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Order Tymovirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
Brennan et al. (1999) used the PVX vector in parallel with another great plant virus vector, namely that of cowpea mosaic virus (CPMV), described in Chapter 27. The D2 peptide derived from a S. aureus fibronectin-binding protein (FnBP), aa 1−38, was added N-terminally to the PVX coat, and chimeric virions induced high titers of FnBP-specific antibody in mice.
Bacteria-Derived Alternatives to Live Mycobacterium bovis Bacillus Calmette–Guerin for Nonmuscle Invasive Bladder Cancer Treatment
Published in Ananda M. Chakrabarty, Arsénio M. Fialho, Microbial Infections and Cancer Therapy, 2019
Esther Julián, Estela Noguera-Ortega
Mycolyl transferases are a complex of three antigenic proteins (Ag85 A, B, and C) present in both the cytosol and the CW of all mycobacteria species. This Ag85 complex has been identified as a major secreted protein of actively replicating M. tuberculosis. Their function is the transport of trehalose monomycolate to trehalose dimycolate (TDM) and arabinogalactan mycolate (AGM). The antigen 85B (also known as alpha antigen, MPT59, or antigen 6) triggers a strong Th1 immune response when used to stimulate immune cells. Its immunological properties led to the use of this antigen as the basis for subunit vaccines to prevent tuberculosis. Moreover, Ag85 is a fibronectin-binding protein.
Role of Bacteria in Dermatological Infections
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Thirukannamangai Krishnan Swetha, Shunmugiah Karutha Pandian
The surface-associated pilus proteins and M-proteins of GAS strains involved in skin and throat infections are found to be different, which are discriminated in clinical settings using T-antigen and M-protein serotyping (Cogen et al., 2008). The T-antigen genes sheltered in FCT region (i.e., loci of Fibronectin, collagen-binding protein, and T-antigen) encode pilus proteins and adhesins, which establish mechanical stabilization of covalent bonds and supports endurance of shearing forces formed during initial attachment of GAS to integrin found on host extracellular matrix (ECM) (Bessen, 2016). Also, the interaction of host integrin α5β1 with bacterial fibronectin-binding protein is reported to promote invasion by eliciting the cellular signaling pathways, which in turn, leads to conformational changes of host cytoskeletal actin (Walker et al., 2014).
Osteomyelitis and pyomyositis due to Staphylococcus aureus in an osteomalacic adult with multiple fractures
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Masumi Ogawa, Takatoshi Kitazawa, Yusuke Yoshino, Koji Morita, Toshio Ishikawa, Yasuo Ota
Normal bone is highly resistant to infection, which can only occur as a result of very large inocula, trauma, or the presence of foreign bodies [8]. S. aureus binds to fibronectin via the fibronectin-binding protein on its surface [9,10]. In animal models of rib fracture, fibronectin expression transiently increased in the fracture callus during fracture healing [11]. In other animal studies, rabbits with fractures and S. aureus bacteremia developed hematogenous osteomyelitis in the metaphysis of the bone with closed fracture [12,13]. Acute hematogenous osteomyelitis occurring at the site of closed fractures is rare [14]. In this present case, we speculated that during the fracture healing process, S. aureus was disseminated from a distant infection focus to the fractured bone and surrounding damaged muscle and eventually caused the formation of multifocal hematogenous osteomyelitis and muscle abscesses.
Pathobionts: mechanisms of survival, expansion, and interaction with host with a focus on Clostridioides difficile
Published in Gut Microbes, 2021
Harish Chandra, Krishna Kant Sharma, Olli H. Tuovinen, Xingmin Sun, Pratyoosh Shukla
Adhesion to the mucosal surfaces through the expression of flagellar proteins in pathobionts provides another opportunity for colonization and pathogenicity. The C. difficile flagellar proteins flagellin and flagella cap protein encoded by the fliC and fliD genes, respectively, have been implicated in C. difficile colonization and pathogenicity by adherence to the mucus in a murine study.59 Mutant strains that lack flagella components have been implicated in poor adherence to mucus and manifestation of low virulence. In this regard, c-diGMP has been shown to play a vital role in flagellar expression, biofilm formation, and adhesion.62 Elevated levels of c-diGMPs have been reported to downregulate flagellar expression and inhibit toxin synthesis and motility via binding to riboswitch upstream of the flgB operon.62 Additionally, c-diGMP induces the expression of type IV pili that interact with intestinal epithelium cells that facilitate the biofilm formation.63 There are other virulence proteins (Spo0A,Cwp66, Cwp84, S-layer protein A, and adhesin fibronectin-binding protein A) that facilitate C. difficile adhesion and biofilm formation.64 Therefore, upon selection and expansion, the pathobiont can use various tactics such as toxins, cell wall proteins, and flagellar proteins to disrupt the host intestinal barrier, leading to severe colitis in the host.
The distinct effects of aspirin on platelet aggregation induced by infectious bacteria
Published in Platelets, 2020
Nadji Hannachi, Jean-Pierre Baudoin, Arsha Prasanth, Gilbert Habib, Laurence Camoin-Jau
Several bacterial strains, such as staphylococci, streptococci, and enterococci play pivotal roles in the etiology of IE [5,6]. These roles are based on the presence of proteins and/or receptors on the surface of these bacteria that directly or indirectly interact with platelets. S. aureus is currently considered to be the main causative agent of IE [5]. S. aureus expresses surface proteins belonging to the microbial surface components that recognize the family of adhesive matrix molecules (MSCRAMM) such as clumping factor (ClfA and ClfB) and fibronectin-binding protein (Fnbp A and FnbpB). These molecules allow bacteria to adhere to tissues and induce platelet aggregation [3,7]. Furthermore, because of the presence of coagulases, S. aureus contributes to the development of fibrino-platelet vegetation during staphylococcal endocarditis [7,8].