Assessment of the efficacy of an autogenous vaccine against Yersinia pseudotuberculosis in young Merino sheep

2018 ◽  
Vol 67 (1) ◽  
pp. 27-35
Author(s):  
KJ Stanger ◽  
H McGregor ◽  
M Marenda ◽  
JM Morton ◽  
JWA Larsen
2008 ◽  
Vol 63 (2) ◽  
pp. 88-92
Author(s):  
Michał Szczyrek ◽  
Anna Mełges ◽  
Alina Olender ◽  
Konrad Jarząbek ◽  
Jacek Postępski

2009 ◽  
Vol 54 (3) ◽  
pp. 239-245 ◽  
Author(s):  
J. M. L. Maia ◽  
L. G. S. Monnazzi ◽  
B. M. M. Medeiros

Virulence ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 638-653
Author(s):  
Anne Marie Krachler ◽  
Natalie Sirisaengtaksin ◽  
Pauline Monteith ◽  
C. E. Timothy Paine ◽  
Christopher J. Coates ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hayley I. Muendlein ◽  
Wilson M. Connolly ◽  
Zoie Magri ◽  
Irina Smirnova ◽  
Vladimir Ilyukha ◽  
...  

AbstractInflammation and cell death are closely linked arms of the host immune response to infection, which when carefully balanced ensure host survival. One example of this balance is the tightly regulated transition from TNFR1-associated pro-inflammatory complex I to pro-death complex II. By contrast, here we show that a TRIF-dependent complex containing FADD, RIPK1 and caspase-8 (that we have termed the TRIFosome) mediates cell death in response to Yersinia pseudotuberculosis and LPS. Furthermore, we show that constitutive binding between ZBP1 and RIPK1 is essential for the initiation of TRIFosome interactions, caspase-8-mediated cell death and inflammasome activation, thus positioning ZBP1 as an effector of cell death in the context of bacterial blockade of pro-inflammatory signaling. Additionally, our findings offer an alternative to the TNFR1-dependent model of complex II assembly, by demonstrating pro-death complex formation reliant on TRIF signaling.


Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 296
Author(s):  
Mabruka Salem ◽  
Maria I. Pajunen ◽  
Jin Woo Jun ◽  
Mikael Skurnik

The Yersinia bacteriophages fPS-2, fPS-65, and fPS-90, isolated from pig stools, have long contractile tails and elongated heads, and they belong to genus Tequatroviruses in the order Caudovirales. The phages exhibited relatively wide host ranges among Yersinia pseudotuberculosis and related species. One-step growth curve experiments revealed that the phages have latent periods of 50–80 min with burst sizes of 44–65 virions per infected cell. The phage genomes consist of circularly permuted dsDNA of 169,060, 167,058, and 167,132 bp in size, respectively, with a G + C content 35.3%. The number of predicted genes range from 267 to 271. The phage genomes are 84–92% identical to each other and ca 85% identical to phage T4. The phage receptors were identified by whole genome sequencing of spontaneous phage-resistant mutants. The phage-resistant strains had mutations in the ompF, galU, hldD, or hldE genes. OmpF is a porin, and the other genes encode lipopolysaccharide (LPS) biosynthetic enzymes. The ompF, galU, and hldE mutants were successfully complemented in trans with respective wild-type genes. The host recognition was assigned to long tail fiber tip protein Gp38, analogous to that of T-even phages such as Salmonella phage S16, specifically to the distal β-helices connecting loops.


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