China
Africa
Explore chapters and articles related to this topic
Bacteriophage Involvement in Neurodegenerative Diseases
Published in David Perlmutter, The Microbiome and the Brain, 2019
We next developed an in vitro model and determined that phage-induced alteration of E. coli abundance lead to PAMP release from E. coli biofilms. Using an amyloid-diagnostic dye, we noted the release of highly immunogenic amyloids (curli-DNA composites) from E. coli biofilms upon E. coli prophage induction. Combining these results with existing data on the immunogenic role of enterobacterial amyloids, these findings suggest that phages indirectly contribute to the release of biofilm PAMPs that could trigger β-cell autoimmunity in type 1 diabetes susceptible hosts.
Neonatal Bacterial Infection
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Koilmani Emmanuvel Rajan, Christopher Karen
The colonization of nasopharynx, oropharynx, or sinuses is the critical prerequisite for the development of bacterial meningitis. The virulent type of the pathogen determines the mechanisms behind invasion and colonization. Adhesion to the host tissue is the essential and initial step in bacterial infection. Bacterial adhesions extend to attach, colonize, and evade most of the defensive mechanisms of the host. The appendage or cell surface components that facilitate bacterial adhesion are called adhesins. Among gram-negative pathogens, pili or fimbriae are the major bacterial adhesive surface structures. They are mostly filamentous and can pass through or between capsular layers. Type 1, P-pili, type IV, and curli are the well-characterized pilus structures in gram-negative bacteria. On the other hand, in gram-positive bacteria, surface proteins, polysaccharides, or lipids displayed the adhesive functions (Kline 2009; Grandgirard and Leib 2010). Adhesins helps meningeal pathogens to successfully colonize the mucosal epithelial surfaces (i.e., respiratory, intestinal, and genitourinary tract) of the host (Kc et al. 2017). E. coli K1, GBS, and N. meningitidis use pili or fibrils to initiate binding in brain microvasculature endothelial cells (BMEC). Occasionally, the toxins released by the bacteria can lower the blood–brain barrier and facilitate penetration. Penetration of the mucosal barrier by the bacteria through or between the epithelial cells is very specific to most of the bacteria (Van Sorge and Doran 2012).
Internalization of Microbial Pathogens by Integrin Receptors and the Binding of the Yersinia pseudotuberculosis Invasin Protein
Published in Yoshikazu Takada, Integrins: The Biological Problems, 2017
The amino terminal heparin-binding domain of fibronectin is also able to adhere to a variety of E. coli strains,17,18,24 but the bacterial structure involved appears to be quite different from that found in the Gram-positive cocci. Binding to E. coli occurs via bundles of distinct surface structures that bear some resemblance to bacterial pili.18 The fine and twisted appearance of these organelles in the electron microscope has earned them the name of curli, which are made of repeated monomers of the curlin subunit.18 The expression of these filamentous structures is under very tight thermoregulatory control, and since most E. coli isolates have the ability to express curli, it appears that there is some selective pressure to maintain fibronectin binding in vivo. The potential in vivo roles will be discussed below.
Clonal groups of extended-spectrum β-lactamase and biofilm producing uropathogenic Escherichia coli in Iran
Published in Pathogens and Global Health, 2022
Ali Qasemi, Fateh Rahimi, Mohammad Katouli
Biofilm formation by UPEC on the surface or inside the bladder epithelial cells, as well as on the urinary catheters, is one of the main causes of bacterial resistance to the host immune system and antimicrobial agents and the persistence of UPEC that often results in recurrent infections [4,43]. Therefore, the study of factors involved in biofilm production can be useful to find the new therapeutic agents for the treatment of chronic and recurrent UTIs. Common antimicrobial strategies for treatment of UTIs may result in emergence and spread of MDR and β-lactamase-producing strains. The fact that more than 40% of the UPEC tested in this study produced curli and cellulose, with majority of strains classified as moderate – and strong-biofilm producers, indicate the important role of biofilm in the pathogenicity of UPEC, as reported previously [4]. There was a significant correlation between the results of biofilm production evaluation methods in our study, as all cellulose and/or curli producing strains were able to form biofilm. In addition, we verified a potential correlation between coexpression ability of curli and cellulose with biofilm production capacity in UPEC strains. Our findings are further supported by previous reports that coproduction of curli and cellulose results in a significant increase in biofilm formation in the strains with rdar morphotype [44]. Despite that we found some strains with strong biofilm formation ability that were negative for curli or cellulose, suggesting that other factors may also affect this process.
Benzyl isocyanate isolated from the leaves of Psidium guajava inhibits Staphylococcus aureus biofilm formation
Published in Biofouling, 2020
Kunal Dutta, Amit Karmakar, Debarati Jana, Saroj Ballav, Sergey Shityakov, Amiya Kumar Panda, Chandradipa Ghosh
It is well-documented in several studies that biofilm formation in S. aureus takes place by both ica-operon dependent and ica-operon independent mechanisms, and this organism produces biofilm at almost the same efficiency by these two mechanisms. There are also reports that environmental activation of icaADBC does not correlate with increased biofilm formation or that the ica operon needs to be essentially present for biofilm formation in S. aureus (Fitzpatrick et al. 2005; Toledo-Arana et al. 2005; Nasr et al. 2012; Figueiredo et al. 2017; Omidi et al. 2020). Moreover, both modes of biofilm formation by S. aureus have clinical importance (Wang et al. 2010). A slime production assay which reflects biofilm formation using Congo Red (CR) agar is a standard biochemical qualitative assay in this regard. This method is employed to make a rough estimation of slime production by the bacteria. CR is a well-known amyloid binding dye (Reichhardt et al. 2016), and binds to S. aureus producing amyloid structures during biofilm formation to give a black coloration (Cohen and Merzendorfer 2019). The black coloration of the CR plate is due to the presence of amyloid curli fibers that help in the formation of exopolysaccharides (EPS) (Cohen and Merzendorfer 2019). Among all other bacterial fibers, curli are distinguishable as they have the property of binding with CR. Herein, by CR assay was employed in identifying this property. It is true that if a bacterium produces curli fibers, it has the capability of producing slime.
Molecules involved in motility regulation in Escherichia coli cells: a review
Published in Biofouling, 2020
Fazlurrahman Khan, Nazia Tabassum, Dung Thuy Nguyen Pham, Sandra Folarin Oloketuyi, Young-Mog Kim
An example of such an effector protein is YcgR. YcgR acts as a negative regulator of flagellar motility (Nieto et al. 2019). YcgR also includes a c-di-GMP binding (PilZ) domain. Hence, the activity of YcgR is affected by the cellular levels of the c-di-GMP (Amikam and Galperin 2006; Paul et al. 2010) (Figure 2A). At high c-di-GMP concentrations, c-di-GMP binds to the YcgR, and a YcgR-c-di-GMP complex is formed (Boehm et al. 2010; Fang and Gomelsky 2010). This complex then binds to a stator protein (MotA). In this way, the YcgR-c-di-GMP complex interferes with the binding of rotor protein FliG to MotA. The flagellar rotation is accomplished via torque generated due to the interaction of rotor protein FliG and stator protein MotA (Newell et al. 2009). Hence, the flagellar motility becomes inhibited by the YcgR-c-di-GMP complex. Interestingly, biofilm formation was also found to be enhanced at high c-di-GMP concentrations as a result of increased expression of curli fimbriae that facilitate the initial surface adhesion of bacterial cells. The activity of FixJ/LuxR family protein CsgD (curlin subunit gene D), a master regulator of curli fimbriae expression and biofilm formation, is regulated by c-di-GMP levels (Pesavento et al. 2008). CsgD activates the transcription of csgBA structural operon encoding curli proteins such as CsgB and CsgA involved in bacterial adhesion to surfaces.