scholarly journals Virulence factors of Actinobacillus actinomycetemcomitans: other putative factors

2000 ◽  
Vol 14 (1) ◽  
pp. 05-11
Author(s):  
Mario Julio AVILA-CAMPOS ◽  
Maria Regina Lorenzetti SIMIONATO ◽  
Silvana CAI ◽  
Márcia Pinto Alves MAYER ◽  
José Luiz DE LORENZO ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Periodontal Disease ◽  
Virulence Factors ◽  
Causative Agent ◽  
Tissue Repair ◽  
Bacteriocin Production ◽  
Actinobacillus Actinomycetemcomitans ◽  
Blood Types ◽  
Wide Range ◽  
Localized Juvenile Periodontitis

Actinobacillus actinomycetemcomitans is implicated as the causative agent of localized juvenile periodontitis. This organism possesses a large number of virulence factors with a wide range of activities and also interfere with tissue repair. Fifty isolates of A. actinomycetemcomitans from 20 periodontal patients were examined to evaluate other putative virulence factors. In this study, the capsule, DNase, coagulase, fibrinolysin, proteolytic, haemolysin and bacteriocin production, haemagglutination, serum sensitivity, epithelial cells attachment, hydrophobicity and virulence of the A. actinomycetemcomitans isolates were evaluated. All the isolates were resistant to the different tested sera. 70% to 94% were alpha-haemolytics and agglutinated all blood types. Most of isolates produced antagonistic substances and they had a low hydrophobicity. None of the isolates was pathogenic for mice. Little is known as to wether these factors may act in the development of periodontal disease, and further studies are required for an application in pathogenic and systematic terms.

scholarly journals Simultaneous lack of catalase and beta-toxin in Staphylococcus aureus leads to increased intracellular survival in macrophages and epithelial cells and to attenuated virulence in murine and ovine models

Microbiology ◽  
2009 ◽  
Vol 155 (5) ◽  
pp. 1505-1515 ◽  
Author(s):  
Susana Martínez-Pulgarín ◽  
Gustavo Domínguez-Bernal ◽  
José A. Orden ◽  
Ricardo de la Fuente
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Epithelial Cells ◽  
Virulence Factors ◽  
Mammary Epithelial Cells ◽  
Intracellular Survival ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells ◽  
Wide Range ◽  
Beta Toxin

Staphylococcus aureus produces a variety of virulence factors that allow it to cause a wide range of infections in humans and animals. In the latter, S. aureus is a leading cause of intramammary infections. The contribution of catalase (KatA), an enzyme implicated in oxidative stress resistance, and beta-toxin (Hlb), a haemolysin, to the pathogenesis of S. aureus is poorly characterized. To investigate the role of these enzymes as potential virulence factors in S. aureus, we examined the intracellular survival of ΔkatA, Δhlb and ΔkatA Δhlb mutants in murine macrophages (J774A.1) and bovine mammary epithelial cells (MAC-T), and their virulence in different murine and ovine models. Catalase was not required for the survival of S. aureus within either J774A.1 or MAC-T cells. However, it was necessary for the intracellular proliferation of the bacterium after invasion of MAC-T cells. In addition, catalase was not needed for the full virulence of S. aureus in mice. Deletion of the hlb gene had no effect on the intracellular survival of S. aureus in J774A.1 cells but did cause a slight increase in survival in MAC-T cells. Furthermore, like catalase, beta-toxin was not required for complete virulence of S. aureus in murine models. Unexpectedly, the ΔkatA Δhlb mutant showed a notably increased persistence in both cell lines, and was significantly less virulent for mice than were the wild-type strain and single mutants. Most interestingly, it was also markedly attenuated in intramammary and subcutaneous infections in ewes and lambs.

Bacteriocin production by Actinobacillus actinomycetemcomitans isolated from the oral cavity of humans with periodontal disease, periodontally healthy subjects and marmosets

2002 ◽  
Vol 153 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Francisca Lúcia Lima ◽  
Flávio F Farias ◽  
José Eustáquio Costa ◽  
Maria Auxiliadora R Carvalho ◽  
Celuta S Alviano ◽  
...  
Keyword(s):  
Oral Cavity ◽  
Periodontal Disease ◽  
Healthy Subjects ◽  
Bacteriocin Production ◽  
Actinobacillus Actinomycetemcomitans

scholarly journals Characterization and Genetic Diversity of Listeria monocytogenes Isolated from Cattle Abortions in Latvia, 2013–2018

2021 ◽  
Vol 8 (9) ◽  
pp. 195
Author(s):  
Žanete Šteingolde ◽  
Irēna Meistere ◽  
Jeļena Avsejenko ◽  
Juris Ķibilds ◽  
Ieva Bergšpica ◽  
...  
Keyword(s):  
Genetic Diversity ◽  
Listeria Monocytogenes ◽  
Virulence Factors ◽  
Causative Agent ◽  
Animal Species ◽  
Clonal Complex ◽  
The Third ◽  
Wide Range ◽  
Sequence Types

Listeria monocytogenes can cause disease in humans and in a wide range of animal species, especially in farm ruminants. The aim of the study was to determine the prevalence and genetic diversity of L. monocytogenes related to 1185 cattle abortion cases in Latvia during 2013–2018. The prevalence of L. monocytogenes among cattle abortions was 16.1% (191/1185). The seasonality of L. monocytogenes abortions was observed with significantly higher occurrence (p < 0.01) in spring (March–May). In 61.0% of the cases, the affected cattle were under four years of age. L. monocytogenes abortions were observed during the third (64.6%) and second (33.3%) trimesters of gestation. Overall, 27 different sequence types (ST) were detected, and four of them, ST29 (clonal complex, CC29), ST37 (CC37), ST451 (CC11) and ST7 (CC7), covered more than half of the L. monocytogenes isolates. Key virulence factors like the prfA-dependent virulence cluster and inlA, inlB were observed in all the analyzed isolates, but lntA, inlF, inlJ, vip were associated with individual sequence types. Our results confirmed that L. monocytogenes is the most important causative agent of cattle abortions in Latvia and more than 20 different STs were observed in L. monocytogenes abortions in cattle.

Role of Suspected Periodontopathogens in Microbiological Monitoring of Periodontitis

1993 ◽  
Vol 7 (2) ◽  
pp. 163-174 ◽  
Author(s):  
G. Dahlén
Keyword(s):  
Periodontal Disease ◽  
Treatment Decision ◽  
Fusobacterium Nucleatum ◽  
The Body ◽  
Actinobacillus Actinomycetemcomitans ◽  
Risk Markers ◽  
Campylobacter Rectus ◽  
Localized Juvenile Periodontitis ◽  
Host Parasite

Periodontal disease is the clinical result of a complex interaction between the host and plaque bacteria. Although a specificity to some degree is found for Actinobacillus actinomycetemcomitans in localized juvenile periodontitis (LJP), it has been difficult to obtain evidence for a specific etiological role of the bacteria associated with periodontal disease in adults. What we see is the net result of host-parasite interactions which in an unpredictable moment accumulate and exceed the threshold of tissue integrity. This hypothesis is concomitant with the view of periodontal disease as a polymicrobial infection, predominantly anaerobic, which occurs commonly in the oral cavity or elsewhere in the body. Some micro-organisms (risk markers) occur more frequently than others and may significantly determine the outcome of this host-parasite interaction. Microbiological sampling and analysis seem to be of limited value in risk assessment; however, they can be used as tools in diagnosis in LJP patients and acute infections, and in treatment decision and therapy control in "refractory" patients. Suspected pathogens (risk markers) are Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and some species of spirochetes, while the roles of Prevotella intermedia, Bacteroides forsythus, Fusobacterium nucleatum, Campylobacter rectus, and Peptostreptococcus micros are more uncertain. The presence of periodontopathogens as well as enterics, Staphylococcus aureus and Candida especially, should be considered in patients with systemic individual disorders-e.g., diabetes mellitus, neutropenia, agranulocytosis, and AIDS-or with implants.

scholarly journals Beyond the Specific Plaque Hypothesis: Are Highly Leukotoxic Strains of Actinobacillus Actinomycetemcomitans a Paradigm for Periodontal Pathogenesis?

2001 ◽  
Vol 12 (2) ◽  
pp. 116-124 ◽  
Author(s):  
J.M. Guthmiller ◽  
E.T. Lolly ◽  
J. Korostoff
Keyword(s):  
Virulence Factors ◽  
Periodontal Diseases ◽  
Actinobacillus Actinomycetemcomitans ◽  
Pathogenic Potential ◽  
Periodontal Bacteria ◽  
Genes Encoding ◽  
Localized Juvenile Periodontitis ◽  
Different Populations

Actinobacillus actinomycetemcomitans is a facultative anaerobe implicated in a variety of periodontal diseases. Its presence is most closely associated with localized juvenile periodontitis (LJP), although the exact role of the organism in this and other periodontal diseases is not entirely clear. While A. actinomycetemcomitans produces several different putative virulence factors, the most widely studied is the leukotoxin. The leukotoxin selectively kills polymorphonuclear leukocytes and macrophages in vitro, constituting the host's first line of defense. Interestingly, even though all strains of A. actinomycetemcomitans have the genes encoding the leukotoxin, there is variability in leukotoxin expression. Differences in the structure of the promoter region of the leukotoxin gene operon were shown to correlate directly with levels of leukotoxin production. Highly leukotoxic forms appear to exhibit increased pathogenic potential, as evidenced by recent studies that have shown a significant association between the prevalence of such strains and the occurrence of LJP in several different populations. This represents the first demonstration of an association between a particular subset of a pathogenic species and a specific periodontal disease. Early identification of A. actinomycetemcomitans by microbial and genetic assays to evaluate leukotoxicity may enhance the efficacy of preventive and/or therapeutic techniques. Future investigations should continue to evaluate pathogenic variations of additional virulence factors expressed in vivo, not only of A. actinomycetemcomitans, but also of other periodontal bacteria and infectious disease pathogens.

scholarly journals Coronatine contributes to Pseudomonas cannabina pv. alisalensis virulence by overcoming both stomatal and apoplastic defenses in dicot and monocot plants

2021 ◽  
Author(s):  
Nanami Sakata ◽  
Takako Ishiga ◽  
Shunsuke Masuo ◽  
Yoshiteru Hashimoto ◽  
Yasuhiro Ishiga
Keyword(s):  
Virulence Factors ◽  
Causative Agent ◽  
Green Manure ◽  
Bacterial Blight ◽  
Host Plants ◽  
Deletion Mutants ◽  
Tomato Dc3000 ◽  
Wide Range ◽  
Infection Processes ◽  
Green Manure Crops

Pseudomonas cannabina pv. alisalensis (Pcal) is a causative agent of bacterial blight of crucifer including cabbage, radish, and broccoli. Importantly, Pcal can infect not only a wide range of Brassicaceae, but also green manure crops such as oat. However, Pcal virulence mechanisms have not been investigated and are not fully understood. We focused on coronatine (COR) function, which is one of the well-known P. syringae pv. tomato DC3000 virulence factors, in Pcal infection processes on both dicot and monocot plants. Cabbage and oat plants dip-inoculated with a Pcal KB211 COR mutant (ΔcmaA) exhibited reduced virulence compared to Pcal WT. Moreover, ΔcmaA failed to reopen stomata on both cabbage and oat, suggesting that COR facilitates Pcal entry through stomata into both plants. Furthermore, cabbage and oat plants syringe-infiltrated with ΔcmaA also showed reduced virulence, suggesting that COR is involved in overcoming not only stomatal-based defense, but also apoplastic defense. Indeed, defense related genes, including PR1 and PR2, were highly expressed in plants inoculated with ΔcmaA compared to Pcal WT, indicating that COR suppresses defense-related genes of both cabbage and oat. Additionally, SA accumulation increases after ΔcmaA inoculation compared to Pcal WT. Taken together, COR contributes to cause disease by suppressing stomatal-based defense and apoplastic defense in both dicot and monocot plants. Here, we investigated COR functions in the interaction of Pcal and different host plants (dicot and monocot plants) using genetically and biochemically defined COR deletion mutants.

scholarly journals SARS-CoV-2 drives JAK1/2-dependent local complement hyperactivation

2021 ◽  
Vol 6 (58) ◽  
pp. eabg0833
Author(s):  
Bingyu Yan ◽  
Tilo Freiwald ◽  
Daniel Chauss ◽  
Luopin Wang ◽  
Erin West ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Clinical Manifestations ◽  
Lung Epithelial Cells ◽  
Complement Factor ◽  
Respiratory Epithelial Cells ◽  
Signature Genes ◽  
Wide Range ◽  
Lung Epithelial ◽  
Gene Transcripts ◽  
Respiratory Epithelial

Patients with coronavirus disease 2019 (COVID-19) present a wide range of acute clinical manifestations affecting the lungs, liver, kidneys and gut. Angiotensin converting enzyme (ACE) 2, the best-characterized entry receptor for the disease-causing virus SARS-CoV-2, is highly expressed in the aforementioned tissues. However, the pathways that underlie the disease are still poorly understood. Here, we unexpectedly found that the complement system was one of the intracellular pathways most highly induced by SARS-CoV-2 infection in lung epithelial cells. Infection of respiratory epithelial cells with SARS-CoV-2 generated activated complement component C3a and could be blocked by a cell-permeable inhibitor of complement factor B (CFBi), indicating the presence of an inducible cell-intrinsic C3 convertase in respiratory epithelial cells. Within cells of the bronchoalveolar lavage of patients, distinct signatures of complement activation in myeloid, lymphoid and epithelial cells tracked with disease severity. Genes induced by SARS-CoV-2 and the drugs that could normalize these genes both implicated the interferon-JAK1/2-STAT1 signaling system and NF-κB as the main drivers of their expression. Ruxolitinib, a JAK1/2 inhibitor, normalized interferon signature genes and all complement gene transcripts induced by SARS-CoV-2 in lung epithelial cell lines, but did not affect NF-κB-regulated genes. Ruxolitinib, alone or in combination with the antiviral remdesivir, inhibited C3a protein produced by infected cells. Together, we postulate that combination therapy with JAK inhibitors and drugs that normalize NF-κB-signaling could potentially have clinical application for severe COVID-19.

scholarly journals Pseudomonas aeruginosa PA80 is a cystic fibrosis isolate deficient in RhlRI quorum sensing

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Syed A. K. Shifat Ahmed ◽  
Michelle Rudden ◽  
Sabrina M. Elias ◽  
Thomas J. Smyth ◽  
Roger Marchant ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Virulence Factors ◽  
Genomic Islands ◽  
Clinical Strain ◽  
Whole Genome ◽  
Synonymous Mutations ◽  
Wide Range

AbstractPseudomonas aeruginosa uses quorum sensing (QS) to modulate the expression of several virulence factors that enable it to establish severe infections. The QS system in P. aeruginosa is complex, intricate and is dominated by two main N-acyl-homoserine lactone circuits, LasRI and RhlRI. These two QS systems work in a hierarchical fashion with LasRI at the top, directly regulating RhlRI. Together these QS circuits regulate several virulence associated genes, metabolites, and enzymes in P. aeruginosa. Paradoxically, LasR mutants are frequently isolated from chronic P. aeruginosa infections, typically among cystic fibrosis (CF) patients. This suggests P. aeruginosa can undergo significant evolutionary pathoadaptation to persist in long term chronic infections. In contrast, mutations in the RhlRI system are less common. Here, we have isolated a clinical strain of P. aeruginosa from a CF patient that has deleted the transcriptional regulator RhlR entirely. Whole genome sequencing shows the rhlR locus is deleted in PA80 alongside a few non-synonymous mutations in virulence factors including protease lasA and rhamnolipid rhlA, rhlB, rhlC. Importantly we did not observe any mutations in the LasRI QS system. PA80 does not appear to have an accumulation of mutations typically associated with several hallmark pathoadaptive genes (i.e., mexT, mucA, algR, rpoN, exsS, ampR). Whole genome comparisons show that P. aeruginosa strain PA80 is closely related to the hypervirulent Liverpool epidemic strain (LES) LESB58. PA80 also contains several genomic islands (GI’s) encoding virulence and/or resistance determinants homologous to LESB58. To further understand the effect of these mutations in PA80 QS regulatory and virulence associated genes, we compared transcriptional expression of genes and phenotypic effects with isogenic mutants in the genetic reference strain PAO1. In PAO1, we show that deletion of rhlR has a much more significant impact on the expression of a wide range of virulence associated factors rather than deletion of lasR. In PA80, no QS regulatory genes were expressed, which we attribute to the inactivation of the RhlRI QS system by deletion of rhlR and mutation of rhlI. This study demonstrates that inactivation of the LasRI system does not impact RhlRI regulated virulence factors. PA80 has bypassed the common pathoadaptive mutations observed in LasR by targeting the RhlRI system. This suggests that RhlRI is a significant target for the long-term persistence of P. aeruginosa in chronic CF patients. This raises important questions in targeting QS systems for therapeutic interventions.

scholarly journals An In Vitro Cell Culture Model for Pyoverdine-Mediated Virulence

Pathogens ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 9
Author(s):  
Donghoon Kang ◽  
Natalia V. Kirienko
Keyword(s):  
Cell Culture ◽  
Virulence Factors ◽  
Model Organisms ◽  
Cell Culture Model ◽  
Chronic Infections ◽  
In Vitro Cell Culture ◽  
Mitochondrial Homeostasis ◽  
Culture Model ◽  
Wide Range

Pseudomonas aeruginosa is a multidrug-resistant, opportunistic pathogen that utilizes a wide-range of virulence factors to cause acute, life-threatening infections in immunocompromised patients, especially those in intensive care units. It also causes debilitating chronic infections that shorten lives and worsen the quality of life for cystic fibrosis patients. One of the key virulence factors in P. aeruginosa is the siderophore pyoverdine, which provides the pathogen with iron during infection, regulates the production of secreted toxins, and disrupts host iron and mitochondrial homeostasis. These roles have been characterized in model organisms such as Caenorhabditis elegans and mice. However, an intermediary system, using cell culture to investigate the activity of this siderophore has been absent. In this report, we describe such a system, using murine macrophages treated with pyoverdine. We demonstrate that pyoverdine-rich filtrates from P. aeruginosa exhibit substantial cytotoxicity, and that the inhibition of pyoverdine production (genetic or chemical) is sufficient to mitigate virulence. Furthermore, consistent with previous observations made in C. elegans, pyoverdine translocates into cells and disrupts host mitochondrial homeostasis. Most importantly, we observe a strong correlation between pyoverdine production and virulence in P. aeruginosa clinical isolates, confirming pyoverdine’s value as a promising target for therapeutic intervention. This in vitro cell culture model will allow rapid validation of pyoverdine antivirulents in a simple but physiologically relevant manner.

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