Browse
Submit Data
Databases
API
Help

Dataset Information

29 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chitosan coupling makes microbial biofilms susceptible to antibiotics.

ABSTRACT: Microbial biofilms, prevalent in nature and inherently resistant to both antimicrobial agents and host defenses, can cause serious problems in the chemical, medical and pharmaceutical industries. Herein we demonstrated that conjugation of an aminoglycoside antibiotic (streptomycin) to chitosan could efficiently damage established biofilms and inhibit biofilm formation. This method was suitable to eradiate biofilms formed by Gram-positive organisms, and it appeared that antibiotic contents, molecular size and positive charges of the conjugate were the key to retain this anti-biofilm activity. Mechanistic insight demonstrated chitosan conjugation rendered streptomycin more accessible into biofilms, thereby available to interact with biofilm bacteria. Thus, this work represent an innovative strategy that antibiotic covalently linked to carbohydrate carriers can overcome antibiotic resistance of microbial biofilms, and might provide a comprehensive solution to combat biofilms in industrial and medical settings.

SUBMITTER: Zhang A

PROVIDER: S-EPMC3842539 | biostudies-literature | 2013 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Chitosan coupling makes microbial biofilms susceptible to antibiotics.

Zhang Amin A Mu Haibo H Zhang Wuxia W Cui Guoting G Zhu Jie J Duan Jinyou J

Scientific reports 20131128

Microbial biofilms, prevalent in nature and inherently resistant to both antimicrobial agents and host defenses, can cause serious problems in the chemical, medical and pharmaceutical industries. Herein we demonstrated that conjugation of an aminoglycoside antibiotic (streptomycin) to chitosan could efficiently damage established biofilms and inhibit biofilm formation. This method was suitable to eradiate biofilms formed by Gram-positive organisms, and it appeared that antibiotic contents, molec ...[more]

PMID: 24284335

Similar Datasets

Secondary Effects of Antibiotics on Microbial Biofilms.

Project description:Biofilms are assemblages of microorganisms attached to each other, or to a surface, and encased in a protective, self-produced matrix. Such associations are now recognized as the predominant microbial growth mode. The physiology of cells in biofilms differs from that of the planktonic cells on which most research has been conducted. Consequently, there are significant gaps in our knowledge of the biofilm lifestyle. Filling this gap is particularly important, given that biofilm cells may respond differently to antibiotics than do planktonic cells of the same species. Understanding the effects of antibiotics on biofilms is of paramount importance for clinical practice due to the increased levels of antibiotic resistance and resistance dissemination in biofilms. From a wider environmental perspective antibiotic exposure can alter the ecology of biofilms in nature, and hence disrupt ecosystems. Biofilm cells display increased resilience toward antibiotics. This resilience is often explained by mechanisms and traits such as decreased antibiotic penetration, metabolically inactive persister cells, and intrinsic resistance by members of the biofilm community. Together, these factors suggest that cells in biofilms are often exposed to subinhibitory concentrations of antimicrobial agents. Here we discuss how cells in biofilms are affected by the presence of antibiotics at subinhibitory concentrations, and the possible ramifications of such secondary effects for healthcare and the environment.

| S-EPMC7492572 | biostudies-literature

Designed α-sheet peptides disrupt uropathogenic E. coli biofilms rendering bacteria susceptible to antibiotics and immune cells.

Project description:Uropathogenic Escherichia coli account for the largest proportion of nosocomial infections in the United States. Nosocomial infections are a major source of increased costs and treatment complications. Many infections are biofilm associated, rendering antibiotic treatments ineffective or cause additional complications (e.g., microbiome depletion). This work presents a potentially complementary non-antibiotic strategy to fight nosocomial infections by inhibiting the formation of amyloid fibrils, a proteinaceous structural reinforcement known as curli in E. coli biofilms. Despite extensive characterization of the fibrils themselves and their associated secretion system, mechanistic details of curli assembly in vivo remain unclear. We hypothesized that, like other amyloid fibrils, curli polymerization involves a unique secondary structure termed "α-sheet". Biophysical studies herein confirmed the presence of α-sheet structure in prefibrillar species of CsgA, the major component of curli, as it aggregated. Binding of synthetic α-sheet peptides to the soluble α-sheet prefibrillar species inhibited CsgA aggregation in vitro and suppressed amyloid fibril formation in biofilms. Application of synthetic α-sheet peptides also enhanced antibiotic susceptibility and dispersed biofilm-resident bacteria for improved uptake by phagocytic cells. The ability of synthetic α-sheet peptides to reduce biofilm formation, improve antibiotic susceptibility, and enhance clearance by macrophages has broad implications for combating biofilm-associated infections.

| S-EPMC10247742 | biostudies-literature

How do environment-dependent switching rates between susceptible and persister cells affect the dynamics of biofilms faced with antibiotics?

Project description:Persisters form sub-populations of stress-tolerant cells that play a major role in the capacity of biofilms to survive and recover from disturbances such as antibiotic treatments. The mechanisms of persistence are diverse and influenced by environmental conditions, and persister populations are more heterogeneous than formerly suspected. We used computational modeling to assess the impact of three switching strategies between susceptible and persister cells on the capacity of bacterial biofilms to grow, survive and recover from antibiotic treatments. The strategies tested were: (1) constant switches, (2) substrate-dependent switches and (3) antibiotic-dependent switches. We implemented these strategies in an individual-based biofilm model and simulated antibiotic shocks on virtual biofilms. Because of limited available data on switching rates in the literature, nine parameter sets were assessed for each strategy. Substrate and antibiotic-dependent switches allowed high switching rates without affecting the growth of the biofilms. Compared to substrate-dependent switches, constant and antibiotic-dependent switches were associated with higher proportions of persisters in the top of the biofilms, close to the substrate source, which probably confers a competitive advantage within multi-species biofilms. The constant and substrate-dependent strategies need a compromise between limiting the wake-up and death of persisters during treatments and leaving the persister state fast enough to recover quickly after antibiotic-removal. Overall, the simulations gave new insights into the relationships between the dynamics of persister populations in biofilms and their dynamics of growth, survival and recovery when faced with disturbances.

| S-EPMC5854711 | biostudies-literature

Microbial biofilms

Project description:Diabetic wound biofilms raw sequence reads

| PRJNA304940 | ENA

Marine Microbial Biofilms

Project description:Marine Microbial Biofilms Amplicon Raw sequence reads

| PRJNA978954 | ENA

Cannabinoid receptor 2 evolutionary gene loss makes parrots more susceptible to neuroinflammation.

Project description:In vertebrates, cannabinoids modulate neuroimmune interactions through two cannabinoid receptors (CNRs) conservatively expressed in the brain (CNR1, syn. CB1) and in the periphery (CNR2, syn. CB2). Our comparative genomic analysis indicates several evolutionary losses in the CNR2 gene that is involved in immune regulation. Notably, we show that the CNR2 gene pseudogenized in all parrots (Psittaciformes). This CNR2 gene loss occurred because of chromosomal rearrangements. Our positive selection analysis suggests the absence of any specific molecular adaptations in parrot CNR1 that would compensate for the CNR2 loss in the modulation of the neuroimmune interactions. Using transcriptomic data from the brains of birds with experimentally induced sterile inflammation we highlight possible functional effects of such a CNR2 gene loss. We compare the expression patterns of CNR and neuroinflammatory markers in CNR2-deficient parrots (represented by the budgerigar, Melopsittacus undulatus and five other parrot species) with CNR2-intact passerines (represented by the zebra finch, Taeniopygia guttata). Unlike in passerines, stimulation with lipopolysaccharide resulted in neuroinflammation in the parrots linked with a significant upregulation of expression in proinflammatory cytokines (including interleukin 1 beta (IL1B) and 6 (IL6)) in the brain. Our results indicate the functional importance of the CNR2 gene loss for increased sensitivity to brain inflammation.

| S-EPMC9727682 | biostudies-literature

The use of chitosan to damage Cryptococcus neoformans biofilms.

Project description:The use of indwelling medical devices (e.g. pacemakers, prosthetic joints, catheters, etc) continues to increase, yet these devices are all too often complicated by infections with biofilm-forming microbes with increased resistance to antimicrobial agents and host defense mechanisms. We investigated the ability of chitosan, a polymer isolated from crustacean exoskeletons, to damage biofilms formed by the pathogenic fungus Cryptococcus neoformans. Using 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino) carbonyl]-2H-tetrazolium-hydroxide (XTT) reduction assay and CFU determinations, we showed that chitosan significantly reduced both the metabolic activity of the biofilms and cell viability, respectively. We further demonstrated that chitosan penetrated biofilms and damaged fungal cells using confocal and scanning electron microscopy. Notably, melanization, an important virulence determinant of C. neoformans, did not protect cryptococcal biofilms against chitosan. The chitosan concentrations used in this study to evaluate fungal biofilm susceptibility were not toxic to human endothelial cells. Our results indicate that cryptococcal biofilms are susceptible to treatment with chitosan, suggesting an option for the prevention or treatment of fungal biofilms on indwelling medical devices.

| S-EPMC2783412 | biostudies-literature

Community Composition Determines Activity of Antibiotics against Multispecies Biofilms.

Project description:In young cystic fibrosis (CF) patients, Staphylococcus aureus is typically the most prevalent organism, while in adults, Pseudomonas aeruginosa is the major pathogen. More recently, it was observed that also Streptococcus anginosus plays an important role in exacerbations of respiratory symptoms. These species are often coisolated from CF lungs, yet little is known about whether antibiotic killing of one species is influenced by the presence of others. In the present study, we compared the activities of various antibiotics against S. anginosus, S. aureus, and P. aeruginosa when grown in monospecies biofilms with the activity observed in a multispecies biofilm. Our results show that differences in antibiotic activity against species grown in mono- and multispecies biofilms are species and antibiotic dependent. Fewer S. anginosus cells are killed by antibiotics that interfere with cell wall synthesis (amoxicillin plus sulbactam, cefepime, imipenem, meropenem, and vancomycin) in the presence of S. aureus and P. aeruginosa, while for ciprofloxacin, levofloxacin, and tobramycin, no difference was observed. In addition, we observed that the cell-free supernatant of S. aureus, but not that of P. aeruginosa biofilms, also caused this decrease in killing. Overall, S. aureus was more affected by antibiotic treatment in a multispecies biofilm, while for P. aeruginosa, no differences were observed between growth in mono- or multispecies biofilms. The results of the present study suggest that it is important to take the community composition into account when evaluating the effect of antimicrobial treatments against certain species in mixed biofilms.

| S-EPMC5571329 | biostudies-literature

Microbial biofilms and breast tissue expanders.

Project description:We previously developed and validated a vortexing-sonication technique for detection of biofilm bacteria on the surface of explanted prosthetic joints. Herein, we evaluated this technique for diagnosis of infected breast tissue expanders and used it to assess colonization of breast tissue expanders. From April 2008 to December 2011, we studied 328 breast tissue expanders at Mayo Clinic, Rochester, MN, USA. Of seven clinically infected breast tissue expanders, six (85.7%) had positive cultures, one of which grew Propionibacterium species. Fifty-two of 321 breast tissue expanders (16.2%, 95% CI, 12.3-20.7%) without clinical evidence of infection also had positive cultures, 45 growing Propionibacterium species and ten coagulase-negative staphylococci. While vortexing-sonication can detect clinically infected breast tissue expanders, 16 percent of breast tissue expanders appear to be asymptomatically colonized with normal skin flora, most commonly, Propionibacterium species.

| S-EPMC3730356 | biostudies-literature

Cooperation and conflict in microbial biofilms.

Project description:Biofilms, in which cells attach to surfaces and secrete slime (polymeric substances), are central to microbial life. Biofilms are often thought to require high levels of cooperation because extracellular polymeric substances are a shared resource produced by one cell that can be used by others. Here we examine this hypothesis by using a detailed individual-based simulation of a biofilm to investigate the outcome of evolutionary competitions between strains that differ in their level of polymer production. Our model includes a biochemical description of the carbon fluxes for growth and polymer production, and it explicitly calculates diffusion-reaction effects and the resulting solute gradients in the biofilm. An emergent property of these simple but realistic mechanistic assumptions is a strong evolutionary advantage to extracellular polymer production. Polymer secretion is altruistic to cells above a focal cell: it pushes later generations in their lineage up and out into better oxygen conditions, but it harms others; polymer production suffocates neighboring nonpolymer producers. This property, analogous to vertical growth in plants, suggests that polymer secretion provides a strong competitive advantage to cell lineages within mixed-genotype biofilms: global cooperation is not required. Our model fundamentally changes how biofilms are expected to respond to changing social conditions; the presence of multiple strains in a biofilm should promote rather than inhibit polymer secretion.

| S-EPMC1783407 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data