Статті в журналах: "Bacterial virulence factors"

1

Kurmasheva, Naziia, Vyacheslav Vorobiev, Margarita Sharipova, Tatyana Efremova, and Ayslu Mardanova. "The Potential Virulence Factors ofProvidencia stuartii: Motility, Adherence, and Invasion." BioMed Research International 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/3589135.

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Providencia stuartiiis the most commonProvidenciaspecies capable of causing human infections. CurrentlyP. stuartiiis involved in high incidence of urinary tract infections in catheterized patients. The ability of bacteria to swarm on semisolid (viscous) surfaces and adhere to and invade host cells determines the specificity of the disease pathogenesis and its therapy. In the present study we demonstrated morphological changes ofP. stuartiiNK cells during migration on the viscous medium and discussed adhesive and invasive properties utilizing the HeLa-M cell line as a host model. To visualize the interaction ofP. stuartiiNK bacterial cells with eukaryotic cellsin vitroscanning electron and confocal microscopy were performed. We found that bacteriaP. stuartiiNK are able to adhere to and invade HeLa-M epithelial cells and these properties depend on the age of bacterial culture. Also, to invade the host cells the infectious dose of the bacteria is essential. The microphotographs indicate that after incubation of bacterialP. stuartiiNK cells together with epithelial cells the bacterial cells both were adhered onto and invaded into the host cells.

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Goebel, W., T. Chakraborty, and J. Kreft. "Bacterial hemolysins as virulence factors." Antonie van Leeuwenhoek 54, no. 5 (1988): 453–63. http://dx.doi.org/10.1007/bf00461864.

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Chizhikov, Vladimir, Avraham Rasooly, Konstantin Chumakov, and Dan D. Levy. "Microarray Analysis of Microbial Virulence Factors." Applied and Environmental Microbiology 67, no. 7 (July 1, 2001): 3258–63. http://dx.doi.org/10.1128/aem.67.7.3258-3263.2001.

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ABSTRACT Hybridization with oligonucleotide microchips (microarrays) was used for discrimination among strains of Escherichia coli and other pathogenic enteric bacteria harboring various virulence factors. Oligonucleotide microchips are miniature arrays of gene-specific oligonucleotide probes immobilized on a glass surface. The combination of this technique with the amplification of genetic material by PCR is a powerful tool for the detection of and simultaneous discrimination among food-borne human pathogens. The presence of six genes (eaeA, slt-I,slt-II, fliC, rfbE, andipaH) encoding bacterial antigenic determinants and virulence factors of bacterial strains was monitored by multiplex PCR followed by hybridization of the denatured PCR product to the gene-specific oligonucleotides on the microchip. The assay was able to detect these virulence factors in 15 Salmonella,Shigella, and E. coli strains. The results of the chip analysis were confirmed by hybridization of radiolabeled gene-specific probes to genomic DNA from bacterial colonies. In contrast, gel electrophoretic analysis of the multiplex PCR products used for the microarray analysis produced ambiguous results due to the presence of unexpected and uncharacterized bands. Our results suggest that microarray analysis of microbial virulence factors might be very useful for automated identification and characterization of bacterial pathogens.

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Flores-Díaz, Marietta, Laura Monturiol-Gross, Claire Naylor, Alberto Alape-Girón, and Antje Flieger. "Bacterial Sphingomyelinases and Phospholipases as Virulence Factors." Microbiology and Molecular Biology Reviews 80, no. 3 (June 15, 2016): 597–628. http://dx.doi.org/10.1128/mmbr.00082-15.

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SUMMARYBacterial sphingomyelinases and phospholipases are a heterogeneous group of esterases which are usually surface associated or secreted by a wide variety of Gram-positive and Gram-negative bacteria. These enzymes hydrolyze sphingomyelin and glycerophospholipids, respectively, generating products identical to the ones produced by eukaryotic enzymes which play crucial roles in distinct physiological processes, including membrane dynamics, cellular signaling, migration, growth, and death. Several bacterial sphingomyelinases and phospholipases are essential for virulence of extracellular, facultative, or obligate intracellular pathogens, as these enzymes contribute to phagosomal escape or phagosomal maturation avoidance, favoring tissue colonization, infection establishment and progression, or immune response evasion. This work presents a classification proposal for bacterial sphingomyelinases and phospholipases that considers not only their enzymatic activities but also their structural aspects. An overview of the main physiopathological activities is provided for each enzyme type, as are examples in which inactivation of a sphingomyelinase- or a phospholipase-encoding gene impairs the virulence of a pathogen. The identification of sphingomyelinases and phospholipases important for bacterial pathogenesis and the development of inhibitors for these enzymes could generate candidate vaccines and therapeutic agents, which will diminish the impacts of the associated human and animal diseases.

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5

Lantz, M. S. "Are bacterial proteases important virulence factors?" Journal of Periodontal Research 32, no. 1 (January 1997): 126–32. http://dx.doi.org/10.1111/j.1600-0765.1997.tb01393.x.

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Sharma, Aditya Kumar, Neha Dhasmana, Neha Dubey, Nishant Kumar, Aakriti Gangwal, Meetu Gupta, and Yogendra Singh. "Bacterial Virulence Factors: Secreted for Survival." Indian Journal of Microbiology 57, no. 1 (November 5, 2016): 1–10. http://dx.doi.org/10.1007/s12088-016-0625-1.

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Cepas, Virginio, and Sara M. Soto. "Relationship between Virulence and Resistance among Gram-Negative Bacteria." Antibiotics 9, no. 10 (October 20, 2020): 719. http://dx.doi.org/10.3390/antibiotics9100719.

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Bacteria present in the human body are innocuous, providing beneficial functions, some of which are necessary for correct body function. However, other bacteria are able to colonize, invade, and cause damage to different tissues, and these are categorised as pathogens. These pathogenic bacteria possess several factors that enable them to be more virulent and cause infection. Bacteria have a great capacity to adapt to different niches and environmental conditions (presence of antibiotics, iron depletion, etc.). Antibiotic pressure has favoured the emergence and spread of antibiotic-resistant bacteria worldwide. Several studies have reported the presence of a relationship (both positive and negative, and both direct and indirect) between antimicrobial resistance and virulence among bacterial pathogens. This review studies the relationship among the most important Gram-negative bacteria (Escherichia coli and Pseudomonas aeruginosa) taking into account two points of view: (i) the effect the acquisition of resistance has on virulence, and (ii) co-selection of resistance and virulence. The relationship between resistance and virulence among bacteria depends on the bacterial species, the specific mechanisms of resistance and virulence, the ecological niche, and the host.

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Warrier, Anjali, Kapaettu Satyamoorthy, and Thokur Sreepathy Murali. "Quorum-sensing regulation of virulence factors in bacterial biofilm." Future Microbiology 16, no. 13 (September 2021): 1003–21. http://dx.doi.org/10.2217/fmb-2020-0301.

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Chronic polymicrobial wound infections are often characterized by the presence of bacterial biofilms. They show considerable structural and functional heterogeneity, which influences the choice of antimicrobial therapy and wound healing dynamics. The hallmarks of biofilm-associated bacterial infections include elevated antibiotic resistance and extreme pathogenicity. Biofilm helps bacteria to evade the host defense mechanisms and persist longer in the host. Quorum-sensing (QS)-mediated cell signaling primarily regulates biofilm formation in chronic infections and plays a major role in eliciting virulence. This review focuses on the QS mechanisms of two major bacterial pathogens, Staphylococcus aureus and Pseudomonas aeruginosa and explains how they interact in the wound microenvironment to regulate biofilm development and virulence. The review also provides an insight into the treatment modalities aimed at eradicating polymicrobial biofilms. This information will help us develop better diagnostic modalities and devise effective treatment regimens to successfully manage and overcome severe life-threatening bacterial infections.

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Zúñiga-Bahamon, Andrés, Fabián Tobar, Juan Fernando Duque, and Pedro Moreno. "Acinetobacter baumannii: Resistance and Virulence mediated through bacterial type IV secretion system." Revista Estomatología 21, no. 2 (September 29, 2017): 37–45. http://dx.doi.org/10.25100/re.v21i2.5765.

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Introduction: Type IV Bacterial Secretion Systems (TFSS) have a variety of biological functions such as the exchange of genetic material with other bacteria and virulent translocation of DNA with its effector proteins into host cells. A. baumannii is a pathogen that causes infections in humans and exhibits high rates of multidrug resistance to drugs. Objective: To relate how type IV secretion systems is associated with patterns of resistance and virulence in A. baumannii. Materials and Methods: Exhaustive search in PMC (NCBI) using a set of keywords was performed. Results: The search yielded 133 articles. Fourteen articles were analysed to determine the bacterial secretion system and the resistant and virulence of AA. baumannii. Conclusions: Systems of bacterial type IV secretion present in A. baumannii are crucial in understanding the patterns of virulence and resistance. Key words: Pathogenicity, type four secretion system (T4SS), A. baumannii, virulence factors, multidrug bacterial resistance (MDR), horizontal gene transfer (HGT).

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Ansari, Shamshul, and Yoshio Yamaoka. "Helicobacter pylori Virulence Factors Exploiting Gastric Colonization and its Pathogenicity." Toxins 11, no. 11 (November 19, 2019): 677. http://dx.doi.org/10.3390/toxins11110677.

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Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world’s population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the bacteria must overcome harsh gastric conditions. H. pylori has a well-developed mechanism by which it can survive in a very acidic niche. Despite bacterial factors, gastric environmental factors and host genetic constituents together play a co-operative role for gastric pathogenicity. The virulence factors include bacterial colonization factors BabA, SabA, OipA, and HopQ, and the virulence factors necessary for gastric pathogenicity include the effector proteins like CagA, VacA, HtrA, and the outer membrane vesicles. Bacterial factors are considered more important. Here, we summarize the recent information to better understand several bacterial virulence factors and their role in the pathogenic mechanism.

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Oogai, Yuichi, Miki Matsuo, Masahito Hashimoto, Fuminori Kato, Motoyuki Sugai, and Hitoshi Komatsuzawa. "Expression of Virulence Factors by Staphylococcus aureus Grown in Serum." Applied and Environmental Microbiology 77, no. 22 (September 16, 2011): 8097–105. http://dx.doi.org/10.1128/aem.05316-11.

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ABSTRACTStaphylococcus aureusproduces many virulence factors, including toxins, immune-modulatory factors, and exoenzymes. Previous studies involving the analysis of virulence expression were mainly performed byin vitroexperiments using bacterial medium. However, whenS. aureusinfects a host, the bacterial growth conditions are quite different from those in a medium, which may be related to the different expression of virulence factors in the host. In this study, we investigated the expression of virulence factors inS. aureusgrown in calf serum. The expression of many virulence factors, including hemolysins, enterotoxins, proteases, and iron acquisition factors, was significantly increased compared with that in bacterial medium. In addition, the expression of RNA III, a global regulon for virulence expression, was significantly increased. This effect was partially restored by the addition of 300 μM FeCl3into serum, suggesting that iron depletion is associated with the increased expression of virulence factors in serum. In chemically defined medium without iron, a similar effect was observed. In a mutant withagrinactivated grown in serum, the expression of RNA III,psm, andsec4was not increased, while other factors were still induced in the mutant, suggesting that another regulatory factor(s) is involved. In addition, we found that serum albumin is a major factor for the capture of free iron to prevent the supply of iron to bacteria grown in serum. These results indicate thatS. aureusexpresses virulence factors in adaptation to the host environment.

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12

Silva, Laura Nunes, Karine Rigon Zimmer, Alexandre José Macedo, and Danielle Silva Trentin. "Plant Natural Products Targeting Bacterial Virulence Factors." Chemical Reviews 116, no. 16 (July 20, 2016): 9162–236. http://dx.doi.org/10.1021/acs.chemrev.6b00184.

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Abe, Akio, Takeshi Matsuzawa, and Asaomi Kuwae. "Type-III effectors: Sophisticated bacterial virulence factors." Comptes Rendus Biologies 328, no. 5 (May 2005): 413–28. http://dx.doi.org/10.1016/j.crvi.2005.02.008.

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Highsmith, Anita K., and William R. Jarvis. "Klebsiella pneumoniae:Selected Virulence Factors that Contribute to Pathogenicity." Infection Control 6, no. 2 (February 1985): 75–77. http://dx.doi.org/10.1017/s0195941700062640.

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AbstractKlebsiella pneumoniaeinfections occur in humans of all ages, however the highest risk groups appear to be infants, the elderly and the immunocompromised. One or more virulence factors may contribute to pathogenicity in humans. In this article we review three factors that may mediate virulence: cell wall receptors, capsular polysaccharide, and endotoxin.First, the presence of cell wall receptors enablesK. pneumoniaeto attach to the host cell, thereby altering the bacterial surface so that phagocytosis by polymorphonuclear leukocytes and macrophages is impaired and invasion of the non-phagocytic host cell is facilitated. Second, invasion of the host cell is also facilitated by the large polysaccharide capsule surrounding the bacterial cell; in addition this capsule acts as a barrier and protects the bacteria from phagocytosis. Third,K. pneumoniaeproduces an endotoxin that appears to be independent of factors that determine receptors and capsular characteristics. Marked interspecies differences in endotoxin production may correlate with virulence. Although some or all of these factors may ultimately determine virulence, the interaction of these factors in vivo has made it difficult to assess the relative contribution of any one of these virulence factors. The pathogenic mechanisms ofK. pneumoniaethat ultimately determine virulence remain unclear and will require further study.

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Ellis, Terri N., and Meta J. Kuehn. "Virulence and Immunomodulatory Roles of Bacterial Outer Membrane Vesicles." Microbiology and Molecular Biology Reviews 74, no. 1 (March 2010): 81–94. http://dx.doi.org/10.1128/mmbr.00031-09.

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SUMMARY Outer membrane (OM) vesicles are ubiquitously produced by Gram-negative bacteria during all stages of bacterial growth. OM vesicles are naturally secreted by both pathogenic and nonpathogenic bacteria. Strong experimental evidence exists to categorize OM vesicle production as a type of Gram-negative bacterial virulence factor. A growing body of data demonstrates an association of active virulence factors and toxins with vesicles, suggesting that they play a role in pathogenesis. One of the most popular and best-studied pathogenic functions for membrane vesicles is to serve as natural vehicles for the intercellular transport of virulence factors and other materials directly into host cells. The production of OM vesicles has been identified as an independent bacterial stress response pathway that is activated when bacteria encounter environmental stress, such as what might be experienced during the colonization of host tissues. Their detection in infected human tissues reinforces this theory. Various other virulence factors are also associated with OM vesicles, including adhesins and degradative enzymes. As a result, OM vesicles are heavily laden with pathogen-associated molecular patterns (PAMPs), virulence factors, and other OM components that can impact the course of infection by having toxigenic effects or by the activation of the innate immune response. However, infected hosts can also benefit from OM vesicle production by stimulating their ability to mount an effective defense. Vesicles display antigens and can elicit potent inflammatory and immune responses. In sum, OM vesicles are likely to play a significant role in the virulence of Gram-negative bacterial pathogens.

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LIHUA, LIN, WANG JIANHUI, YU JIALIN, LI YAYIN, and LIU GUANXIN. "Effects of Allicin on the Formation of Pseudomonas aeruginosa Biofilm and the Production of Quorum-Sensing Controlled Virulence Factors." Polish Journal of Microbiology 62, no. 3 (2013): 243–51. http://dx.doi.org/10.33073/pjm-2013-032.

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The Gram-negative Pseudomonas aeruginosa bacterial pathogen is reputed for its resistance to multiple antibiotics, and this property is strongly associated with the development of biofilms. Bacterial biofilms form by aggregation of microorganisms on a solid surface and secretion of an extracellular polysaccharide substances that acts as a physical protection barrier for the encased bacteria. In addition, the P aeruginosa quorum-sensing system contributes to antibiotic resistance by regulating the expression of several virulence factors, including exotoxin A, elastase, pyoverdin and rhamnolipid. The organosulfur compound allicin, derived from garlic, has been shown to inhibit both surface-adherence of bacteria and production of virulence factors. In this study, the effects of allicin on P aeruginosa biofilm formation and the production of quorum-sensing controlled virulence factors were investigated. The results demonstrated that allicin could inhibit early bacterial adhesion, reduce EPS secretion, and down-regulate virulence factors' production. Collectively, these findings suggest the potential of allicin as a therapeutic agent for controlling P aeruginosa biofilm.

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Sinclair, Paul. "Virulence Factors ofHelicobacter pylori." Canadian Journal of Gastroenterology 5, no. 6 (1991): 214–18. http://dx.doi.org/10.1155/1991/761642.

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Much attention has recently been focused onHelicobacter pylori(formerlyCampylobacter pylori). It is strongly implicated as the causative agent in chronic gastritis, and may be involved in gastric and duodenal ulcers, although the latter has not been confirmed. Several virulence factors have been documented, although their involvement in the pathogenes is ofH pyloriis not proven.H pyloriwould appear to have one natural reservoir, ie, the gastric mucosa of humans. To avoid this harsh environment, it is postulated thatH pyloripossesses several characteristics which enhance survival. Strong urease enzymes produced by these organism reduce urea to ammonia and appear to create a locally elevated environment with respect to pH. The spiral shape of the cells and their flagellar motility allow them to wind themselves into the mucous layer of the stomach. Some evidence exists for the production of strong proteolytic activity, hence degrading the mucous barrier and increasing permeability for the organism. Cyroroxin excreted by the bacteria may have some effect on the surrounding cells, with the possible lysis and release of bacterial growth factors. There is evidence that a chemotactic response is present due to these growth factors and their higher concentration in the intracellular spaces. The presence of specific and nonspecific adhesion has also been demonstrated, thus allowing the bacterium, once at the epithelial cell surface, to attach and avoid being washed off by movement within the stomach. Although treatment with antimicrobials eradicates the organism and improves symptoms of peptic ulcer patients, there is no indication that the same occurs in nonulcer dyspepsia patients. Further work is essential to describe the virulence mechanisms ofH pyloriand the possible pathogenic role of the organism.

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Wang, Li, Seiko Makino, Ashim Subedee, and Adam J. Bogdanove. "Novel Candidate Virulence Factors in Rice Pathogen Xanthomonas oryzae pv. oryzicola as Revealed by Mutational Analysis." Applied and Environmental Microbiology 73, no. 24 (November 2, 2007): 8023–27. http://dx.doi.org/10.1128/aem.01414-07.

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ABSTRACT Bacterial leaf streak, caused by Xanthomonas oryzae pv. oryzicola, is an important disease of rice. Transposon-mediated mutational analysis of the pathogen with a quantitative assay revealed candidate virulence factors including genes involved in the pathogenesis of other phytopathogenic bacteria, virulence factors of animal pathogens, and genes not previously associated with virulence.

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Kazmierczak, Mark J., Martin Wiedmann, and Kathryn J. Boor. "Alternative Sigma Factors and Their Roles in Bacterial Virulence." Microbiology and Molecular Biology Reviews 69, no. 4 (December 2005): 527–43. http://dx.doi.org/10.1128/mmbr.69.4.527-543.2005.

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SUMMARY Sigma factors provide promoter recognition specificity to RNA polymerase holoenzyme, contribute to DNA strand separation, and then dissociate from the core enzyme following transcription initiation. As the regulon of a single sigma factor can be composed of hundreds of genes, sigma factors can provide effective mechanisms for simultaneously regulating expression of large numbers of prokaryotic genes. One newly emerging field is identification of the specific roles of alternative sigma factors in regulating expression of virulence genes and virulence-associated genes in bacterial pathogens. Virulence genes encode proteins whose functions are essential for the bacterium to effectively establish an infection in a host organism. In contrast, virulence-associated genes can contribute to bacterial survival in the environment and therefore may enhance the capacity of the bacterium to spread to new individuals or to survive passage through a host organism. As alternative sigma factors have been shown to regulate expression of both virulence and virulence-associated genes, these proteins can contribute both directly and indirectly to bacterial virulence. Sigma factors are classified into two structurally unrelated families, the σ70 and the σ54 families. The σ70 family includes primary sigma factors (e.g., Bacillus subtilis σA) as well as related alternative sigma factors; σ54 forms a distinct subfamily of sigma factors referred to as σN in almost all species for which these proteins have been characterized to date. We present several examples of alternative sigma factors that have been shown to contribute to virulence in at least one organism. For each sigma factor, when applicable, examples are drawn from multiple species.

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Liu, Bo, Dandan Zheng, Siyu Zhou, Lihong Chen, and Jian Yang. "VFDB 2022: a general classification scheme for bacterial virulence factors." Nucleic Acids Research 50, no. D1 (November 30, 2021): D912—D917. http://dx.doi.org/10.1093/nar/gkab1107.

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Abstract The virulence factor database (VFDB, http://www.mgc.ac.cn/VFs/) is dedicated to presenting a comprehensive knowledge base and a versatile analysis platform for bacterial virulence factors (VFs). Recent developments in sequencing technologies have led to increasing demands to analyze potential VFs within microbiome data that always consist of many different bacteria. Nevertheless, the current classification of VFs from various pathogens is based on different schemes, which create a chaotic situation and form a barrier for the easy application of the VFDB dataset for future panbacterial metagenomic analyses. Therefore, based on extensive literature mining, we recently proposed a general category of bacterial VFs in the database and reorganized the VFDB dataset accordingly. Thus, all known bacterial VFs from 32 genera of common bacterial pathogens collected in the VFDB are well grouped into 14 basal categories along with over 100 subcategories in a hierarchical architecture. The new coherent and well-defined VFDB dataset will be feasible and applicable for future panbacterial analysis in terms of virulence factors. In addition, we introduced a redesigned JavaScript-independent web interface for the VFDB website to make the database readily accessible to all users with various client settings worldwide.

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Jaafar, Firas Nabeeh, Majid Ahmed AL-Bayati, Hadeel Kareem Musafer, Maan Abdul Azeez, and Zahraa Kareem Raheem. "Quorum Sensing and its Correlation with Virulence Factors." South Asian Research Journal of Pharmaceutical Sciences 4, no. 3 (June 10, 2022): 60–69. http://dx.doi.org/10.36346/sarjps.2022.v04i03.003.

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Quorum sensing (QS) is cell to cell signaling mechanism that enables bacteria collectively control gene expression in response to their population density, or it is bacterial communicate with one another using chemical signals. There are three types of signaling molecules: Acyl-homoserinelactonase (AHLs), Auto-inducer peptides (AIPs) and Autoinducer-2 (AI-2). Q.S was first observed and described in bioluminescence bacterium V.fischeri.In V. fischeri, several kinds of quorum sensing system were identified. At first, lux system was found and regulates the luciferase operon and light production. LuxIwas isolated as an AHL synthase while LuxR was isolated as a transcriptional activator of the luciferase operon. At low cell density, LuxOrepresses LitR, which is a positive regulator of the expression of LuxR. Quorum quenching (QQ) refers to the mechanism by which bacterial communication can be interrupted, or it is the process of preventing QS by disrupting the signaling.The first major QS-disrupting strategy that has been studied is the interference with the detection of the AIs and the second one is the inactivation/degradations of the signal molecules.

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Drevets, Douglas A. "Listeria monocytogenes Virulence Factors That Stimulate Endothelial Cells." Infection and Immunity 66, no. 1 (January 1, 1998): 232–38. http://dx.doi.org/10.1128/iai.66.1.232-238.1998.

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ABSTRACT Listeria monocytogenes infection of endothelial cells upregulates surface expression of adhesion molecules and stimulates neutrophil adhesion to infected cell monolayers. The experiments presented here tested the roles of specific bacterial virulence factors as triggers for this inflammatory phenotype and function. Human umbilical vein endothelial cell (HUVEC) monolayers were infected with wild-type L. monocytogenes or L. monocytogenesmutants; then surface expression of E-selectin and neutrophil adhesion were measured. The results showed that Δhly andprfA mutants were the most crippled, requiring 100-fold more mutant bacteria than wild-type bacteria for analogous stimulation. By comparison, L. monocytogenes mutants with deletions ofactA, inlA, inlB,inlAB, plcA, and plcB resembled their parent strains, and a ΔplcA ΔplcB mutant displayed decreased intracellular growth rate but only a minor decrease in stimulation of E-selectin or neutrophil adhesion. Other experiments showed that cytochalasin D-treated HUVEC monolayers bound bacteria, but internalization and increased surface E-selectin and intercellular adhesion molecule-1 expression were profoundly inhibited. However, cytochalasin D had no effect on the HUVEC response to stimulation with lipopolysaccharide or tumor necrosis factor alpha. These data suggest that listeriolysin O production by infecting L. monocytogenes contributes to increased expression of surface E-selectin and intercellular adhesion molecule-1, but neither it nor intracellular replication are directly responsible for this event. Nonetheless it is possible that listeriolysin O potentiates the effect(s) of an other molecule(s) that directly triggers this response. Additionally, cellular invasion by L. monocytogenes appears to be critical for initiating the HUVEC response, potentially by providing a signal which results in upregulation of the necessary bacterial genes.

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Khayyat, Ahdab N., Hisham A. Abbas, Mamdouh F. A. Mohamed, Hani Z. Asfour, Maan T. Khayat, Tarek S. Ibrahim, Mahmoud Youns, et al. "Not Only Antimicrobial: Metronidazole Mitigates the Virulence of Proteus mirabilis Isolated from Macerated Diabetic Foot Ulcer." Applied Sciences 11, no. 15 (July 26, 2021): 6847. http://dx.doi.org/10.3390/app11156847.

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Diabetic foot ulcers are recognized to be a severe complication of diabetes, increasing the risk of amputation and death. The bacterial infection of Diabetic foot ulcers with virulent and resistant bacteria as Proteus mirabilis greatly worsens the wound and may not be treated with conventional therapeutics. Developing new approaches to target bacterial virulence can be helpful to conquer such infections. In the current work, we evaluated the anti-virulence activities of the widely used antibacterial metronidazole. The minimum inhibitory concentrations (MIC) and minimum biofilm eradication concentrations (MEBC) were determined for selected antibiotics which P. mirabilis was resistant to them in the presence and absence of metronidazole in sub-MIC. The effect of metronidazole in sub-MIC on P. mirabilis virulence factors as production of exoenzymes, motilities, adhesion and biofilm formation, were evaluated. Furthermore, molecular docking of metronidazole into P. mirabilis adhesion and essential quorum sensing (QS) proteins, was performed. The results revealed a significant ability of metronidazole to in-vitro inhibit P. mirabilis virulence factors and antagonize its essential proteins. Moreover, metronidazole markedly decreased the MICs and MBECs of tested antibiotics. Conclusively, metronidazole in sub-MIC is a plausible anti-virulence and anti-QS agent that can be combined to other antibiotics as anti-virulence adjuvant to defeat aggressive infections.

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Costerton, William J., Lucio Montanaro, Naomi Balaban, and Carla Renata Arciola. "Prospecting Gene Therapy of Implant Infections." International Journal of Artificial Organs 32, no. 9 (September 2009): 689–95. http://dx.doi.org/10.1177/039139880903200919.

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Infection still represents one of the most serious and ravaging complications associated with prosthetic devices. Staphylococci and enterococci, the bacteria most frequently responsible for orthopedic postsurgical and implant-related infections, express clinically relevant antibiotic resistance. The emergence of antibiotic-resistant bacteria and the slow progress in identifying new classes of antimicrobial agents have encouraged research into novel therapeutic strategies. The adoption of antisense or “antigene” molecules able to silence or knock-out bacterial genes responsible for their virulence is one possible innovative approach. Peptide nucleic acids (PNAs) are potential drug candidates for gene therapy in infections, by silencing a basic gene of bacterial growth or by tackling the antibiotic resistance or virulence factors of a pathogen. An efficacious contrast to bacterial genes should be set up in the first stages of infection in order to prevent colonization of periprosthesis tissues. Genes encoding bacterial factors for adhesion and colonization (biofilm and/or adhesins) would be the best candidates for gene therapy. But after initial enthusiasm for direct antisense knock-out or silencing of essential or virulence bacterial genes, difficulties have emerged; consequently, new approaches are now being attempted. One of these, interference with the regulating system of virulence factors, such as agr, appears particularly promising.

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Gao, Peng, Pak Leung Ho, Bingpeng Yan, Kong Hung Sze, Julian Davies, and Richard Yi Tsun Kao. "Suppression of Staphylococcus aureus virulence by a small-molecule compound." Proceedings of the National Academy of Sciences 115, no. 31 (July 16, 2018): 8003–8. http://dx.doi.org/10.1073/pnas.1720520115.

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Emerging antibiotic resistance among bacterial pathogens has necessitated the development of alternative approaches to combat drug-resistance-associated infection. The abolition of Staphylococcus aureus virulence by targeting multiple-virulence gene products represents a promising strategy for exploration. A multiplex promoter reporter platform using gfp-luxABCDE dual-reporter plasmids with selected promoters from S. aureus-virulence-associated genes was used to identify compounds that modulate the expression of virulence factors. One small-molecule compound, M21, was identified from a chemical library to reverse virulent S. aureus into its nonvirulent state. M21 is a noncompetitive inhibitor of ClpP and alters α-toxin expression in a ClpP-dependent manner. A mouse model of infection indicated that M21 could attenuate S. aureus virulence. This nonantibiotic compound has been shown to suppress the expression of multiple unrelated virulence factors in S. aureus, suggesting that targeting a master regulator of virulence is an effective way to control virulence. Our results illustrate the power of chemical genetics in the modulation of virulence gene expression in pathogenic bacteria.

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Escosura-Muñiz, Alfredo de la, Kristina Ivanova, and Tzanko Tzanov. "Electrical Evaluation of Bacterial Virulence Factors Using Nanopores." ACS Applied Materials & Interfaces 11, no. 14 (March 19, 2019): 13140–46. http://dx.doi.org/10.1021/acsami.9b02382.

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Chen, L. "VFDB: a reference database for bacterial virulence factors." Nucleic Acids Research 33, Database issue (December 17, 2004): D325—D328. http://dx.doi.org/10.1093/nar/gki008.

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SLOTS, JÖRGEN, and GUNNAR DAHLÉN. "Subgingival microorganisms and bacterial virulence factors in periodontitis." European Journal of Oral Sciences 93, no. 2 (April 1985): 119–27. http://dx.doi.org/10.1111/j.1600-0722.1985.tb01319.x.

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Mock, Michèle, and Agnes Ullmann. "Calmodulin-activated bacterial adenylate cyclases as virulence factors." Trends in Microbiology 1, no. 5 (August 1993): 187–92. http://dx.doi.org/10.1016/0966-842x(93)90089-a.

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Tan, Y. P., Q. Lin, X. H. Wang, S. Joshi, C. L. Hew, and K. Y. Leung. "Comparative Proteomic Analysis of Extracellular Proteins of Edwardsiella tarda." Infection and Immunity 70, no. 11 (November 2002): 6475–80. http://dx.doi.org/10.1128/iai.70.11.6475-6480.2002.

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ABSTRACT A comparison of extracellular proteins of virulent and avirulent Edwardsiella tarda strains revealed several major, virulent-strain-specific proteins. Proteomic analysis identified two of the proteins in the virulent strain PPD130/91 as flagellin and SseB, which are virulence factors in bacterial pathogens. PCR amplification and DNA sequencing confirmed the presence of the genes that encode these proteins. Our results clearly demonstrated the potency of the proteomic approach in identifying virulence factors.

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Abd El-Aleam, Rehab H., Riham F. George, Hanan H. Georgey, and Hamdy M. Abdel-Rahman. "Bacterial virulence factors: a target for heterocyclic compounds to combat bacterial resistance." RSC Advances 11, no. 58 (2021): 36459–82. http://dx.doi.org/10.1039/d1ra06238g.

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Gauthier, Annick, Marilyn L. Robertson, Michael Lowden, J. Antonio Ibarra, José Luis Puente, and B. Brett Finlay. "Transcriptional Inhibitor of Virulence Factors in Enteropathogenic Escherichia coli." Antimicrobial Agents and Chemotherapy 49, no. 10 (October 2005): 4101–9. http://dx.doi.org/10.1128/aac.49.10.4101-4109.2005.

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ABSTRACT The type III secretion system (TTSS) is a key virulence mechanism of many important gram-negative bacterial pathogens. The TTSS is conserved among different bacterial pathogens, and mutations and deletions to the system significantly decrease virulence, making the TTSS an important potential therapeutic target. We have developed a high-throughput assay to search for inhibitors of the TTSS. We screened a commercial library of 20,000 small molecules for their ability to inhibit type III secretion by enteropathogenic Escherichia coli (EPEC). After discarding compounds that had no effect on secretion, inhibited bacterial growth, and/or caused degradation of EPEC-secreted proteins, the search was focused on a class of compounds that, while not direct inhibitors of type III secretion, inhibit expression of TTSS-related genes and other genes involved in virulence. This class of compounds does not affect bacterial viability or motility, indicating that it is not significantly affecting the expression of essential genes and is specific to virulence-associated genes. Transcriptional fusion assays confirmed that virulence-associated promoters were more sensitive to inhibition by this class of compounds. Overall, we have identified a class of compounds that can be used as a tool to probe the mechanism(s) that regulates virulence gene expression in EPEC.

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Spidlova, Petra, Pavla Stojkova, Anders Sjöstedt, and Jiri Stulik. "Control of Francisella tularensis Virulence at Gene Level: Network of Transcription Factors." Microorganisms 8, no. 10 (October 21, 2020): 1622. http://dx.doi.org/10.3390/microorganisms8101622.

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Regulation of gene transcription is the initial step in the complex process that controls gene expression within bacteria. Transcriptional control involves the joint effort of RNA polymerases and numerous other regulatory factors. Whether global or local, positive or negative, regulators play an essential role in the bacterial cell. For instance, some regulators specifically modify the transcription of virulence genes, thereby being indispensable to pathogenic bacteria. Here, we provide a comprehensive overview of important transcription factors and DNA-binding proteins described for the virulent bacterium Francisella tularensis, the causative agent of tularemia. This is an unexplored research area, and the poorly described networks of transcription factors merit additional experimental studies to help elucidate the molecular mechanisms of pathogenesis in this bacterium, and how they contribute to disease.

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Alonzo, Francis, Gary C. Port, Min Cao, and Nancy E. Freitag. "The Posttranslocation Chaperone PrsA2 Contributes to Multiple Facets of Listeria monocytogenes Pathogenesis." Infection and Immunity 77, no. 7 (May 18, 2009): 2612–23. http://dx.doi.org/10.1128/iai.00280-09.

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ABSTRACT Listeria monocytogenes is an intracellular bacterial pathogen whose virulence depends on the regulated expression of numerous secreted bacterial factors. As for other gram-positive bacteria, many proteins secreted by L. monocytogenes are translocated across the bacterial membrane in an unfolded state to the compartment existing between the membrane and the cell wall. This compartment presents a challenging environment for protein folding due to its high density of negative charge, high concentrations of cations, and low pH. We recently identified PrsA2 as a gene product required for L. monocytogenes virulence. PrsA2 was identified based on its increased secretion by strains containing a mutationally activated form of prfA, the key regulator of L. monocytogenes virulence gene expression. The prsA2 gene product is one of at least two predicted peptidyl-prolyl cis/trans-isomerases encoded by L. monocytogenes; these proteins function as posttranslocation protein chaperones and/or foldases. In this study, we demonstrate that PrsA2 plays a unique and important role in L. monocytogenes pathogenesis by promoting the activity and stability of at least two critical secreted virulence factors: listeriolysin O (LLO) and a broad-specificity phospholipase. Loss of PrsA2 activity severely attenuated virulence in mice and impaired bacterial cell-to-cell spread in host cells. In contrast, mutants lacking prsA1 resembled wild-type bacteria with respect to intracellular growth and cell-to-cell spread as well as virulence in mice. PrsA2 is thus distinct from PrsA1 in its unique requirement for the stability and full activity of L. monocytogenes-secreted factors that contribute to host infection.

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Fugier, Emilie, Georgios Pappas, and Jean-Pierre Gorvel. "Virulence factors in brucellosis: implications for aetiopathogenesis and treatment." Expert Reviews in Molecular Medicine 9, no. 35 (December 2007): 1–10. http://dx.doi.org/10.1017/s1462399407000543.

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Brucellaspecies are responsible for the global zoonotic disease brucellosis. These intracellular pathogens express a set of factors – including lipopolysaccharides, virulence regulator proteins and phosphatidylcholine – to ensure their full virulence. Some virulence factors are essential for invasion of the host cell, whereas others are crucial to avoid elimination by the host. They allowBrucellaspp. to survive and proliferate within its replicative vacuole and enable the bacteria to escape detection by the host immune system. Several strategies have been used to develop animal vaccines against brucellosis, but no adequate vaccine yet exists to cure the disease in humans. This is probably due to the complicated pathophysiology of humanBrucellaspp. infection, which is different than in animal models. Here we reviewBrucellaspp. virulence factors and how they control bacterial trafficking within the host cell.

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Henderson, Brian. "An overview of protein moonlighting in bacterial infection." Biochemical Society Transactions 42, no. 6 (November 17, 2014): 1720–27. http://dx.doi.org/10.1042/bst20140236.

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We are rapidly returning to a world in which bacterial infections are a major health issue. Pathogenic bacteria are able to colonize and cause pathology due to the possession of virulence factors such as adhesins, invasins, evasins and toxins. These are generally specifically evolved proteins with selective actions. It is, therefore, surprising that most human bacterial pathogens employ moonlighting proteins as virulence factors. Currently, >90 bacterial species employ one or more moonlighting protein families to aid colonization and induce disease. These organisms employ 90 moonlighting bacterial protein families and these include enzymes of the glycolytic pathway, tricarboxylic acid (TCA) cycle, hexosemonophosphate shunt, glyoxylate cycle and a range of other metabolic enzymes, proteases, transporters and, also, molecular chaperones and protein-folding catalysts. These proteins have homologues in eukaryotes and only a proportion of the moonlighting proteins employed are solely bacterial in origin. Bacterial moonlighting proteins can be divided into those with single moonlighting functions and those with multiple additional biological actions. These proteins contribute significantly to the population of virulence factors employed by bacteria and some are obvious therapeutic targets. Where examined, bacterial moonlighting proteins bind to target ligands with high affinity. A major puzzle is the evolutionary mechanism(s) responsible for bacterial protein moonlighting and a growing number of highly homologous bacterial moonlighting proteins exhibit widely different moonlighting actions, suggesting a lack in our understanding of the mechanism of evolution of protein active sites.

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Sun, Hongmin. "The Interaction Between Pathogens and the Host Coagulation System." Physiology 21, no. 4 (August 2006): 281–88. http://dx.doi.org/10.1152/physiol.00059.2005.

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There is mounting evidence that the hemostatic system is critical in host responses to bacterial infection. Invasive bacteria have evolved virulence strategies to interact with host hemostatic factors such as plasminogen and fibrinogen for infection. Furthermore, genetic variations in host hemostatic factors also influence host response to bacterial infection.

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Abaturov, А. Е., and Т. А. Kryuchko. "Inhibition of bacterial virulence factors as a method of treating bacterial pneumonia." CHILD`S HEALTH 13, no. 2 (April 27, 2018): 224–31. http://dx.doi.org/10.22141/2224-0551.13.2.2018.129557.

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39

Sudheesh, Ponnerassery S., Aliya Al-Ghabshi, Nashwa Al-Mazrooei, and Saoud Al-Habsi. "Comparative Pathogenomics of Bacteria Causing Infectious Diseases in Fish." International Journal of Evolutionary Biology 2012 (May 22, 2012): 1–16. http://dx.doi.org/10.1155/2012/457264.

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Fish living in the wild as well as reared in the aquaculture facilities are susceptible to infectious diseases caused by a phylogenetically diverse collection of bacterial pathogens. Control and treatment options using vaccines and drugs are either inadequate, inefficient, or impracticable. The classical approach in studying fish bacterial pathogens has been looking at individual or few virulence factors. Recently, genome sequencing of a number of bacterial fish pathogens has tremendously increased our understanding of the biology, host adaptation, and virulence factors of these important pathogens. This paper attempts to compile the scattered literature on genome sequence information of fish pathogenic bacteria published and available to date. The genome sequencing has uncovered several complex adaptive evolutionary strategies mediated by horizontal gene transfer, insertion sequence elements, mutations and prophage sequences operating in fish pathogens, and how their genomes evolved from generalist environmental strains to highly virulent obligatory pathogens. In addition, the comparative genomics has allowed the identification of unique pathogen-specific gene clusters. The paper focuses on the comparative analysis of the virulogenomes of important fish bacterial pathogens, and the genes involved in their evolutionary adaptation to different ecological niches. The paper also proposes some new directions on finding novel vaccine and chemotherapeutic targets in the genomes of bacterial pathogens of fish.

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Diggle, Stephen P. "Microbial communication and virulence: lessons from evolutionary theory." Microbiology 156, no. 12 (December 1, 2010): 3503–12. http://dx.doi.org/10.1099/mic.0.045179-0.

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At the heart of tackling the huge challenge posed by infectious micro-organisms is the overwhelming need to understand their nature. A major question is, why do some species of bacteria rapidly kill their host whilst others are relatively benign? For example, Yersinia pestis, the causative organism of plague, is a highly virulent human pathogen whilst the closely related Yersinia pseudotuberculosis causes a much less severe disease. Using molecular techniques such as mutating certain genes, microbiologists have made significant advances over recent decades in elucidating the mechanisms that govern the production of virulence factors involved in causing disease in many bacterial species. There are also evolutionary and ecological factors which will influence virulence. Many of these ideas have arisen through the development of evolutionary theory and yet there is strikingly little empirical evidence testing them. By applying both mechanistic and adaptive approaches to microbial behaviours we can begin to address questions such as, what factors influence cooperation and the evolution of virulence in microbes and can we exploit these factors to develop new antimicrobial strategies?

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Johnson, J. R. "Virulence factors in Escherichia coli urinary tract infection." Clinical Microbiology Reviews 4, no. 1 (January 1991): 80–128. http://dx.doi.org/10.1128/cmr.4.1.80.

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Uropathogenic strains of Escherichia coli are characterized by the expression of distinctive bacterial properties, products, or structures referred to as virulence factors because they help the organism overcome host defenses and colonize or invade the urinary tract. Virulence factors of recognized importance in the pathogenesis of urinary tract infection (UTI) include adhesins (P fimbriae, certain other mannose-resistant adhesins, and type 1 fimbriae), the aerobactin system, hemolysin, K capsule, and resistance to serum killing. This review summarizes the virtual explosion of information regarding the epidemiology, biochemistry, mechanisms of action, and genetic basis of these urovirulence factors that has occurred in the past decade and identifies areas in need of further study. Virulence factor expression is more common among certain genetically related groups of E. coli which constitute virulent clones within the larger E. coli population. In general, the more virulence factors a strain expresses, the more severe an infection it is able to cause. Certain virulence factors specifically favor the development of pyelonephritis, others favor cystitis, and others favor asymptomatic bacteriuria. The currently defined virulence factors clearly contribute to the virulence of wild-type strains but are usually insufficient in themselves to transform an avirulent organism into a pathogen, demonstrating that other as-yet-undefined virulence properties await discovery. Virulence factor testing is a useful epidemiological and research tool but as yet has no defined clinical role. Immunological and biochemical anti-virulence factor interventions are effective in animal models of UTI and hold promise for the prevention of UTI in humans.

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Åhlund, Monika K., Patrik Rydén, Anders Sjöstedt, and Svenja Stöven. "Directed Screen of Francisella novicida Virulence Determinants Using Drosophila melanogaster." Infection and Immunity 78, no. 7 (May 17, 2010): 3118–28. http://dx.doi.org/10.1128/iai.00146-10.

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ABSTRACT Francisella tularensis is a highly virulent, facultative intracellular human pathogen whose virulence mechanisms are not well understood. Occasional outbreaks of tularemia and the potential use of F. tularensis as a bioterrorist agent warrant better knowledge about the pathogenicity of this bacterium. Thus far, genome-wide in vivo screens for virulence factors have been performed in mice, all however restricted by the necessity to apply competition-based, negative-selection assays. We wanted to individually evaluate putative virulence determinants suggested by such assays and performed directed screening of 249 F. novicida transposon insertion mutants by using survival of infected fruit flies as a measure of bacterial virulence. Some 20% of the genes tested were required for normal virulence in flies; most of these had not previously been investigated in detail in vitro or in vivo. We further characterized their involvement in bacterial proliferation and pathogenicity in flies and in mouse macrophages. Hierarchical cluster analysis of mutant phenotypes indicated a functional linkage between clustered genes. One cluster grouped all but four genes of the Francisella pathogenicity island and other loci required for intracellular survival. We also identified genes involved in adaptation to oxidative stress and genes which might induce host energy wasting. Several genes related to type IV pilus formation demonstrated hypervirulent mutant phenotypes. Collectively, the data demonstrate that the bacteria in part use similar virulence mechanisms in mammals as in Drosophila melanogaster but that a considerable proportion of the virulence factors active in mammals are dispensable for pathogenicity in the insect model.

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Vranes, J., A. Antolovic-Pozgain, M. Senjug, and B. Bedenic. "P820 Escherichia coli virulence factors in chronic bacterial prostatitis." International Journal of Antimicrobial Agents 29 (March 2007): S207. http://dx.doi.org/10.1016/s0924-8579(07)70661-1.

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Boquet, Patrice, and Emmanuel Lemichez. "Bacterial virulence factors targeting Rho GTPases: parasitism or symbiosis?" Trends in Cell Biology 13, no. 5 (May 2003): 238–46. http://dx.doi.org/10.1016/s0962-8924(03)00037-0.

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QUINN, F., G. NEWMAN, and C. KING. "In search of virulence factors of human bacterial disease." Trends in Microbiology 5, no. 1 (January 1997): 20–26. http://dx.doi.org/10.1016/s0966-842x(97)81770-2.

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Azeredo da Silveira, Samareh, and Antonio Perez. "Liposomes as novel anti-infectives targeting bacterial virulence factors?" Expert Review of Anti-infective Therapy 13, no. 5 (April 8, 2015): 531–33. http://dx.doi.org/10.1586/14787210.2015.1028367.

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Brauner, A., U. Flodin, B. Hylander, and C. G. Östenson. "Bacteriuria, Bacterial Virulence and Host Factors in Diabetic Patients." Diabetic Medicine 10, no. 6 (July 1993): 550–54. http://dx.doi.org/10.1111/j.1464-5491.1993.tb00119.x.

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Herbert, Mark A., Catriona JE Beveridge, and Nigel J. Saunders. "Bacterial virulence factors in neonatal sepsis: group B streptococcus." Current Opinion in Infectious Diseases 17, no. 3 (June 2004): 225–29. http://dx.doi.org/10.1097/00001432-200406000-00009.

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Rahme, L. G., F. M. Ausubel, H. Cao, E. Drenkard, B. C. Goumnerov, G. W. Lau, S. Mahajan-Miklos, et al. "Plants and animals share functionally common bacterial virulence factors." Proceedings of the National Academy of Sciences 97, no. 16 (August 1, 2000): 8815–21. http://dx.doi.org/10.1073/pnas.97.16.8815.

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Tseng, Chin-Chung, Jiunn-Jong Wu, Ming-Cheng Wang, Lien-I. Hor, Yen-Hsiu Ko, and Jeng-Jong Huang. "Host and Bacterial Virulence Factors Predisposing to Emphysematous Pyelonephritis." American Journal of Kidney Diseases 46, no. 3 (September 2005): 432–39. http://dx.doi.org/10.1053/j.ajkd.2005.05.019.

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