Helicobacter pylori virulence factors and the host immune response: implications for therapeutic vaccination

2003 ◽  
Vol 11 (3) ◽  
pp. 134-138 ◽  
Author(s):  
Christian Prinz ◽  
Nadia Hafsi ◽  
Petra Voland
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Host Immune Response ◽  
Therapeutic Vaccination

Virulence of Enterococcus faecalis and Impact of Genome‐wide approaches

2011 ◽  
Vol 1 (1) ◽  
pp. 16-24
Author(s):  
Rakesh Kumar Patidar ◽  
Mithilesh Kumar Gupta ◽  
Vinod Singh
Keyword(s):  
Immune Response ◽  
Enterococcus Faecalis ◽  
Virulence Factors ◽  
Host Immune Response ◽  
Oral Infection ◽  
Bacterial Virulence ◽  
Host Defenses ◽  
Opportunistic Pathogens ◽  
New Therapies

Enterococci are well recognized opportunistic pathogens in human and animal infections. Enterococcus faecalis have attracted much attention in recent times due to their increased recognition as an oral infection. The severity of these infections depends on the host immune response and on the presence of virulence factors. Bacterial virulence factors enable a host to replicate and disseminate within a host in part by subverting or eluding host defenses. Application of genome‐wide approaches has led to the identification of new virulence factors that may serve as targets for new therapies. This review discusses the virulence factors of E. faecalis and impact of genome‐wide approaches.

scholarly journals Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk

2010 ◽  
Vol 23 (4) ◽  
pp. 713-739 ◽  
Author(s):  
Lydia E. Wroblewski ◽  
Richard M. Peek ◽  
Keith T. Wilson
Keyword(s):  
Gastric Cancer ◽  
Immune Response ◽  
Helicobacter Pylori ◽  
Clinical Outcomes ◽  
Disease Risk ◽  
Host Immune Response ◽  
Gastric Epithelium ◽  
Junctional Complex ◽  
Pathogenic Potential ◽  
H Pylori

SUMMARY Helicobacter pylori is a gastric pathogen that colonizes approximately 50% of the world's population. Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer, which is the second leading cause of cancer-related deaths worldwide. Once H. pylori colonizes the gastric environment, it persists for the lifetime of the host, suggesting that the host immune response is ineffective in clearing this bacterium. In this review, we discuss the host immune response and examine other host factors that increase the pathogenic potential of this bacterium, including host polymorphisms, alterations to the apical-junctional complex, and the effects of environmental factors. In addition to host effects and responses, H. pylori strains are genetically diverse. We discuss the main virulence determinants in H. pylori strains and the correlation between these and the diverse clinical outcomes following H. pylori infection. Since H. pylori inhibits the gastric epithelium of half of the world, it is crucial that we continue to gain understanding of host and microbial factors that increase the risk of developing more severe clinical outcomes.

scholarly journals Brucella Hijacks Host-Mediated Palmitoylation To Stabilize and Localize PrpA to the Plasma Membrane

2018 ◽  
Vol 86 (11) ◽  
Author(s):  
Juan M. Spera ◽  
Francisco Guaimas ◽  
María M. Corvi ◽  
Juan E. Ugalde
Keyword(s):  
Immune Response ◽  
Plasma Membrane ◽  
Host Cell ◽  
Virulence Factors ◽  
Cell Activity ◽  
Host Immune Response ◽  
Content Type ◽  
Cell Plasma ◽  
The Individual ◽  
Cellular Immune

ABSTRACT Brucellaceae are a group of pathogenic intracellular bacteria with the ability to modulate the host response, both at the individual cell level and systemically. One of the hallmarks of the virulence process is the capacity of the bacteria to downregulate the adaptive and acquired host immune response through a plethora of virulence factors that directly impact several key signaling cascades. PrpA is one of those virulence factors that alters, via its polyclonal B-cell activity, the humoral and cellular immune responses of the host, ultimately favoring the establishment of a chronic infection. Even though PrpA affects B cells, it directly targets macrophages, triggering a response that ultimately affects B lymphocytes. In the present article we report that PrpA is S-palmitoylated in two N-terminal cysteine residues by the host cell and that this modification is necessary for its biological activity. Our results demonstrate that S-palmitoylation promotes PrpA migration to the host cell plasma membrane and stabilizes the protein during infection. These findings add a new mechanism exploited by this highly evolved pathogen to modulate the host immune response.

scholarly journals The Immune Interplay between the Host and the Pathogen inAspergillus fumigatusLung Infection

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Helioswilton Sales-Campos ◽  
Ludmilla Tonani ◽  
Cristina Ribeiro Barros Cardoso ◽  
Márcia Regina Von Zeska Kress
Keyword(s):  
Immune Response ◽  
Virulence Factors ◽  
Host Immune Response ◽  
Protective Role ◽  
Acquired Immunity ◽  
Therapeutic Approaches ◽  
Complex Interplay ◽  
Th17 Response ◽  
Pathogen Virulence ◽  
Fine Regulation

The interplay betweenAspergillus fumigatusand the host immune response in lung infection has been subject of studies over the last years due to its importance in immunocompromised patients. The multifactorial virulence factors ofA. fumigatusare related to the fungus biological characteristics, for example, structure, ability to grow and adapt to high temperatures and stress conditions, besides capability of evading the immune system and causing damage to the host. In this context, the fungus recognition by the host innate immunity occurs when the pathogen disrupts the natural and chemical barriers followed by the activation of acquired immunity. It seems clear that a Th1 response has a protective role, whereas Th2 reactions are often associated with higher fungal burden, and Th17 response is still controversial. Furthermore, a fine regulation of the effector immunity is required to avoid excessive tissue damage associated with fungal clearance, and this role could be attributed to regulatory T cells. Finally, in this work we reviewed the aspects involved in the complex interplay between the host immune response and the pathogen virulence factors, highlighting the immunological issues and the importance of its better understanding to the development of novel therapeutic approaches for invasive lung aspergillosis.

scholarly journals Yeast-Host Interactions: Anadenanthera colubrina Modulates Virulence Factors of C. albicans and Inflammatory Response In Vitro

2021 ◽  
Vol 12 ◽  
Author(s):  
Carolina Medeiros de Almeida Maia ◽  
Silvana Pasetto ◽  
Cassiano Francisco Weege Nonaka ◽  
Edja Maria Melo de Brito Costa ◽  
Ramiro Mendonça Murata
Keyword(s):  
Immune Response ◽  
Antifungal Activity ◽  
Virulence Factors ◽  
Fungal Infections ◽  
Oral Candidiasis ◽  
Host Immune Response ◽  
Host Cells ◽  
Broth Microdilution Method ◽  
Cytokines Secretion

Oral candidiasis is one of the most common fungal infections in humans. Its incidence has increased widely, as well as the antifungal resistance, demanding for the search for novel antifungal therapeutic agents. Anadenanthera colubrina (Vell.) Brenan is a plant species that has been proven to possess pharmacological effects, including antifungal and anti-inflammatory activities. This study evaluated in vitro the effects of standardized A. colubrina extract on virulence factors of Candida albicans and its regulation on immune response through C. albicans-host interaction. Antifungal activity was evaluated by Broth Microdilution Method against reference Candida strains (C. albicans, C. glabrata, C. tropicalis; C. dubliniensis). Anti-biofilm effect was performed on C. albicans mature biofilm and quantified by CFU/mL/g of biofilm dry weight. Proleotlytic enzymatic activities of proteinase and phospholipase were assessed by Azocasein and Phosphatidylcholine assays, respectively. Cytotoxicity effect was determined by Cell Titer Blue Viability Assay on Human Gingival Fibroblasts. Co-cultured model was used to analyze C. albicans coexisting with HGF by Scanning Electron Microscopy and fluorescence microscopies; gene expression was assessed by RT-PCR of C. albicans enzymes (SAP-1, PLB-1) and of host inflammatory cytokines (IL-6, IL-8, IL-1β, IL-10). Cytokines secretion was analysed by Luminex. The extract presented antifungal effect with MIC<15.62 μg/ml against Candida strains. Biofilm and proteolytic activity were significant reduced at 312.4 μg/ml (20 × 15.62 μg/ml) extract concentration. Cell viability was maintained higher than 70% in concentrations up to 250 μg/ml (LD50 = 423.3 μg/ml). Co-culture microscopies demonstrated a substantial decreased in C. albicans growth and minimal toxicity against host cells. Gene expressions of SAP-1/PLB-1 were significantly down-regulated and host immune response was modulated by a significant decreased on IL-6 and IL-8 cytokines secretion. A. colubrina had antifungal activity on Candida strains, antibiofilm, and anti-proteolytic enzyme effects against C. albicans. Presented low cytotoxicity to the host cells and modulatory effects on the host immune response.

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