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Pathogenicity and Virulence
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Once adherent to host cells, some pathogens, of which V. cholerae represents a classic example, maintain a strictly extracellular habitation, while others prefer to live within selected host cells other than polymorphonuclear leukocytes (PMN) and macrophages, the co-called “professional phagocytes.” Life within host cells affords protection from a potentially hostile environment and access to a nutrient-rich cytoplasm. To achieve this end, several intracellular microbes have evolved ways of inducing their endocytosis by nonphagocytic cells of the host. Proteins which adhere to the host cell, activate host cell signals, and mediate the use of host cell machinery to allow entry of the bacteria into the cell are called invasins. The invasins of Listeria, Yersinia, Salmonella, and Shigella have been identified within recent years using in vitro cell culture systems.
Mucosal interactions with enteropathogenic bacteria
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Nadine Cerf-Bensussan, Pamela Schnupf, Valérie Gaboriau-Routhiau, Philippe J. Sansonetti
Other pathogens have evolved molecules that can harness host transmembrane cell-adhesion receptors and trigger intracellular cascades that lead to epithelial cell invasion. This “zipper” strategy is used by Yersinia spp. and Listeria spp. to invade PPs (Figure 25.4). Depending on temperature, pH, and growth phase, two strains of enteropathogenic Yersinia, Y. enterocolitica and Y. pseudotuberculosis, express invasin (Inv), a 101 kDa outer membrane protein encoded by a 70 kb virulence plasmid called pYV. Bacterial Inv binds β1 integrins on the luminal surface of M cells. Inv binding results in the clustering of β1 integrins and subsequent activation of a signaling cascade that induces cytoskeleton rearrangements and bacterial internalization. Studies using inv mutants suggest that Inv is critical for dissemination from the intestinal lumen (even in animals lacking PPs) and for abscess formation in mesenteric lymph nodes but dispensable for overall virulence. Besides Yersinia, other bacteria may target host β1 integrins to adhere to the mucosa. For example, H. pylori uses its type IV secretion system (T4SS) to target β1 integrins and subsequently translocate its effector protein CagA, a protein with carcinogenic properties. Thus, an adhesin called CagL is present at the T4SS pilus surface. This adhesin was shown to bridge and activate the α5β1 integrin on the basolateral membrane of gastric epithelial cells.
Disease Prediction and Drug Development
Published in Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam, Introduction to Computational Health Informatics, 2019
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam
The proteins characterized as common virulence-factors include: 1) adhesins – bacterial cell-surface proteins that allow the pathogen to get attached to host cells; 2) toxins – an antigenic substance produced by the pathogens toxic to the human-cells; 3) invasins – bacterial-cell proteins that penetrate and damage host human-cell and are responsible for the spread of pathogens; 4) secretion systems – protein complexes that secrete virulence-factors to invade the host cells and 5) iron uptake system – proteins involved in taking iron from the environment.
Protein-losing enteropathy caused by Yersinia enterocolitica colitis
Published in Paediatrics and International Child Health, 2021
Lara Ferreira, Raquel Amaral, Fernanda Gomes, José Cabral
Y. enterocolitica can be transmitted via water, soil, animals and food. Human major pathogenic serogroups are O:3, O:5,27, O:8 and O:9 [7]. Raw pork products such as neck trimmings, tonsillar tissue, tongue and tripe are important sources of yersinioses [8–10] which can present as abdominal pain, loose, watery or bloody stools, fever and septicaemia [8,11,12]. Y. enterocolitica adheres to gut epithelial cells and invades them via invasin and other surface proteins such as yersinia outer membrane proteins (Yops). It then localises in lymphoid tissue within the gut wall and in mesenteric lymph nodes [7,13]. Yersiniosis is commonly diagnosed by positive stool culture and it can also be isolated in culture from mesenteric lymph nodes, pharyngeal exudates, peritoneal fluid or blood. Serology or Western blotting, which uses Yops as antigens for antibody detection is more sensitive and specific than stool culture or other serological methods of diagnosing yersinia-associated complications [12,13].
Effects of bacterial physiological states and bacterial species on host–microbe interactions
Published in Biofouling, 2018
Lijia Huang, Jinfeng Zeng, Caroline Bosch-Tijhof, Junqi Ling, Xi Wei, Cor van Loveren, Wim Crielaard, Dong Mei Deng
Bacterial intracellular invasion into host cells often requires adherence of the bacterial cells to a host cell (Yilmaz and Lamont 2004). It was suggested that the attachment of bacteria triggered the rearrangements of the membrane and cytoskeleton of the host cells and led to the internalization of the bacterial cells (Yilmaz and Lamont 2004). In the present experimental setup, a maximum number of planktonic cells were in close contact with epithelial cells in the sedimented cell group, while this number was likely much less in the free-floating cell group. The pilot experiment indicated that the centrifugation condition used in this study did not influence the rate of bacterial cell internalization (data not shown). Moreover, the study of Young et al. (2000) showed that invasin mutant strains of Yersinia enterocolitica displayed similar invasion rates with and without centrifugation. These results indicate that centrifugation itself does not increase bacterial invasion. Therefore, the considerable differences in bacterial internalization observed in this study are likely due to the differences in host–microbe cell contacts between free-floating and sedimented cell groups.
Mucoadhesive drug delivery systems: a promising noninvasive approach to bioavailability enhancement. Part II: formulation considerations
Published in Expert Opinion on Drug Delivery, 2023
Radha Kulkarni, Suraj Fanse, Diane J. Burgess
Mucoadhesive polymers can be grouped as specific and nonspecific. Specific polymers are biological molecules that recognize and thus bind or adhere to specific target chemical structures on the surface of cells or in the mucus. Most of specific mucoadhesive polymers are derived from plant origin. One classic example of this subtype is lectins. They are nonimmune glycoproteins that are mostly of plant origin and are capable of recognizing different combinations of polysaccharides or glycoconjugates. Since the surface of cells is covered with a multitude of sugar arrays, these polymers bind very well to cell surfaces and thus are mucoadhesive. Common sources of lectin include plants of the family Solanaceae (tomato) and Fabaceae (pea). Another type of specific mucoadhesive polymers includes bacterial polymers such as fibrins and invasins. Fibrins play an important role in the pathogenicity of certain organisms such as Escherichia coli by allowing them to bind/adhere to specific tissue sites [34]. Invasin is a membrane protein derived from Yersinia pseudotuberculosis and has the biological function to adhere to the cell wall and has been used to develop polymeric nanospheres for targeted drug delivery [35]. Nonspecific biopolymers are usually synthetic polymers, which will adhere to most cell surfaces and/or mucus, i.e. they lack specificity for a particular substrate; for example polyacrylic acid and carboxymethylcellulose. They can bind to the mucus layer via different types of interactions such as positively charged polymers (chitosans), which interact with the negatively charged mucin through electrostatic interactions, or poly(acrylic acids) such as carbopol and polycarbophil, which swell on contact with water to form viscous gels and may bind through the mechanism of mucin entanglement or hydrogen bonding [36].