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Fungal ABC transporters and microbial interactions in natural environments.

In natural environments, microorganisms are exposed to a wide variety of antibiotic compounds produced by competing organisms. Target organisms have evolved various mechanisms of natural resistance to these metabolites. In this study, the role of ATP-binding cassette (ABC) transporters in interactions between the plant-pathogenic fungus Botrytis cinerea and antibiotic-producing Pseudomonas bacteria was investigated in detail. We discovered that 2,4-diacetylphloroglucinol, phenazine-1-carboxylic acid and phenazine-1-carboxamide (PCN), broad-spectrum antibiotics produced by Pseudomonas spp., induced expression of several ABC transporter genes in B. cinerea. Phenazines strongly induced expression of BcatrB, and deltaBcatrB mutants were significantly more sensitive to these antibiotics than their parental strain. Treatment of B. cinerea germlings with PCN strongly affected the accumulation of [14C]fludioxonil, a phenylpyrrole fungicide known to be transported by BcatrB, indicating that phenazines also are transported by BcatrB. Pseudomonas strains producing phenazines displayed a stronger antagonistic activity in vitro toward ABcatrB mutants than to the parental B. cinerea strain. On tomato leaves, phenazine-producing Pseudomonas strains were significantly more effective in reducing gray mold symptoms incited by a ABcatrB mutant than by the parental strain. We conclude that the ABC transporter BcatrB provides protection to B. cinerea in phenazine-mediated interactions with Pseudomonas spp. Collectively, these results indicate that fungal ABC transporters can play an important role in antibiotic-mediated interactions between bacteria and fungi in plant-associated environments. The implications of these findings for the implementation and sustainability of crop protection by antagonistic microorganisms are discussed.

ATP-Binding Cassette Transporters↗

Innate immunity in host-microbial interactions: beyond B27 in the spondyloarthropathies.

The spondyloarthropathies are diseases influenced by genetic predisposition and, to a varying extent, infectious triggers. A causal role for bacterial infections is most clear for reactive arthritis. Recent insights into arthritogenic components of bacteria may set the stage for a better understanding of disease pathogenesis, the role of heat shock proteins in antigen processing and immune activation, and the adjuvant effect of CpG-DNA. Recent developments in the area of innate immunity broaden current concepts of genetically defined factors in host-pathogen interactions. In particular, the biology of toll-like receptors as important elements in the innate immune response to pathogens is being defined. These factors in innate immunity may have important implications for sequelae of infections, such as reactive arthritis.

Animals↗

Microbial interactions in sediment communities.

Mineralization of organic matter in aquatic ecosystems with shallow waters occurs to a large extent in their sediments under anoxic conditions. This is achieved by a community of bacteria, which are the catalysts in a sequence of processes. Of the two possible terminal processes, methanogenesis and sulphate reduction, the first usually dominates in freshwater systems, whereas in estuarine and marine sediments electrons are mainly channelled to sulphate. Interactions between sulphate-reducing and methanogenic bacteria are described. Sulphate-reducing bacteria also show interactions with fermentative bacteria. After a brief description of properties of sulphate-reducing and fermentative bacteria occurring in sediments, examples are given of interactions between them. This is followed by the presentation of some results obtained from studies on competition for L-lactate between organisms belonging to both groups. It is shown that sulphate-reducing bacteria could successfully compete for L-lactate when this was available in growth-limiting amounts with sufficient sulphate and iron. Finally, a brief discussion is given of ecological niches of sulphide-oxidizing bacteria thriving in the upper sediment layers.

Anaerobiosis↗

The role of microbial interactions in infectious disease.

The occurrence of infectious disease is affected by interaction between microorganisms in three ways. The indigenous flora (commensal microorganisms) of some mucous surfaces provide one of the main protective mechanisms against infection by pathogens (disease-producing microbes). The commensal populations interfere with the establishment of pathogens on mucous membranes by evoking anaerobic conditions, by competing for space and nutrients and by producing inhibitors. How, at the beginning of successful infection, pathogens in relatively small numbers overcome this protective activity of the commensal population is unknown. Although not a general phenomenon, some pathogens exacerbate the effects of others. The best examples are the potentiation of bacterial infections by existing viral infections: mucosal adherence and penetration by bacteria are enhanced and phagocytic defences against them weakened. Some microorganisms that are unable to produce significant disease on their own may combine with others to cause serious sickness. The harmful effects of these combinations of microorganisms can be explained by the multifactorial nature of pathogenicity (virulence), i.e. the capacity to produce disease. Although each member of the mixed population cannot alone produce the full complement of factors needed for disease production, the complement can be attained by combining contributions from different members.

Bacteria↗

Dialysis membrane technique for ultrastructural studies of microbial interactions.

A dialysis membrane technique was developed that enabled ultrastructural investigations of the interaction of nematode-trapping fungi and their nematode prey. It allowed the sectioning of individual traps that had been selected by light microscopy and was used in kinetic studies on trap formation, nematode capture, and subsequent nematode digestion. The method can also be used for enzyme cytochemical experiments.

Animals↗

Effect of microbial interaction on the colonization rate of Actinomyces viscosus or Streptococcus mutans in the dental plaque of rats.

The resident oral microflora of conventional Osborne-Mendel rats was challenged with Actinomyces viscosus or Streptococcus mutans strains. The adherence of the inoculated organism to the tooth surface and the subsequent growth were studied by means of viable counts determination. The initial growth rate of S. mutans in conventional rats was lower than in mono-associated gnotobiotic rats (doubling time, td = 5 h versus td = 1.1 h). The delayed start of growth and the low initial growth rate indicated that a competitive interaction between S. mutans and the resident microflora occurred. The initial growth rate of A. viscosus in conventional rats (td = 3.1 h) was approximately the same as that in gnotobiotic rats (td = 2.8 h). The start of growth of A. viscosus was only slightly delayed compared with the start in gnotobiotic rats. These results suggest a neutralistic relationship between A. viscosus and the resident microflora. A. viscosus reached a stationary level about 7 days after inoculation, whereas the S. mutans strains did not reach stationary levels until 2 weeks after inoculation.

Actinomyces↗

Human intestinal epithelial cells are broadly unresponsive to Toll-like receptor 2-dependent bacterial ligands: implications for host-microbial interactions in the gut.

Intestinal epithelial cells (IEC) interact with a high density of Gram-positive bacteria and are active participants in mucosal immune responses. Recognition of Gram-positive organisms by Toll-like receptor (TLR)2 induces proinflammatory gene expression by diverse cells. We hypothesized that IEC are unresponsive to Gram-positive pathogen-associated molecular patterns and sought to characterize the functional responses of IEC to TLR2-specific ligands. Human colonic epithelial cells isolated by laser capture microscopy and IEC lines (Caco-2, T84, HT-29) were analyzed for expression of TLR2, TLR6, TLR1, and Toll inhibitory protein (Tollip) mRNA by RT-PCR and quantitative real-time PCR. Response to Gram-positive bacterial ligands was measured by NF-kappa B reporter gene activation and IL-8 secretion. TLR2 protein expression was analyzed by immunofluorescence and flow cytometry. Colonic epithelial cells and lamina propria cells from both uninflamed and inflamed tissue demonstrate low expression of TLR2 mRNA compared with THP-1 monocytes. IECs were unresponsive to TLR2 ligands including the staphylococcal-derived Ags phenol soluble modulin, peptidoglycan, and lipotechoic acid and the mycobacterial-derived Ag soluble tuberculosis factor. Transgenic expression of TLR2 and TLR6 restored responsiveness to phenol soluble modulin and peptidoglycan in IEC. In addition to low levels of TLR2 protein expression, IEC also express high levels of the inhibitory molecule Tollip. We conclude that IEC are broadly unresponsive to TLR2 ligands secondary to deficient expression of TLR2 and TLR6. The relative absence of TLR2 protein expression by IEC and high level of Tollip expression may be important in preventing chronic proinflammatory cytokine secretion in response to commensal Gram-positive bacteria in the gut.

Bacterial Toxins↗

[Some features of tonsillar microflora and microbial interaction (in normal and pathological states)].

The description of a new method for the determination of interaction between bacterial strains isolated from the mucous membrane of tonsils of healthy children and patients with chronic tonsillitis. In the analysis of mutual influence of symbionts on the hemolytic, lecitovitellase, lysozyme and antilysozyme activity of microbes isolated from healthy children no changes in the expression of these pathogenicity and persistence factors have been detected in the overwhelming majority of cases (70.8-89.9%). In the microflora of sick children interactions were synergic with respect to pathogenicity factors in 35.2-46.7% of cases and antagonistic in 18.7-31.3% of cases.

Adolescent↗