scholarly journals Helicobacter pylori Resists the Antimicrobial Activity of Calprotectin via Lipid A Modification and Associated Biofilm Formation

mBio ◽  
2015 ◽  
Vol 6 (6) ◽  
Author(s):  
Jennifer A. Gaddy ◽  
Jana N. Radin ◽  
Thomas W. Cullen ◽  
Walter J. Chazin ◽  
Eric P. Skaar ◽  
...  
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Cell Surface ◽  
Biofilm Formation ◽  
Lipid A ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Content Type ◽  
Bacterial Fitness ◽  
H Pylori

ABSTRACTHelicobacter pyloriis one of several pathogens that persist within the host despite a robust immune response.H. pylorielicits a proinflammatory response from host epithelia, resulting in the recruitment of immune cells which manifests as gastritis. Relatively little is known about howH. pylorisurvives antimicrobials, including calprotectin (CP), which is present during the inflammatory response. The data presented here suggest that one wayH. pylorisurvives the nutrient sequestration by CP is through alteration of its outer membrane. CP-treatedH. pyloridemonstrates increased bacterial fitness in response to further coculture with CP. Moreover, CP-treatedH. pyloricultures form biofilms and demonstrate decreased cell surface hydrophobicity. In response to CP, theH. pyloriLpx lipid A biosynthetic enzymes are not fully functional. The lipid A molecules observed inH. pyloricultures treated with CP indicate that the LpxF, LpxL, and LpxR enzyme functions are perturbed. Transcriptional analysis oflpxF,lpxL, andlpxRindicates that metal restriction by CP does not control this pathway through transcriptional regulation. Analyses ofH. pylorilpx mutants reveal that loss of LpxF and LpxL results in increased fitness, similar to what is observed in the presence of CP; moreover, these mutants have significantly increased biofilm formation and reduced cell surface hydrophobicity. Taken together, these results demonstrate a novel mechanism ofH. pyloriresistance to the antimicrobial activity of CP via lipid A modification strategies and resulting biofilm formation.IMPORTANCEHelicobacter pylorievades recognition of the host's immune system by modifying the lipid A component of lipopolysaccharide. These results demonstrate for the first time that the lipid A modification pathway is influenced by the host's nutritional immune response.H. pylori's exposure to the host Mn- and Zn-binding protein calprotectin perturbs the function of 3 enzymes involved in the lipid A modification pathway. Moreover, CP treatment ofH. pylori, or mutants with an altered lipid A, exhibit increased bacterial fitness and increased biofilm formation. This suggests thatH. pylorimodifies its cell surface structure to survive under the stress imposed by the host immune response. These results provide new insights into the molecular mechanisms that influence the biofilm lifestyle and how endotoxin modification, which rendersH. pyloriresistant to cationic antimicrobial peptides, can be inactivated in response to sequestration of nutrient metals.

scholarly journals Membrane Vesicle Formation as a Multiple-Stress Response Mechanism Enhances Pseudomonas putida DOT-T1E Cell Surface Hydrophobicity and Biofilm Formation

2012 ◽  
Vol 78 (17) ◽  
pp. 6217-6224 ◽  
Author(s):  
Thomas Baumgarten ◽  
Stefanie Sperling ◽  
Jana Seifert ◽  
Martin von Bergen ◽  
Frank Steiniger ◽  
...  
Keyword(s):  
Stress Response ◽  
Cell Surface ◽  
Pseudomonas Putida ◽  
Biofilm Formation ◽  
Membrane Vesicle ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Outer Membrane Vesicles ◽  
Stress Factors ◽  
Content Type

ABSTRACTAmong the adaptive responses of bacteria to rapid changes in environmental conditions, those of the cell envelope are known to be the most crucial. Therefore, several mechanisms with which bacteria change their cell surface and membranes in the presence of different environmental stresses have been elucidated. Among these mechanisms, the release of outer membrane vesicles (MV) in Gram-negative bacteria has attracted particular research interest because of its involvement in pathogenic processes, such as that ofPseudomonas aeruginosabiofilm formation in cystic fibrosis lungs. In this study, we investigated the role of MV formation as an adaptive response ofPseudomonas putidaDOT-T1E to several environmental stress factors and correlated it to the formation of biofilms. In the presence of toxic concentrations of long-chain alcohols, under osmotic stress caused by NaCl, in the presence of EDTA, and after heat shock, cells of this strain released MV within 10 min in the presence of a stressor. The MV formed showed similar size and charge properties, as well as comparable compositions of proteins and fatty acids. MV release caused a significant increase in cell surface hydrophobicity, and an enhanced tendency to form biofilms was demonstrated in this study. Therefore, the release of MV as a stress response could be put in a physiological context.

scholarly journals The Helicobacter pylori Autotransporter ImaA (HP0289) Modulates the Immune Response and Contributes to Host Colonization

2012 ◽  
Vol 80 (7) ◽  
pp. 2286-2296 ◽  
Author(s):  
William E. Sause ◽  
Andrea R. Castillo ◽  
Karen M. Ottemann
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Membrane Protein ◽  
Outer Membrane ◽  
Outer Membrane Protein ◽  
Dependent Manner ◽  
Wild Type ◽  
Content Type ◽  
H Pylori ◽  
Murine Infections

ABSTRACTThe human pathogenHelicobacter pyloriemploys a diverse collection of outer membrane proteins to colonize, persist, and drive disease within the acidic gastric environment. In this study, we sought to elucidate the function of the host-induced geneHP0289, which encodes an uncharacterized outer membrane protein. We first generated an isogenicH. pylorimutant that lacksHP0289and found that the mutant has a colonization defect in single-strain infections and is greatly outcompeted in mouse coinfection experiments with wild-typeH. pylori. Furthermore, we used protease assays and biochemical fractionation coupled with an HP0289-targeted peptide antibody to verify that the HP0289 protein resides in the outer membrane. Our previous findings showed that theHP0289promoter is upregulated in the mouse stomach, and here we demonstrate thatHP0289expression is induced under acidic conditions in an ArsRS-dependent manner. Finally, we have shown that theHP0289mutant induces greater expression of the chemokine interleukin-8 (IL-8) and the cytokine tumor necrosis factor alpha (TNF-α) in gastric carcinoma cells (AGS). Similarly, transcription of the IL-8 homolog keratinocyte-derived chemokine (KC) is elevated in murine infections with the HP0289 mutant than in murine infections with wild-typeH. pylori. On the basis of this phenotype, we renamed HP0289 ImaA forimmunomodulatoryautotransporter protein. Our work has revealed that genes inducedin vivoplay an important role inH. pyloripathogenesis. Specifically, the outer membrane protein ImaA modulates a component of the host inflammatory response, and thus may allowH. pylorito fine tune the host immune response based on ImaA expression.

scholarly journals Quercetin inhibits virulence properties of Porphyromas gingivalis in periodontal disease

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zhiyan He ◽  
Xu Zhang ◽  
Zhongchen Song ◽  
Lu Li ◽  
Haishuang Chang ◽  
...  
Keyword(s):  
Cell Surface ◽  
Periodontal Disease ◽  
Biofilm Formation ◽  
Cell Structure ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Laser Scanning Microscopy ◽  
Confocal Laser ◽  
Antimicrobial Effects ◽  
Virulence Properties

Abstract Porphyromonas gingivalis is a causative agent in the onset and progression of periodontal disease. This study aims to investigate the effects of quercetin, a natural plant product, on P. gingivalis virulence properties including gingipain, haemagglutinin and biofilm formation. Antimicrobial effects and morphological changes of quercetin on P. gingivalis were detected. The effects of quercetin on gingipains activities and hemolytic, hemagglutination activities were evaluated using chromogenic peptides and sheep erythrocytes. The biofilm biomass and metabolism with different concentrations of quercetin were assessed by the crystal violet and MTT assay. The structures and thickness of the biofilms were observed by confocal laser scanning microscopy. Bacterial cell surface properties including cell surface hydrophobicity and aggregation were also evaluated. The mRNA expression of virulence and iron/heme utilization was assessed using real time-PCR. Quercetin exhibited antimicrobial effects and damaged the cell structure. Quercetin can inhibit gingipains, hemolytic, hemagglutination activities and biofilm formation at sub-MIC concentrations. Molecular docking analysis further indicated that quercetin can interact with gingipains. The biofilm became sparser and thinner after quercetin treatment. Quercetin also modulate cell surface hydrophobicity and aggregation. Expression of the genes tested was down-regulated in the presence of quercetin. In conclusion, our study demonstrated that quercetin inhibited various virulence factors of P. gingivalis.

scholarly journals Variation in Cell Surface Hydrophobicity among Cryptococcus neoformans Strains Influences Interactions with Amoebas

mSphere ◽  
2020 ◽  
Vol 5 (2) ◽  
Author(s):  
Raghav Vij ◽  
Carina Danchik ◽  
Conor Crawford ◽  
Quigly Dragotakes ◽  
Arturo Casadevall
Keyword(s):  
Cell Surface ◽  
Cryptococcus Neoformans ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Natural Soil ◽  
Order Structure ◽  
Hydroxyl Groups ◽  
Biophysical Properties ◽  
Content Type ◽  
Biophysical Parameter

ABSTRACT Cryptococcus neoformans and Cryptococcus gattii are pathogenic fungi that cause significant morbidity and mortality. Cell surface hydrophobicity (CSH) is a biophysical parameter that influences the adhesion of fungal cells or spores to biotic and abiotic surfaces. C. neoformans is encased by polysaccharide capsule that is highly hydrophilic and is a critical determinant of virulence. In this study, we report large differences in the CSH of some C. neoformans and C. gattii strains. The capsular polysaccharides of C. neoformans strains differ in repeating motifs and therefore vary in the number of hydroxyl groups, which, along with higher-order structure of the capsule, may contribute to the variation in hydrophobicity that we observed. We found that cell wall composition, in the context of chitin-chitosan content, does not influence CSH. For C. neoformans, CSH correlated with phagocytosis by natural soil predator Acanthamoeba castellanii. Furthermore, capsular binding of the protective antibody (18B7), but not the nonprotective antibody (13F1), altered the CSH of C. neoformans strains. Variability in CSH could be an important characteristic in comparing the biological properties of cryptococcal strains. IMPORTANCE The interaction of a microbial cell with its environment is influenced by the biophysical properties of a cell. The affinity of the cell surface for water, defined by the cell surface hydrophobicity (CSH), is a biophysical parameter that varies among different strains of Cryptococcus neoformans. The CSH influences the phagocytosis of the yeast by its natural predator in the soil, the amoeba. Studying variation in biophysical properties like CSH gives us insight into the dynamic host-predator interaction and host-pathogen interaction in a damage-response framework.

scholarly journals Effect of Eugenol on Cell Surface Hydrophobicity, Adhesion, and Biofilm ofCandida tropicalisandCandida dubliniensisIsolated from Oral Cavity of HIV-Infected Patients

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Suelen Balero de Paula ◽  
Thais Fernanda Bartelli ◽  
Vanessa Di Raimo ◽  
Jussevania Pereira Santos ◽  
Alexandre Tadachi Morey ◽  
...  
Keyword(s):  
Cell Surface ◽  
Oral Cavity ◽  
Biofilm Formation ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Planktonic Cells ◽  
Hydrophobic Behavior ◽  
Significant Difference ◽  
Substrate Surfaces ◽  
Sessile Cells

MostCandidaspp. infections are associated with biofilm formation on host surfaces. Cells within these communities display a phenotype resistant to antimicrobials and host defenses, so biofilm-associated infections are difficult to treat, representing a source of reinfections. The present study evaluated the effect of eugenol on the adherence properties and biofilm formation capacity ofCandida dubliniensisandCandida tropicalisisolated from the oral cavity of HIV-infected patients. All isolates were able to form biofilms on different substrate surfaces. Eugenol showed inhibitory activity against planktonic and sessile cells ofCandidaspp. No metabolic activity in biofilm was detected after 24 h of treatment. Scanning electron microscopy demonstrated that eugenol drastically reduced the number of sessile cells on denture material surfaces. MostCandidaspecies showed hydrophobic behavior and a significant difference in cell surface hydrophobicity was observed after exposure of planktonic cells to eugenol for 1 h. Eugenol also caused a significant reduction in adhesion of mostCandidaspp. to HEp-2 cells and to polystyrene. These findings corroborate the effectiveness of eugenol againstCandidaspecies other thanC. albicans, reinforcing its potential as an antifungal applied to limit both the growth of planktonic cells and biofilm formation on different surfaces.

scholarly journals Factors associated with adherence to and biofilm formation on polystyrene byStenotrophomonas maltophilia: the role of cell surface hydrophobicity and motility

2008 ◽  
Vol 287 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Arianna Pompilio ◽  
Raffaele Piccolomini ◽  
Carla Picciani ◽  
Domenico D'Antonio ◽  
Vincenzo Savini ◽  
...  
Keyword(s):  
Cell Surface ◽  
Biofilm Formation ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Factors Associated

scholarly journals Biofilm Formation and Cell Surface Properties among Pathogenic and Nonpathogenic Strains of the Bacillus cereus Group

2009 ◽  
Vol 75 (20) ◽  
pp. 6616-6618 ◽  
Author(s):  
Sandrine Auger ◽  
Nalini Ramarao ◽  
Christine Faille ◽  
Agnès Fouet ◽  
Stéphane Aymerich ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cell Surface ◽  
Bacillus Cereus ◽  
Digestive Tract ◽  
Biofilm Formation ◽  
Cell Surface Hydrophobicity ◽  
Surface Hydrophobicity ◽  
Bacillus Cereus Group ◽  
Cell Surface Properties ◽  
Tract Infections

ABSTRACT Biofilm formation by 102 Bacillus cereus and B. thuringiensis strains was determined. Strains isolated from soil or involved in digestive tract infections were efficient biofilm formers, whereas strains isolated from other diseases were poor biofilm formers. Cell surface hydrophobicity, the presence of an S layer, and adhesion to epithelial cells were also examined.

scholarly journals Cholesterol Enhances Helicobacter pylori Resistance to Antibiotics and LL-37

2011 ◽  
Vol 55 (6) ◽  
pp. 2897-2904 ◽  
Author(s):  
David J. McGee ◽  
Alika E. George ◽  
Elizabeth A. Trainor ◽  
Katherine E. Horton ◽  
Ellen Hildebrandt ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Lipid A ◽  
Polymyxin B ◽  
Defined Medium ◽  
Vital Role ◽  
Content Type ◽  
The Two Cultures ◽  
H Pylori ◽  
The Impact

ABSTRACTThe human gastric pathogenHelicobacter pyloristeals host cholesterol, modifies it by glycosylation, and incorporates the glycosylated cholesterol onto its surface via a cholesterol glucosyltransferase, encoded bycgt. The impact of cholesterol onH. pyloriantimicrobial resistance is unknown.H. pyloristrain 26695 was cultured in Ham's F12 chemically defined medium in the presence or absence of cholesterol. The two cultures were subjected to overnight incubations with serial 2-fold dilutions of 12 antibiotics, six antifungals, and seven antimicrobial peptides (including LL-37 cathelicidin and human alpha and beta defensins). Of 25 agents tested, cholesterol-grownH. pyloricells were substantially more resistant (over 100-fold) to nine agents than wereH. pyloricells grown without cholesterol. These nine agents included eight antibiotics and LL-37.H. pyloriwas susceptible to the antifungal drug pimaricin regardless of cholesterol presence in the culture medium. Acgtmutant retained cholesterol-dependent resistance to most antimicrobials but displayed increased susceptibility to colistin, suggesting an involvement of lipid A. Mutation oflpxE, encoding lipid A1-phosphatase, led to loss of cholesterol-dependent resistance to polymyxin B and colistin but not other antimicrobials tested. Thecgtmutant was severely attenuated in gerbils, indicating that glycosylation is essentialin vivo. These findings suggest that cholesterol plays a vital role in virulence and contributes to the intrinsic antibiotic resistance ofH. pylori.

Sign in / Sign up

Export Citation Format

Share Document