Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Microbial interactions”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,549 records · Page 86Linked to original sources
PubMed1996

Study of interaction effects of polyacrylic acid polymers (carbopol 940) on antimicrobial activity of methyl parahydroxybenzoate against some gram-negative, gram-positive bacteria and yeast.

Cosmetic or pharmaceutical formulations containing hydrophilic polymers of natural or synthetic origin, may be more exposed to successful microbial contamination because of a polymer-preservative interaction. The experimental data reported in this paper relate to the possible interference of Carbopol 940 with methyl parahydroxybenzoate. Results show that this hydrophilic polymer, widely employed in many formulations, exerts, on the contrary, an interesting synergism on microbicidal activity of the preserving agent against E. coli and P. Aeruginosa. A reduction in microbicidal activity against S. aureus and C. albicans is observed for a polymer concentration higher than that needed for anti-Gram-negative synergy.

Acrylic Resins↗
PubMed1999

Lung surfactant proteins (SP-A and SP-D) in non-adaptive host responses to infection.

The lung surfactant proteins A and D (SP-A and SP-D) are collectins composed of C-type lectin domains attached to collagen regions. SP-A and SP-D are mainly found in the surfactant covering the pulmonary epithelial cells, but are also produced by cells lining the gastrointestinal tract. The main role of SP-A and SP-D is to interact directly with carbohydrate on the surface of microbial pathogens, thereby initiating a variety of effector mechanisms. This review focuses on the non-adaptive host responses of SP-A and SP-D to infection. Interaction of SP-A and SP-D with phagocytes is discussed and the structure and function of the putative receptors for SP-A and SP-D is presented. SP-A and SP-D seem to be regulated in a way similar to acute-phase proteins in the course of inflammation and evidence for the involvement of SP-A and SP-D as immunomodulators as well as their role in clearing allergens and modulating effector mechanisms in allergic reactions is discussed.

Adaptation, Physiological↗
PubMed2000

Pathophysiologic basis of sepsis: considerations for future strategies of intervention.

OBJECTIVE: To analyze the implications for therapeutic advances in the treatment of sepsis and septic shock based on the mechanisms underlying the response to microbial infection. DATA SOURCES: Clinical trials and experimental models designed to determine the key mechanisms involved in cellular and molecular processes of inflammatory reactions. STUDY SELECTION: Analyses of normal immune reactions to microbial infection, processes involved in the development of sepsis, and reasons for frequent failure of regimens based on current therapeutic rationales. DATA EXTRACTION/SYNTHESIS: Review of the data suggests that the dysregulation of the immune system resulting in sepsis/septic shock is ineffectually blocked by interfering with the action of inflammatory mediators or cascades, as these processes may be too complex to be easily antagonized. Rather, blockade of the action of microbial products or of the intracellular processes activated by receptor interaction with these products may provide a more promising therapeutic alternative. CONCLUSIONS: The sepsis syndrome induced by microbial pathogens reflects excessive stimulation of the processes of innate immunity. Bacterial components reacting with specific receptors activate intracellular processes, resulting in the release of excessive amounts of mediators of inflammation as well as triggering multiple complex proteolytic cascades. Blockade or antagonism of the actions of individual intermediary messenger molecules has proved therapeutically unsuccessful, because blockade of mediators alone does not block the direct activation of processes such as coagulation and complement. The dysregulation that characterizes sepsis may be amenable to blockade of the bacterial components or to the intracellular pathways triggered by these products.

Humans↗
PubMed2003

Dynamics of microbial communities on marine snow aggregates: colonization, growth, detachment, and grazing mortality of attached bacteria.

We studied the dynamics of microbial communities attached to model aggregates (4-mm-diameter agar spheres) and the component processes of colonization, detachment, growth, and grazing mortality. Agar spheres incubated in raw seawater were rapidly colonized by bacteria, followed by flagellates and ciliates. Colonization can be described as a diffusion process, and encounter volume rates were estimated at about 0.01 and 0.1 cm(3) h(-1) for bacteria and flagellates, respectively. After initial colonization, the abundances of flagellates and ciliates remained approximately constant at 10(3) to 10(4) and approximately 10(2) cells sphere(-1), respectively, whereas bacterial populations increased at a declining rate to >10(7) cells sphere(-1). Attached microorganisms initially detached at high specific rates of approximately 10(-2) min(-1), but the bacteria gradually became irreversibly attached to the spheres. Bacterial growth (0 to 2 day(-1)) was density dependent and declined hyperbolically when cell density exceeded a threshold. Bacterivorous flagellates grazed on the sphere surface at an average saturated rate of 15 bacteria flagellate(-1) h(-1). At low bacterial densities, the flagellate surface clearance rate was approximately 5 x 10(-7) cm(2) min(-1), but it declined hyperbolically with increasing bacterial density. Using the experimentally estimated process rates and integrating the component processes in a simple model reproduces the main features of the observed microbial population dynamics. Differences between observed and predicted population dynamics suggest, however, that other factors, e.g., antagonistic interactions between bacteria, are of importance in shaping marine snow microbial communities.

Animals↗
PubMed1999

IL-6 levels in gingival crevicular fluid (GCF) from patients with non-insulin dependent diabetes mellitus (NIDDM), adult periodontitis and healthy subjects.

Cytokines play an important role in the pathology associated with chronic inflammatory diseases. One of these cytokines, interleukin 6 (IL-6) is a major mediator of the host response to tissue injury, infection and bone resorption. In the present study, gingival crevicular fluid (GCF) level of IL-6 was determined in patients with non-insulin dependent diabetes mellitus (NIDDM) with periodontitis, adult periodontitis, and healthy controls by use of an enzyme linked immunosorbent assay (ELISA). Twenty-four NIDDM patients with periodontitis, twenty-four adult periodontitis and twenty-four healthy controls were selected for the study. GCF sampling was performed on the vestibular aspects of maxillary incisors and canine teeth. Plaque index (PI), gingival index (GI), gingival bleeding time index (GBTI), probing depth (PD) and probing attachment levels (PAL) were recorded from each sampling area and also the entire dentition. NIDDM and adult periodontitis patients had numerous sites with radiographic evidence of alveolar bone resorption, loss of attachment and pocket depth greater than 3 mm. The mean GCF IL-6 level was 2.43 +/- 0.97 ng/ml in NIDDM patients, 1.31 +/- 0.92 ng/ml in adult periodontitis and 0.62 +/- 0.58 ng/ml in healthy subjects, respectively (p < 0.05). GCF IL-6 levels were markedly higher in NIDDM and adult periodontitis groups compared to the healthy controls. No correlation was found between GCF IL-6 levels and all clinical parameters. These findings suggested that GCF IL-6 levels were significantly higher in the area of inflammation and periodontal destruction locally. The high IL-6 levels in NIDDM patients might be due to different microbial flora in periodontal pockets and altered immune system. Future studies are needed to evaluate the complex interaction among IL-6 GCF levels, host response and local microbial environment in the NIDDM patients.

Adolescent↗
PubMed2005

Application of two types of CIM tube column for purification of microbial enzymes.

Chromatography conditions for two types of convection interaction media (CIM) tube monolithic column, DEAE-8 and C4-8, were investigated using three enzymes from different microorganisms. The enzymes were adsorbed on a CIM DEAE-8 tube column under the same conditions as conventional DEAE columns. The CIM C4-8 tube column required a high concentration of ammonium sulfate compared to the conventional C4 column for adsorbing the enzymes. The separation of enzymes on the CIM tube column chromatography was not affected at flow rates between 0.15 and 1.25 volumes of the column per min. Both columns were successfully applied to the purification of enzymes from crude enzyme solution. Thus, both CIM tube monolithic columns proved useful in greatly reducing the purification time, and could be used at any stage of enzyme purification.

Adsorption↗
PubMed1998

Molecular basis of host-pathogen interaction in septic shock.

Specific mechanisms of recognition of microbial products have been developed by host cells. Among these mechanisms, recognition of lipopolysaccharide of Gram-negative bacteria by CD14, a glycoprotein expressed at the surface of myelomonocytic cells, plays a major role. There is increasing evidence that CD14 also serves as a receptor for other microbial products including peptidoglycan of Gram-positive bacteria. A common theme is that CD14 represents a key molecule in innate immunity. Recognition of microbial products by host cells leads to cell activation and production of a large array of mediators that are necessary for the development of controlled inflammatory processes. When the activation process is out of control, such as in septic shock, these mediators can be detrimental to the host.

Animals↗
PubMed2002

Interactions between novel micro-organisms and intestinal flora.

Microbial strains traditionally used to ferment food have a long history of safe use and are, therefore, considered as generally recognised as safe. Many of these micro-organisms have also functional attributes and are included among probiotics. New species and strains of bacteria with desirable technological and functional properties are constantly being identified; in addition, micro-organisms can be engineered by recently developed biotechnological tools in order to accelerate strain improvement. Although the potentialities of novel micro-organisms with better probiotic and technological properties are promising, it cannot be assumed that they share the safety record of traditional micro-organisms, since they may pose unique challenges for human health. The risk assessment and safety evaluation of novel micro-organisms must focus, primarily, on their potential harmful effects, both direct and indirect, upon host resident intestinal microflora. Genetically modified micro-organisms need further assessment for the complete characterisation of the DNA rearrangement and of the final product, in order to establish the "substantial equivalence" with the parental strain.

Fermentation↗
PubMedDate not supplied

Role of surfactant protein A (SP-A)/lipid interactions for SP-A functions in the lung.

Surfactant protein A (SP-A), an oligomeric glycoprotein, is a member of a group of proteins named collectins that contain collagen-like and Ca(2+)-dependent carbohydrate recognition domains. SP-A interacts with a broad range of amphipathic lipids (glycerophospholipids, sphingophospholipids, glycosphingolipids, lipid A, and lipoglycans) that are present in surfactant or microbial membranes. This review summarizes SP-A/lipid interaction studies regarding the lipid system used (i.e., phospholipid vesicles, phospholipid monolayers, and lipids immobilized on silica or adsorbed on a solid support). The effect of calcium, ionic strength, and pH on the binding of SP-A to lipids and the subsequent lipid aggregation process is discussed. Current evidence suggests that hydrophobic-binding forces are involved in the peripherical association of SP-A to membranes. It is also proposed that fluid and liquid-ordered phase coexistence in surfactant membranes might favor partition of SP-A into those membranes. The binding of SP-A to surfactant membranes containing hydrophobic surfactant peptides makes possible the formation of a membrane reservoir in the alveolar fluid that is protected by SP-A against inactivation and improves the rate of surfactant film formation. In addition, the interaction of SP-A with membranes might enhance the affinity of SP-A for terminal carbohydrates of glycolipids or glycoproteins on the surface of invading microorganisms.

Animals↗
PubMed2004

Synergistic interaction in simultaneous exposure to Streptomyces californicus and Stachybotrys chartarum.

The microbial exposure associated with health complaints in moldy houses consists of a heterogeneous group of components, including both living and dead bacteria, fungi, and their metabolites and active compounds. However, little is known about the interactions between different microbes and their metabolites, although the cytotoxicity and inflammatory potential of certain individual microbes have been reported. In this study, we investigated the inflammatory responses of mouse RAW264.7 macrophages after exposure to six indoor air microbes (Aspergillus versicolor, Penicillium spinulosum, Stachybotrys chartarum, Bacillus cereus, Mycobacterium terrae, and Pseudomonas fluorescens) alone and together with the actinomycete Streptomyces californicus. The production of nitric oxide, levels of the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6), and cytotoxicity were measured. The coexposure to Sta. chartarum and Str. californicus caused a synergistic increase in the production of IL-6 but not other cytokines. In further experiments, the metabolites from Sta. chartarum or from closely related fungi (atranones B and E, satratoxin G, trichodermin, 7-alpha-hydroxytrichodermol, staplabin, and SMTP-7) and the known fungal toxins sterigmatocystin, citrinin, and ochratoxin A were each tested with Str. californicus. The testing revealed a synergistic response in TNF-alpha and IL-6 production after coexposure to Str. californicus with both trichodermin and 7-alpha-hydroxytrichodermol. Finally, the synergistic inflammatory response caused by Str. californicus and trichodermin together was studied by analyzing for the presence of nuclear factor-kappa-B (NF-kappa-B) in nuclear extracts of the exposed cells. The exposure to Str. californicus induced the binding of NF-kappa-B proteins to the NF-kappa-B consensus sequence as well as to the natural NF-kappa-B site of the IL-6 promoter. Adding trichodermin to the exposure did not increase the DNA binding.

Animals↗
PubMed1999

A natural variant of the cysteine protease virulence factor of group A Streptococcus with an arginine-glycine-aspartic acid (RGD) motif preferentially binds human integrins alphavbeta3 and alphaIIbbeta3.

The human pathogenic bacterium group A Streptococcus produces an extracellular cysteine protease [streptococcal pyrogenic exotoxin B (SpeB)] that is a critical virulence factor for invasive disease episodes. Sequence analysis of the speB gene from 200 group A Streptococcus isolates collected worldwide identified three main mature SpeB (mSpeB) variants. One of these variants (mSpeB2) contains an Arg-Gly-Asp (RGD) sequence, a tripeptide motif that is commonly recognized by integrin receptors. mSpeB2 is made by all isolates of the unusually virulent serotype M1 and several other geographically widespread clones that frequently cause invasive infections. Only the mSpeB2 variant bound to transfected cells expressing integrin alphavbeta3 (also known as the vitronectin receptor) or alphaIIbbeta3 (platelet glycoprotein IIb-IIIa), and binding was blocked by a mAb that recognizes the streptococcal protease RGD motif region. In addition, mSpeB2 bound purified platelet integrin alphaIIbbeta3. Defined beta3 mutants that are altered for fibrinogen binding were defective for SpeB binding. Synthetic peptides with the mSpeB2 RGD motif, but not the RSD sequence present in other mSpeB variants, blocked binding of mSpeB2 to transfected cells expressing alphavbeta3 and caused detachment of cultured human umbilical vein endothelial cells. The results (i) identify a Gram-positive virulence factor that directly binds integrins, (ii) identify naturally occurring variants of a documented Gram-positive virulence factor with biomedically relevant differences in their interactions with host cells, and (iii) add to the theme that subtle natural variation in microbial virulence factor structure alters the character of host-pathogen interactions.

Alleles↗
PubMed2004

Cell-to-cell signalling in Escherichia coli and Salmonella enterica.

Cell-to-cell signalling in prokaryotes that leads to co-ordinated behaviour has been termed quorum sensing. This type of signalling can have profound impacts on microbial community structure and host-microbe interactions. The Gram-negative quorum-sensing systems were first discovered and extensively characterized in the marine Vibrios. Some components of the Vibrio systems are present in the classical genetic model organisms Escherichia coli and Salmonella enterica. Both organisms encode a signal receptor of the LuxR family, SdiA, but not a corresponding signal-generating enzyme. Instead, SdiA of Salmonella detects and responds to signals generated only by other microbial species. Conversely, E. coli and Salmonella encode the signal-generating component of a second system (a LuxS homologue that generates AI-2), but the sensory apparatus for AI-2 differs substantially from the Vibrio system. The only genes currently known to be regulated by AI-2 in Salmonella encode an active uptake and modification system for AI-2. Therefore, it is not yet clear whether Salmonella uses AI-2 as a signal molecule or whether AI-2 has some other function. In E. coli, the functions of both SdiA and AI-2 are unclear due to pleiotropy. Genetic strategies to identify novel signalling systems have been performed with E. coli and Providencia stuartii. Several putative signalling systems have been identified, one that uses indole as a signal and another that releases what appears to be a peptide. The latter system has homologues in E. coli and Salmonella, as well as other bacteria, plants and animals. In fact, the protease components from Providencia and Drosophila are functionally interchangeable.

Bacterial Proteins↗
PubMed2006

Host-microbe interactions: shaping the evolution of the plant immune response.

The evolution of the plant immune response has culminated in a highly effective defense system that is able to resist potential attack by microbial pathogens. The primary immune response is referred to as PAMP-triggered immunity (PTI) and has evolved to recognize common features of microbial pathogens. In the coevolution of host-microbe interactions, pathogens acquired the ability to deliver effector proteins to the plant cell to suppress PTI, allowing pathogen growth and disease. In response to the delivery of pathogen effector proteins, plants acquired surveillance proteins (R proteins) to either directly or indirectly monitor the presence of the pathogen effector proteins. In this review, taking an evolutionary perspective, we highlight important discoveries over the last decade about the plant immune response.

Bacteria↗
PubMed1995

A critical assessment of the agar dilution chequerboard technique for studying in-vitro antimicrobial interactions using a representative beta-lactam, aminoglycoside and fluoroquinolone.

The agar dilution chequerboard technique of studying antimicrobial interactions was assessed by testing a representative beta-lactam (piperacillin/tazobactam), aminoglycoside (gentamicin) and fluoroquinolone (ciprofloxacin) against themselves, that is piperacillin/tazobactam plus piperacillin/tazobactam, gentamicin plus gentamicin and ciprofloxacin plus ciprofloxacin. In addition, combinations of piperacillin/tazobactam plus gentamicin or ciprofloxacin were also tested against Enterobacteriaceae and Acinetobacter spp. in triplicate. The agar dilution chequerboard technique did not reliably show addition when agents were combined with themselves, and there was also considerable variation when beta-lactam plus aminoglycoside or fluoroquinolone combinations when tested in triplicate. These observations, and problems with the design of the method, indicate that the chequerboard technique should be used only with adequate controls and replication, and then interpreted with extreme caution; ideally, it should not be used as a method of assessing antimicrobial interactions.

Acinetobacter↗
PubMed2005

Phytohormones mediate volatile emissions during the interaction of compatible and incompatible pathogens: the role of ethylene in Pseudomonas syringae infected tobacco.

Interactions between the phytohormones ethylene, salicylic acid (SA), and jasmonic acid (JA) are thought to regulate the specificity of induced plant defenses against microbial pathogens and herbivores. However, the nature of these interactions leading to induced plant volatile emissions during pathogen infection is unclear. We previously demonstrated that a complex volatile blend including (E)-beta-ocimene, methyl salicylate (MeSA), and numerous sesquiterpenes was released by tobacco plants, Nicotiana tabacum K326, infected with an avirulent/incompatible strain of Pseudomonas syringae pv. tomato (Pst DC3000). In contrast, a volatile blend, mainly consisting of MeSA and two unidentified sesquiterpenes, was released by plants infected with P. syringae pv. tabaci (Pstb) in a virulent/compatible interaction. In this study, we examined the interaction of multiple pathogen stresses, phytohormone signaling, and induced volatile emissions in tobacco. Combined pathogen infection involved the inoculation of one leaf with Pst DC 3000 and of a second leaf, from the same plant, with Pstb. Combined infection reduced emissions of ocimene and MeSA compared to plants infected with Pst DC 3000 alone, but with no significant changes in total sesquiterpene emissions. In the compatible interaction, Pstb elicited a large ethylene burst with a peak emission occurring 3 days after inoculation. In contrast, the incompatible interaction involving Pst DC3000 displayed no such ethylene induction. Pstb-induced ethylene production was not significantly altered by Pst DC3000 in the combined infection. We postulated that Pstb-induced ethylene production may play a regulatory role in altering the typical volatile emission in tobacco in response to Pst DC3000 infection. To clarify the role of ethylene, we dynamically applied ethylene to the headspace of tobacco plants following infection with Pst DC3000. Consistent with Pstb-induced ethylene, exogenous ethylene reduced both ocimene and MeSA emissions, and selectively altered the ratios and amounts of induced sesquiterpene emissions. Our findings suggest that ethylene can regulate the magnitude and blend of induced volatile emissions during pathogen infection.

Cyclopentanes↗
PubMed1999

In-vitro interactions of itraconazole with flucytosine against clinical isolates of Cryptococcus neoformans.

Treatment failures can occur in AIDS patients infected with Cryptococcus neoformans, despite aggressive antifungal therapy. Combination regimens with additive or synergic drugs could provide additional options for treating cryptococcosis. We studied the effects of itraconazole combined with flucytosine against 16 strains of C. neoformans var. neoformans. Combination therapy revealed different results for the various strains, including synergy (fractional inhibitory concentration (FIC) index 0.5, 63% of the interactions), addition (FIC >0.5 to 1.0, 31% of the interactions) and indifference (FIC >1.0 to <2.0, 6% of the interactions). Antagonism (FIC >2.0) was not observed. The efficacy of combination therapy was confirmed by quantitative cfu and killing curve assays. In particular, killing curves conducted in replicating cells showed that the addition of itraconazole prevented the development of flucytosine-resistant mutants of C. neoformans. These data show that the combination of itraconazole and flucytosine is significantly more active than either drug alone against C. neoformans in vitro.

Antifungal Agents↗
PubMed1996

Effect of nitric oxide on staphylococcal killing and interactive effect with superoxide.

The role of reactive nitrogen intermediates (RNI) such as nitric oxide (.NO) in host defense against pyogenic microorganisms is unclear, and the actual interactive effect of RNI and reactive oxidative intermediates (ROI) for microbial killing has not been determined. Since, in nature, ROI and RNI might be generated together within any local infection, we evaluated the separate and interactive effects of .NO and O2- on staphylococcal survival by using a simplified system devoid of eukaryotic cells. These studies showed that prolonged exposure of staphylococci to .NO does not result in early loss of viability but instead is associated with a dose-related delayed loss of viability. This effect is abrogated by the presence of hemoglobin, providing further evidence that the effect is RNI associated. Superoxide-mediated killing also is dose related, but in contrast to RNI-mediated killing, it is rapid and occurs within 2 h of exposure. We further show that the interaction of .NO and O(2)- results in decreased O(2)--mediated staphylococcal killing at early time points. .NO, however, appears to enhance or stabilize microbial killing over prolonged periods of incubation. This study did not produce evidence of early synergism of ROI and RNI, but it does suggest that .NO may contribute to host defense, especially when ROI-mediated killing is compromised.

Dose-Response Relationship, Drug↗
PubMed2005

Interactions between LPS and lung surfactant proteins.

After penetration into the lower airways, bacterial lipopolysaccharide (LPS) interacts with alveolar cells in a fluid environment consisting of pulmonary surfactant, a lipid-protein complex which prevents alveolar collapsing and participates in lung defense. The two hydrophilic surfactant components SP-A and SP-D are proteins with collagen-like and lectin domains (collectins) able to interact with carbohydrate-containing ligands present on microbial membranes, and with defined regions of LPS. This explains their capacity to damage the bacterial envelope and induce an antimicrobial effect. In addition, they modulate LPS-induced production of pro-inflammatory mediators in leukocytes by interaction with LPS or with leukocyte receptors. A third surfactant component, SP-C, is a small, highly hydrophobic lipopeptide which interacts with lipid A and reduces LPS-induced effects in macrophages and splenocyte cultures. The interaction of the different SPs with CD14 might explain their ability to modulate some LPS responses. Although the alveolar fluid contains other antiLPS and antimicrobial agents, SPs are the most abundant proteins which might contribute to protect the lung epithelium and reduce the incidence of LPS-induced lung injury. The presence of the surfactant collectins SP-A and SP-D in non-pulmonary tissues, such as the female genital tract, extends their field of action to other mucosal surfaces.

Amino Acid Sequence↗