Acidic Microenvironment Determines Antibiotic Susceptibility and Biofilm Formation of Pseudomonas aeruginosa
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Pseudomonas aeruginosa is the most prevalent bacterial species that contribute to cystic fibrosis (CF) respiratory failure. The impaired function of CF transmembrane conductance regulator leads to abnormal epithelial Cl-/HCO3- transport and acidification of airway surface liquid. However, it remains unclear why the CF lung is most commonly infected by Pseudomonas aeruginosa versus other pathogens. We carried out studies to investigate if lower pH helps Pseudomonas aeruginosa adapt and thrive in the CF-like acidic lung environment. Our results revealed that Pseudomonas aeruginosa generally forms more biofilm, induces antibiotic resistance faster in acidic conditions, and can be reversed by returning the acidic environment to physiologically neutral conditions. Pseudomonas aeruginosa appears to be highly adaptive to the CF-like acidic pH environment. By studying the effects of an acidic environment on bacterial response, we may provide a new therapeutic option in preventing chronic Pseudomonas aeruginosa infection and colonization.Keywords:
Multidrug tolerance
Lung infection
Colonisation
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Colonisation
Ectomycorrhiza
Salicaceae
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Pulmonary deterioration after B.cepacia complex (BCC) colonization has a heterogeneous pattern. The aim was to investigate the clinical outcome of BCC colonization in CF patients chronically colonized with P. aeruginosa.CF patients chronically colonized with P. aeruginosa were divided into three groups: intermittent (I), chronic (II) and no colonization (III) with BCC. Body mass index (BMI) percentile and spirometric parameters were analyzed at three different times in each group.Fifty-six patients chronically colonized with P. aeruginosa were included. Of these, 27 also had evidence of BCC colonization (13 intermittent and 14 chronic). BMI percentile was significantly lower among patients chronically colonized by both P. aeruginosa and BCC. Mean values of FEV1 and FVC % were also significantly lower in these patients, both at the time of chronic BCC colonization and 24 months forward.Chronic BCC colonization is associated with significant loss of lung function. Lower BMI might be a risk factor for chronic BCC colonization, preceding these events.
Burkholderia cepacia complex
Lung infection
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Colonisation
Colonisation resistance
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Abstract We investigated the effect of prior colonization of sterile soils by a range of soil microbes on the growth of Ralstonia solanacearum YUIRif43 in an earlier report (Soil Sci. Plant Nutr., 46, 449–459, 2000). Here, we report the effect of prior colonization of tomato roots, the host plant of the pathogen, by soil microbes on succeeding colonization by the pathogen. When the soil microbial community was introduced onto tomato roots, subsequent colonization by YUIRif431ux, a lux-marked mutant of YUIRif43, was remarkably suppressed compared with that in the absence of microorganisms which had previously colonized roots (hereafter referred to as priorcolonists). Soil bacteria, rather than fungi, were mainly responsible for the suppression. Next, the effect of individual microbial strains on the colonization by YUIRif43lux was examined. Some strains did not show any significant suppressive effect on subsequent colonization by YUIRif43Iux, unlike others. All the R. solanacearum strains used in this study, especially R. solanacearum NPSI (a weakly virulent mutant of YUl), were effective prior colonists against colonization by YUIRif431ux, that is, they markedly suppressed subsequent colonization by YUIRif431ux. Most of the strains that were effective prior colonists in soil in the earlier report were also effective at suppressing the colonization of tomato roots by YUIRif43Iux. YUIRif43lux competed on tomato roots with the strains that did not show previously an effect against colonization by YUIRif431ux, while root colonization by YUlRif43lux was reduced by co-inoculation with the strains that previously showed a colonization effect. These results suggested that soil bacteria were likely to be responsible for the suppression of colonization by YUIRif43lux of tomato roots, and that strains belonging to R. solanacearum among individual microbial strains might be the most effective antagonists against colonization by YUIRif431ux. Using Tn5-induced derivatives of a strain, Pseudomonas fluorescens MelRC2, one of the most effective priorcolonists, the contribution of motility, antibiosis, rhizosphere competence to the suppressiveness of P. fluorescens MelRC2 against colonization by YUIRif43lux were examined. Key Words: biological controlcompetitionprior colonization Pseudomonas fluorescens rhizosphere competence
Ralstonia solanacearum
Bacterial wilt
Colonisation
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BEAN ROOT COLONIZATION BY PSEUDOMONAS CEPACIA UPR 5C
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Persister cells are transiently antibiotic-tolerant and dormant subpopulations that are produced to escape the effects of antibiotics within biofilms or planktonic cell populations. Persister cells are of high clinical importance due to their tolerance to antimicrobial agents and subsequent failure in antibiotic treatments. Understanding persister cell formation mechanisms is therefore highly important for developing effective therapeutic strategies against pathogenic bacterial persisters. Several anti-persister compounds have been previously identified via isolation from natural resources or chemical synthesis. Furthermore, a combination of these compounds with antibiotics or non-antibiotic drugs also allows action on multiple targets while reducing the administration frequency. Here, we present a comprehensive overview of the clinical importance and formation mechanisms of persister cells as well as the current treatment strategies against persister cell formations in chronic infections.
Multidrug tolerance
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Bacterial cells may escape the effects of antibiotics without undergoing genetic change; these cells are known as persisters. Unlike resistant cells that grow in the presence of antibiotics, persister cells do not grow in the presence of antibiotics. These persister cells are a small fraction of exponentially growing cells (due to carryover from the inoculum) but become a significant fraction in the stationary phase and in biofilms (up to 1%). Critically, persister cells may be a major cause of chronic infections. The mechanism of persister cell formation is not well understood, and even the metabolic state of these cells is debated. Here, we review studies relevant to the formation of persister cells and their metabolic state and conclude that the best model for persister cells is still dormancy, with the latest mechanistic studies shedding light on how cells reach this dormant state.
Multidrug tolerance
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The opportunistic pathogen Pseudomonas aeruginosa (Pa) is a major concern for immunocompromised and cystic fibrosis patients.Chronic lung infections caused by Pa are generally considered incurable, in part, due to the bacteria's ability to form persister cells. These variants are categorized as being phenotypically dormant and highly tolerant to antibiotic treatment. Currently, the mechanisms involved in Pa persister cell formation is poorly understood. One promising candidate is the Pa filamentation induced by cAMP (FIC) domain containing toxin (PaFicT), which like other FIC toxins transiently inhibits cell growth. Genetic knockout and complementation by single copy chromosomal insertion was used to characterize paficT involvement in Pa persister cell formation. Toxicity and the PaFicT active site were examined by overexpression of wild-type and mutant protein variants. Antibiotic tolerance of PaFicT-induced Pa persister cells, was measured by minimum inhibitory concentration (MIC) analysis and compared to parental mostly non-persister populations. Deletion of paficT resulted in a 7.2-fold reduction in persister cell formation, which was fully complemented by re-insertion of the gene. Expression of PaFicT significantly increased persister cell formation by 5.9-fold, and this phenotype required a functional FIC active site motif. Unlike growing cell populations, PaFicT-induced persister cells were unaffected by 4 h treatment with 10 × MIC meropenem and showed an increased survival of 6.2 × 105-fold to tobramycin under the same conditions. Alternatively, survival of both persisters and parental, mostly non-persister, populations were below detectable levels following amikacin treatment. Results indicate a potential major involvement of PaFicT in Pa persister cell formation and multidrug tolerance.
Multidrug tolerance
Amikacin
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In the conditions of different treatments,studies were made of the variation laws of the colonization rate and colonization intensity when arbuscule mycorrhical fungi(AMF) colonizated Betula albo-sinensis.The result showed that in the natural condition,AMF's colonization and colonization intensity were high.Illumination intensity strengthening increased AMF's colonization and colonization intensity.Temperature rising and carbon dioxide concentration diploidizing promoted AMF's colonization intensity.Treatment of 4～7℃ higher than the present temperature would promote AMF's colonization.Treatments of 2～4℃ higher than the present temperature and carbon dioxide concentration diploidizing were inhibitoryin summer and promotive in autumn.From summer to autumn,AMF's colonization descended,but carbon dioxide concentration diploidizing would increase AMF's colonization.
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