensis strains.


2021 ◽  
Vol 12 ◽  
Author(s):  
Luca Robinson ◽  
Janie Liaw ◽  
Zahra Omole ◽  
Dong Xia ◽  
Arnoud H. M. van Vliet ◽  
...  

The Type VI Secretion System (T6SS) has important roles relating to bacterial antagonism, subversion of host cells, and niche colonisation. Campylobacter jejuni is one of the leading bacterial causes of human gastroenteritis worldwide and is a commensal coloniser of birds. Although recently discovered, the T6SS biological functions and identities of its effectors are still poorly defined in C. jejuni. Here, we perform a comprehensive bioinformatic analysis of the C. jejuni T6SS by investigating the prevalence and genetic architecture of the T6SS in 513 publicly available genomes using C. jejuni 488 strain as reference. A unique and conserved T6SS cluster associated with the Campylobacter jejuni Integrated Element 3 (CJIE3) was identified in the genomes of 117 strains. Analyses of the T6SS-positive 488 strain against the T6SS-negative C. jejuni RM1221 strain and the T6SS-positive plasmid pCJDM202 carried by C. jejuni WP2-202 strain defined the “T6SS-containing CJIE3” as a pathogenicity island, thus renamed as Campylobacter jejuni Pathogenicity Island-1 (CJPI-1). Analysis of CJPI-1 revealed two canonical VgrG homologues, CJ488_0978 and CJ488_0998, harbouring distinct C-termini in a genetically variable region downstream of the T6SS operon. CJPI-1 was also found to carry a putative DinJ-YafQ Type II toxin-antitoxin (TA) module, conserved across pCJDM202 and the genomic island CJIE3, as well as several open reading frames functionally predicted to encode for nucleases, lipases, and peptidoglycan hydrolases. This comprehensive in silico study provides a framework for experimental characterisation of T6SS-related effectors and TA modules in C. jejuni.


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