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Yersinia
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
Xin Wang, Ran Duan, Junrong Liang, Wenpeng Gu, Huaiqi Jing
The virulence of pathogenic Y. enterocolitica is attributed to a 70-kb pYV (plasmid for Yersinia virulence) plasmid and some chromosome-encoded factors. A similarly sized plasmid, termed pCD, is found in Y. pestis,10 and pYV is also present in Y. pseudotuberculosis.11 Despite this common feature, the diseases caused by the two enteropathogenic yersiniae are chronic in nature and obviously different from plague. The virulent plasmid pYV encodes Yersinia adhesin A (YadA) and the Yersinia outer protein (Yop) virulon, a system consisting of secreted proteins called Yops and their dedicated type III secretion system (T3SS) apparatus called Ysc.12 The Ysc apparatus forms a channel composed of several proteins.13 Yop proteins fall into two categories. Some are intracellular effectors, while the others are “translocators” needed to deliver the effectors across the eukaryotic plasma membrane into eukaryotic cells. The translocators (YopB, YopD, LcrV) form a pore in the eukaryotic cell’s plasma membrane. The effector Yops are YopE, YopH, YpkA/YopO, YopP/YopJ, YopM, and YopT.12 The chromosome-encoded virulence factors include ail (attachment and invasion locus), inv (invasin), and yst (Yersinia stable toxin). The high pathogenicity island (HPI) bearing an iron acquisition system only exists in the highly pathogenic biotype 1B strains.14 Many studies have reported the role of biotype 1A strains in foodborne outbreaks, in which the pYV plasmid is absent.15
β-arrestin 2 quenches TLR signaling to facilitate the immune evasion of EPEC
Published in Gut Microbes, 2020
Zijuan Chen, Ruixue Zhou, Yihua Zhang, Doudou Hao, Yu Wang, Shichao Huang, Ningning Liu, Chunmei Xia, Nissan Yissachar, Feng Huang, Yiwei Chu, Dapeng Yan
Toll-like receptor 4 (TLR4) plays a pivotal role in early host defense against gram-negative bacteria. Upon ligand stimulation, TLR4 dimerizes and undergoes conformational change required for association of the adaptor protein myeloid differentiation primary response protein 88 (MyD88), which in turn recruits IL-1 R-associated kinase 4 (IRAK4) and IL-1 R-associated kinase 1 (IRAK1). Tumor necrosis factor receptor-associated factor 6 (TRAF6) is then recruited to the signal complex via interaction with phosphorylated IRAK1, which subsequently associates with the ubiquitin ligases ubiquitin-conjugating enzyme 13 and ubiquitin-conjugating enzyme E2 variant.12,13 This triggers K63-linked polyubiquitination of TRAF6 and the recruitment of transforming growth factor β-activated kinase (TAK1)/TAK1-binding protein 1/2 (TAB1/2) complex and induces TAK1 auto-phosphorylation.14 Activated TAK1 promotes the phosphorylation of mitogen-activated protein (MAP) kinases and inhibitor of nuclear factor-κB (IκB)-kinase (IKK), which ultimately leads to the expression of genes encoding cytokines and chemokines.15 Many studies have reported that pathogens had evolved a range of immune evasion strategies to establish a successful infection. Bacterial proteins can modulate key regulators in the TLR signaling pathway to affect the production of cytokines to promote the immune evasion.16,17 For example, Yersinia-secreted LcrV promotes IL-10 secretion in a CD14- and TLR2-dependant manner to suppress immune responses.18
Immunogenicity and protection efficacy of enhanced fitness recombinant Salmonella Typhi monovalent and bivalent vaccine strains against acute toxoplasmosis
Published in Pathogens and Global Health, 2021
Fei-Kean Loh, Sheila Nathan, Sek-Chuen Chow, Chee-Mun Fang
Heterologous antigens could be plasmid encoded or chromosomally integrated for expression in live S. Typhi vaccine. Plasmids can express high levels of antigens, but they tend to impose unacceptable metabolic burden that probably causes eventual plasmid loss. As an alternative, antigens expressed via chromosomal-based gene integration are more stable since the deletion of chromosomal genes is less likely [James E. 8]. However, a single chromosomal gene copy generally reduces the antigen mass, thus expressing insufficient level of antigen to induce an immune response [10]. This is a concern when developing T. gondii vaccines that require multiple antigens to confer cross-protection against the parasite’s changeable life stages. Remarkably, the coupling of plasmid- and chromosome-based antigen expression within single live Salmonella vaccines revealed the potential of gaining stable and adequate antigen expression with high immunity activation properties. Galen et al. constructed an S. Typhi bivalent plague vaccine combining plasmid expression of the F1 antigen and chromosomal expression of LcrV antigen of Yersinia pestis that conferred full protection against lethal pulmonary challenge in BALB/c mice [11]. Following that, Sanapala et al. constructed a trivalent Salmonella Typhimurium delivering LcrV196 and Psn of Yersinia pestis encoded on plasmid and F1 encoded within the chromosome that induced high antibody titers and significant protection against bubonic and pneumonic plague in BALB/c mice [12]. In recent years, Salmonella Choleraesuis has also been adapted as live vector to deliver SaoA antigen and enolase antigen that can confer full protection against Streptococcus suis [13., 2020; 14]. The high immunogenicity of live Salmonella vector achieved has encouraged its application toward vaccine development against a variety of human pathogens including T. gondii.