托福听力背景知识:生物膜

　　Taxonomic diversity

　　Many different bacteria form biofilms, including gram-positive (e.g. Bacillus spp, Listeria monocytogenes, Staphylococcus spp, and lactic acid bacteria, including Lactobacillus plantarum and Lactococcus lactis) and gram-negative species (e.g. Escherichia coli, or Pseudomonas aeruginosa).[37] Cyanobacteria also form biofilms in aquatic environments.[38]

　　Biofilms are formed by bacteria that colonize plants, e.g. Pseudomonas putida, Pseudomonas fluorescens, and related pseudomonads which are common plant-associated bacteria found on leaves, roots, and in the soil, and the majority of their natural isolates form biofilms.[39] Several nitrogen-fixing symbionts of legumes such as Rhizobium leguminosarum and Sinorhizobium meliloti form biofilms on legume roots and other inert surfaces.[39]

　　Along with bacteria, biofilms are also generated by a range of eukaryotic organisms, including fungi e.g. Cryptococcus laurentii[40] and microalgae. Among microalgae, one of the main progenitors of biofilms are diatoms, which colonise both fresh and marine environments worldwide.[41][42]

　　For other species in disease-associated biofilms and biofilms arising from eukaryotes see below.

　　Biofilms and infectious diseases[edit]Biofilms have been found to be involved in a wide variety of microbial infections in the body, by one estimate 80% of all infections.[43] Infectious processes in which biofilms have been implicated include common problems such as bacterial vaginosis, urinary tract infections, catheter infections, middle-ear infections, formation of dental plaque,[44] gingivitis, coating contact lenses,[45] and less common but more lethal processes such as endocarditis, infections in cystic fibrosis, and infections of permanent indwelling devices such as joint prostheses and heart valves.[46][47] More recently it has been noted that bacterial biofilms may impair cutaneous wound healing and reduce topical antibacterial efficiency in healing or treating infected skin wounds.[48] Early detection of biofilms in wounds is crucial to successful chronic wound management. Although many techniques have developed to identify planktonic bacteria in viable wounds, few have been able to quickly and accurately identify bacterial biofilms. Future studies are needed to find means of identifying and monitoring biofilm colonization at the bedside to permit timely initiation of treatment.[49]

　　It has recently been shown that biofilms are present on the removed tissue of 80% of patients undergoing surgery for chronic sinusitis. The patients with biofilms were shown to have been denuded of cilia and goblet cells, unlike the controls without biofilms who had normal cilia and goblet cell morphology.[50] Biofilms were also found on samples from two of 10 healthy controls mentioned. The species of bacteria from intraoperative cultures did not correspond to the bacteria species in the biofilm on the respective patient's tissue. In other words, the cultures were negative though the bacteria were present.[51]

　　Biofilms can also be formed on the inert surfaces of implanted devices such as catheters, prosthetic cardiac valves and intrauterine devices. [52]

　　New staining techniques are being developed to differentiate bacterial cells growing in living animals, e.g. from tissues with allergy-inflammations.[53]

　　Research has shown that sub-therapeutic levels of β-lactam antibiotics induce biofilm formation in Staphylococcus aureus. This sub-therapeutic level of antibiotic may result from the use of antibiotics as growth promoters in agriculture, or during the normal course of antibiotic therapy. The biofilm formation induced by low-level methicillin was inhibited by DNase, suggesting that the sub-therapeutic levels of antibiotic also induce extracellular DNA release.[54] Moreover, from an evolutionary point of view, the creation of the tragedy of the commons in pathogenic microbes may provide advanced therapeutic ways for chronic infections caused by biofilms via genetically engineered invasive cheaters who can invade wild-types ‘cooperators’ of pathogenic bacteria until cooperator populations go to extinction or overall population ‘cooperators and cheaters ’ go to extinction.[55]

　　Dental plaque[edit]Dental plaque is an oral biofilm that adheres to the teeth and consists of many species of both bacteria and fungi (such as Streptococcus mutans and Candida albicans), embedded in salivary polymers and microbial extracellular products. The accumulation of microorganisms subjects the teeth and gingival tissues to high concentrations of bacterial metabolites which results in dental disease.[56]

　　The biofilm on the surface of teeth is frequently subject to oxidative stress[57] and acid stress.[58] Dietary carbohydrates can cause a dramatic decrease in pH in oral biofilms to values of 4 and below (acid stress).[58] A pH of 4 at body temperature of 37 °C causes depurination of DNA, leaving apurinic (AP) sites in DNA,[59] especially loss of guanine.[60]

　　The dental plaque biofilm can result in the disease dental caries if it is allowed to develop over time. An ecologic shift away from balanced populations within the dental biofilm is driven by certain (cariogenic) microbiological populations beginning to dominate when the environment favours them. The shift to an acidogenic, aciduric, and cariogenic microbiological population develops and is maintained by frequent consumption of fermentable dietary carbohydrate. The resulting activity shift in the biofilm (and resulting acid production within the biofilm, at the tooth surface) is associated with an imbalance between demineralization and remineralisation leading to net mineral loss within dental hard tissues (enamel and then dentin), the sign and symptom being a carious lesion. By preventing the dental plaque biofilm from maturing or by returning it back to a non-cariogenic state, dental caries can be prevented and arrested.[61] This can be achieved though the behavioural step of reducing the supply of fermentable carbohydrates (i.e. sugar intake) and frequent removal of the biofilm (i.e. toothbrushing).

　　A peptide pheromone quorum sensing signaling system in S. mutans includes the Competence Stimulating Peptide (CSP) that controls genetic competence.[62][63] Genetic competence is the ability of a cell to take up DNA released by another cell. Competence can lead to genetic transformation, a form of sexual interaction, favored under conditions of high cell density and/or stress where there is maximal opportunity for interaction between the competent cell and the DNA released from nearby donor cells. This system is optimally expressed when S. mutans cells reside in an actively growing biofilm. Biofilm grown S. mutans cells are genetically transformed at a rate 10- to 600-fold higher than S. mutans growing as free-floating planktonic cells suspended in liquid.[62]

　　When the biofilm, containing S. mutans and related oral streptococci, is subjected to acid stress, the competence regulon is induced, leading to resistance to being killed by acid.[58] As pointed out by Michod et al., transformation in bacterial pathogens likely provides for effective and efficient recombinational repair of DNA damages.[64] It appears that S. mutans can survive the frequent acid stress in oral biofilms, in part, through the recombinational repair provided by competence and transformation.

　　Streptococcus pneumoniae[edit]S. pneumoniae is the main cause of community-acquired pneumonia and meningitis in children and the elderly, and of septicemia in HIV-infected persons. When S. pneumonia grows in biofilms, genes are specifically expressed that respond to oxidative stress and induce competence.[65] Formation of a biofilm depends on competence stimulating peptide (CSP). CSP also functions as a quorum-sensing peptide. It not only induces biofilm formation, but also increases virulence in pneumonia and meningitis.