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PubMed2006

Fate determination of the flavin photoreceptions in the cyanobacterial blue light receptor TePixD (Tll0078).

PixD (Tll0078, Slr1694) is a BLUF (sensor of blue light using FAD)-type blue light receptor protein of the thermophilic cyanobacterium Thermosynechococcus elongatus BP-1 and the mesophilic cyanobacterium Synechocystis sp. PCC 6803. BLUF protein is known to show light-induced approximately 10 nm red shift of flavin absorption that is coupled with strengthening of the hydrogen bond between the O(4) of the isoalloxazine ring and a certain amino acid residue. According to the 3D structure of TePixD we determined, O(4) of the ring is linked to Gln50 and Asn32. A survey of flavin-interacting residues by site-directed mutagenesis showed that Gln50 but not Asn32 is essential for the normal red-shifting photoreaction. Here, we further studied the role of Gln50 and its close neighbor Tyr8. All the mutated proteins of Gln50 and Tyr8 (Q50A, Q50N, Y8A and Y8F) lost the normal red-shifting photoreaction. Y8A, Y8F and Q50N, instead, showed a light-induced flavin triplet state and a low yield of subsequent flavin reduction that is analogous to the photocycle of the LOV (light-oxygen-voltage-sensing) domain of phototropins, while Q50A did not. Fourier-transform infrared (FT-IR) analysis of N32A showed that O(4) of the ring is hydrogen-bonded to Asn32 both in the light and dark. These results, together with the 3D structure, indicate that the hydrogen bond network of Tyr8-Gln50-O(4)/N(5) (flavin) is critical for the light reaction of the BLUF domain. Based on the structural and functional similarities of the BLUF and the LOV domain of phototropins, we propose that the interaction between apoprotein and N(5) of flavin determines the photoreaction of the flavin-binding sensors.

Amino Acid Substitution↗
PubMed2001

Spectroscopic characterization of the photocycle intermediates of photoactive yellow protein.

The absorption spectra of photocycle intermediates of photoactive yellow protein mutants were compared with those of the corresponding intermediates of wild type to probe which amino acid residues interact with the chromophore in the intermediate states. B and H intermediates were produced by irradiation and trapped at 80 K, and L intermediates at 193 K. The absorption spectra of these intermediates produced from R52Q were identical to those from wild type, whereas those from E46Q and T50V were 7-15 nm red-shifted as those in the dark states. The absorption spectra of M intermediates were measured by flash photolysis at room temperature. Those of Y42F, T50V, and R52Q were identical to that of wild type, whereas that of E46Q was 11 nm red-shifted. Assuming that the intermediates of mutants have a structure comparable to that of wild type, these findings suggest the following: Glu46 interacts with the chromophore throughout the photocycle, interaction between the chromophore and Thr50 as well as Tyr42 is lost upon the formation of M intermediate, and Arg52 never interacts with the chromophore directly. The hydrogen-bonding network around the phenolic oxygen of the chromophore would be thus maintained until L intermediate decays, and the global conformational change would take place by the loss of the hydrogen bond between the chromophore and Tyr42. This model conflicts with some of the results of previous crystallographic studies, suggesting that the reaction mechanism in the crystal may be different from that in solution.

Amino Acids↗
PubMed2000

Anorexia of infection: current prospects.

The anorexia of infection is part of the host's acute phase response (APR). Despite being beneficial in the beginning, long lasting anorexia delays recovery and is ultimately deleterious. Microbial products such as bacterial cell wall compounds (e.g., lipopolysaccharides and peptidoglycans), microbial nucleic acids (e. g., bacterial DNA and viral double-stranded RNA), and viral glycoproteins trigger the APR and presumably also the anorexia during infections. Microbial products stimulate the production of proinflammatory cytokines (e.g., interleukins [ILs], tumor necrosis factor-alpha, interferons), which serve as endogenous mediators. Several microbial products and cytokines reduce food intake after parenteral administration, suggesting a role of these substances in the anorexia during infection. Microbial products are mainly released and cytokines are produced in the periphery during most infections; they might inhibit feeding through neural and humoral pathways activated by their peripheral actions. Activation of peripheral afferents by locally produced cytokines is involved in several cytokine effects, but is not crucial for the anorectic effect of microbial products and IL-1beta. Cytokines increase leptin expression in the adipose tissue, and leptin may contribute to, but is also not essential for, the anorectic effects of microbial products and cytokines. In addition, a direct action of cytokines and microbial products on the central nervous system (CNS) is presumably involved in the anorexia during infection. Cytokines can reach CNS receptors through circumventricular organs and through active or passive transport mechanisms or they can act through receptors on endothelial cells of the brain vasculature and stimulate the release of subsequent mediators such as eicosanoids. De novo CNS cytokine synthesis occurs in response to peripheral infections, but its role in the accompanying anorexia is still open to discussion. Central mediators of the anorexia during infection appear to be neurochemicals involved in the normal control of feeding, such as serotonin, dopamine, histamine, corticotropin releasing factor, neuropeptide Y, and alpha-melanocyte-stimulating hormone. Reciprocal, synergistic, and antagonistic interactions between various pleiotropic cytokines, and between cytokines and neurochemicals, form a complex network that mediates the anorexia during infection. Current knowledge on the mechanisms involved suggests some therapeutic options for treatment. Substances that block common key steps in cytokine synthesis or cytokine action, or inhibitors of eicosanoid synthesis, may hold more promise than attempts to antagonize specific cytokines. To target the neurochemical mediation of the anorexia during infection may be even more efficient. Future research should address these neurochemical mechanisms and the cytokine actions at the blood-brain barrier. Further unanswered questions concern the modulation of the anorexia during infection by gender and nutritional state.

Acute-Phase Reaction↗
PubMed2006

A systems biology analysis of the Drosophila phagosome.

Phagocytes have a critical function in remodelling tissues during embryogenesis and thereafter are central effectors of immune defence. During phagocytosis, particles are internalized into 'phagosomes', organelles from which immune processes such as microbial destruction and antigen presentation are initiated. Certain pathogens have evolved mechanisms to evade the immune system and persist undetected within phagocytes, and it is therefore evident that a detailed knowledge of this process is essential to an understanding of many aspects of innate and adaptive immunity. However, despite the crucial role of phagosomes in immunity, their components and organization are not fully defined. Here we present a systems biology analysis of phagosomes isolated from cells derived from the genetically tractable model organism Drosophila melanogaster and address the complex dynamic interactions between proteins within this organelle and their involvement in particle engulfment. Proteomic analysis identified 617 proteins potentially associated with Drosophila phagosomes; these were organized by protein-protein interactions to generate the 'phagosome interactome', a detailed protein-protein interaction network of this subcellular compartment. These networks predicted both the architecture of the phagosome and putative biomodules. The contribution of each protein and complex to bacterial internalization was tested by RNA-mediated interference and identified known components of the phagocytic machinery. In addition, the prediction and validation of regulators of phagocytosis such as the 'exocyst', a macromolecular complex required for exocytosis but not previously implicated in phagocytosis, validates this strategy. In generating this 'systems-based model', we show the power of applying this approach to the study of complex cellular processes and organelles and expect that this detailed model of the phagosome will provide a new framework for studying host-pathogen interactions and innate immunity.

Animals↗
PubMed2026

Phylum-wide propionate degradation and its potential connection to poly-gamma-glutamate biosynthesis in Candidatus Cloacimonadota phylum.

The candidate phylum Cloacimonadota is frequently detected in anoxic environments such as anaerobic digestion (AD) reactors, hydrothermal vents, and deep-sea sediments, yet its metabolism remains poorly understood. Metagenomic evidence suggests capacities for amino acid fermentation, carbohydrate degradation, as well as a potential role in syntrophic propionate oxidation (SPO), a key bottleneck in AD. However, a complete methylmalonyl-CoA (mmc) pathway, central to SPO, has not been previously identified in Cloacimonadota genomes. Here, we report results from an acidified lab-scale anaerobic baffled reactor fed with sugar beet pulp, where an increase in the relative abundance of Cloacimonadota correlated with recovery of methanogenesis, resulting in increased methane content in the produced biogas. Metagenomic and metatranscriptomic analyses enabled metabolic reconstruction of the dominant Cloacimonadota operational taxonomic unit (OTU). Furthermore, using a curated database of 204 genome-resolved Cloacimonadota species, we characterized the phylum-level metabolic potential. Comparative genomics revealed alternative proteins, including 2-oxoglutarate:ferredoxin oxidoreductase and aspartate aminotransferase, likely to substitute for missing enzymes in the classical mmc pathway. These proteins were widely distributed and highly conserved across the analyzed Cloacimonadota genomes, suggesting that this variant of the SPO pathway could represent a phylum-specific trait. Moreover, we hypothesize that these alternative pathway steps may link propionate metabolism to protein degradation and poly-γ-glutamate biosynthesis. Network analysis identified the methanogenic archaeon Methanothrix as a potential syntrophic partner, an interaction further supported by propionate-fed enrichment cultures showing co-occurrence of Cloacimonadota and Methanothrix species. Our study sheds light on the Cloacimonadota metabolism, advancing our understanding of their ecological roles and potential for biotechnological applications.

Propionates↗
PubMed1995

1.4 A structure of photoactive yellow protein, a cytosolic photoreceptor: unusual fold, active site, and chromophore.

A photosensing protein directs light energy captured by its chromophore into a photocycle. The protein's structure must accommodate the photocycle and promote the resulting chemical or conformational changes that lead to signal transduction. The 1.4 A crystallographic structure of photoactive yellow protein, determined by multiple isomorphous replacement methods, provides the first view at atomic resolution of a protein with a photocycle. The alpha/beta fold, which differs from the original chain tracing, shows striking similarity to distinct parts of the signal transduction proteins profilin and the SH2 domain. In the dark state structure of photoactive yellow protein, the novel 4-hydroxycinnamyl chromophore, covalently attached to Cys69, is buried within the major hydrophobic core of the protein and is tethered at both ends by hydrogen bonds. In the active site, the yellow anionic form of the chromophore is stabilized by hydrogen bonds from the side chains of Tyr42 and buried Glu46 to the phenolic oxygen atom and by electrostatic complementarity with the positively charged guanidinium group of Arg52. Thr50 further interlocks Tyr42, Glu46, and Arg52 through a network of active site hydrogen bonds. Arg52, located in a concavity of the protein surface adjacent to the dominant patch of negative electrostatic potential, shields the chromophore from solvent and is positioned to form a gateway for the phototactic signal. Overall, the high-resolution structure of photoactive yellow protein supports a mechanism whereby electrostatic interactions create an active site poised for photon-induced rearrangements and efficient protein-mediated signal transduction.

Amino Acid Sequence↗
PubMed1998

Cytokines in sarcoidosis.

Although the cause of sarcoidosis is still unknown, the combination of the characteristic morphologic aspect and the immunohistologic pattern of the sarcoid granulomatous lesions suggest that they are the result of an antigen-driven process. In particular, sarcoid granuloma is considered to be the consequence of an exaggerated immunological response against an undefined antigen which has persisted at the sites of disease involvement. Taking advantage of the availability of pure recombinant cytokines and molecular probes for cytokines and their receptors, in the last few years it has been possible to keenly study the involvement of several cytokines in the pathologic changes associated with sarcoidosis. The purpose of this review is to summarize the interactions between cytokines and their receptors which define regulatory networks ultimately contributing to the sarcoid granuloma formation at sites of disease activity. After a concise overview of the main cytokines involved in the sarcoid inflammatory response, we will briefly discuss the biological effects of Th1 and Th2 cytokines in sarcoid lung and then concentrate on the importance of the local production of those molecules whose release has been recently shown within the lung of patients with sarcoidosis, such as interleukin-12, interleukin-15, and chemokines. Furthermore, we will focus the discussion on the cytokines which, pivotal to the activation of the host defenses, may contribute to lung damage and the consequent lung fibrosis. The final section of this article reviews the lung release of cytokines in the context of recent hypotheses claiming microbial pathogens as putative causative agents of sarcoidosis.

Cytokines↗
PubMed2025

Deciphering microbial and metabolic influences in gastrointestinal diseases-unveiling their roles in gastric cancer, colorectal cancer, and inflammatory bowel disease.

INTRODUCTION: Gastrointestinal disorders (GIDs) affect nearly 40% of the global population, with gut microbiome-metabolome interactions playing a crucial role in gastric cancer (GC), colorectal cancer (CRC), and inflammatory bowel disease (IBD). This study aims to investigate how microbial and metabolic alterations contribute to disease development and assess whether biomarkers identified in one disease could potentially be used to predict another, highlighting cross-disease applicability. METHODS: Microbiome and metabolome datasets from Erawijantari et al. (GC: n = 42, Healthy: n = 54), Franzosa et al. (IBD: n = 164, Healthy: n = 56), and Yachida et al. (CRC: n = 150, Healthy: n = 127) were subjected to three machine learning algorithms, eXtreme gradient boosting (XGBoost), Random Forest, and Least Absolute Shrinkage and Selection Operator (LASSO). Feature selection identified microbial and metabolite biomarkers unique to each disease and shared across conditions. A microbial community (MICOM) model simulated gut microbial growth and metabolite fluxes, revealing metabolic differences between healthy and diseased states. Finally, network analysis uncovered metabolite clusters associated with disease traits. RESULTS: Combined machine learning models demonstrated strong predictive performance, with Random Forest achieving the highest Area Under the Curve(AUC) scores for GC(0.94[0.83-1.00]), CRC (0.75[0.62-0.86]), and IBD (0.93[0.86-0.98]). These models were then employed for cross-disease analysis, revealing that models trained on GC data successfully predicted IBD biomarkers, while CRC models predicted GC biomarkers with optimal performance scores. CONCLUSION: These findings emphasize the potential of microbial and metabolic profiling in cross-disease characterization particularly for GIDs, advancing biomarker discovery for improved diagnostics and targeted therapies.

Humans↗
PubMed2003

Biotechnological approaches to the production of idiotypic vaccines and antiidiotypic antibiotics.

The potential therapeutic activity of a killer toxin produced by the yeast Pichia anomala (PaKT) characterized by its wide spectrum of antimicrobial activity has been exploited through the simulation of its interaction with the specific cell wall receptor (KTR) of PaKT-sensitive microorganisms by the idiotypic network. Killer antiidiotypes (PaKTantiId) produced by idiotypic vaccination with a PaKT-neutralizing monoclonal antibody have proven to confer active and passive immunoprotection in experimental models of systemic and vaginal candidiasis. PaKTantiId-like human anti-KTR antibodies are naturally produced in infections caused by PaKT-sensitive microorganisms. PaKTantiId in its monoclonal and recombinant formats as well as expressed on human commensal bacteria have shown microbicidal activity in vitro and a therapeutic effect in experimental models of infection caused by PaKT-sensitive microorganisms. New perspectives of idiotypic vaccination and antiidiotypic antibiotic therapy and biotechnological approaches to the production of trandisease idiotypic vaccines and wide-spectrum antiidiotypic antibiotics (killer mimotopes) will be discussed as effective tools to fight epidemiologically important mucosal and systemic microbial infections.

Animals↗
PubMed1992

Inflammatory cytokines.

The immune system produces cytokines and other humoral factors to protect the host when threatened by inflammatory agents, microbial invasion, or injury. In some cases this complex defense network successfully restores normal homeostasis, but at other times the overproduction of immunoregulatory mediators may actually prove deleterious to the host. Some examples of immune system-mediated injury have been extensively investigated including anaphylactic shock, autoimmune disease, and immune complex disorders. More recently it has become clear that the cytokine cachectin/tumor necrosis factor (TNF) occupies a key role in the pathophysiology associated with diverse inflammatory states and other serious illnesses including septic shock and cachexia. For example, when cachectin/TNF is produced by resident macrophages during early microbial infection, it mediates an inflammatory response that may alienate and repel the attacking organisms. If the infection spreads, however, the subsequent release of large quantities of cachectin/TNF into the circulation may be catastrophic and trigger a state of lethal shock. These toxic effects occur by direct action of TNF on host cells and by the interaction with a cascade of other endogenous mediators including interleukin-1 and interferon-gamma. The biology of cachectin/TNF will be reviewed, along with the potential for modulating the effects of this pluripotent molecule in a variety of pathologic states.

Animals↗
PubMed2026

Orchard netting impacts on biodiversity leading to cascading effects at the ecosystem level.

Agriculture must ensure food production without further compromising the ecosystem functions upon which it depends. Agricultural practices should therefore avoid harming farmland biodiversity, especially of taxa that supply the key ecosystem services (e.g. pollination, pest control and nutrient uptake) that ultimately support crop production. Orchards are among the largest permanent plantations worldwide and are increasingly characterised by the spread of plastic nets used to protect fruits/nuts from either abiotic (anti-hail, anti-rain, shade nets) or biotic (exclusion nets) hazards. Despite having received little attention to date, these nets may impact natural communities, acting both as physical barriers and as drivers of habitat changes to which biota must respond. Species-level responses to netting depend on the organism's ability to enter the netted environment and successfully exploit available resources. Net-mediated ecological filtering and plastic behavioural responses may alter species interactions, leading to cascading ecological impacts that may create species-poorer 'netted communities' with simplified ecological networks. Such changes may erode biological control potential, other ecosystem functions, and overall system stability. We conducted a systematic review on the effects of protection nets on biota, and reported novel empirical evidence on anti-hail nets' impacts on communities of orchard-dwelling birds, flower-visiting insects, and rodents. In total, we identified 48 studies from the literature, however this literature was strongly biased towards apple orchards, western countries, and pest taxa. Net deployment was highly effective in deterring target pest species, in some cases regardless of their original function, as even weather-protection nets limited pest populations. Side effects on non-target taxa were also often reported, such as decreases in pollinators and natural enemies, and/or increases in secondary pests or microbial diseases. However, most assessments largely disregarded non-pest taxa and the broader ecological consequences of netting. The few studies that addressed the effects of nets at the guild/community level, including our empirical study, confirmed that orchard netting resulted in species-poor assemblages, with possible ecosystem-level consequences. We propose that future assessments should pay more attention to the indirect effects of netting on non-target taxa, and on the supply of crop-supporting ecosystem services mediated by wild species occurring in agroecosystems. Due to the trade-offs between these services and net-mediated crop protection, integrated alternatives should be tested to improve the environmental sustainability of food production and biodiversity conservation in farmed landscapes.

Biodiversity↗
PubMed2005

Aspartate transcarbamylase from the hyperthermophilic archaeon Pyrococcus abyssi. Insights into cooperative and allosteric mechanisms.

Aspartate transcarbamylase (ATCase) (EC 2.1.3.2) from the hyperthermophilic archaeon Pyrococcus abyssi was purified from recombinant Escherichia coli cells. The enzyme has the molecular organization of class B microbial aspartate transcarbamylases whose prototype is the E. coli enzyme. P. abyssi ATCase is cooperative towards aspartate. Despite constraints imposed by adaptation to high temperature, the transition between T- and R-states involves significant changes in the quaternary structure, which were detected by analytical ultracentrifugation. The enzyme is allosterically regulated by ATP (activator) and by CTP and UTP (inhibitors). Nucleotide competition experiments showed that these effectors compete for the same sites. At least two regulatory properties distinguish P. abyssi ATCase from E. coli ATCase: (a) UTP by itself is an inhibitor; (b) whereas ATP and UTP act at millimolar concentrations, CTP inhibits at micromolar concentrations, suggesting that in P. abyssi, inhibition by CTP is the major control of enzyme activity. While V(max) increased with temperature, cooperative and allosteric effects were little or not affected, showing that molecular adaptation to high temperature allows the flexibility required to form the appropriate networks of interactions. In contrast to the same enzyme in P. abyssi cellular extracts, the pure enzyme is inhibited by the carbamyl phosphate analogue phosphonacetate; this difference supports the idea that in native cells ATCase interacts with carbamyl phosphate synthetase to channel the highly thermolabile carbamyl phosphate.

Adenosine Triphosphate↗
PubMed2004

Anabaena sensory rhodopsin: a photochromic color sensor at 2.0 A.

Microbial sensory rhodopsins are a family of membrane-embedded photoreceptors in prokaryotic and eukaryotic organisms. Structures of archaeal rhodopsins, which function as light-driven ion pumps or photosensors, have been reported. We present the structure of a eubacterial rhodopsin, which differs from those of previously characterized archaeal rhodopsins in its chromophore and cytoplasmic-side portions. Anabaena sensory rhodopsin exhibits light-induced interconversion between stable 13-cis and all-trans states of the retinylidene protein. The ratio of its cis and trans chromophore forms depends on the wavelength of illumination, thus providing a mechanism for a single protein to signal the color of light, for example, to regulate color-sensitive processes such as chromatic adaptation in photosynthesis. Its cytoplasmic half channel, highly hydrophobic in the archaeal rhodopsins, contains numerous hydrophilic residues networked by water molecules, providing a connection from the photoactive site to the cytoplasmic surface believed to interact with the receptor's soluble 14-kilodalton transducer.

Anabaena↗
PubMed1993

Role of cytokines and inflammatory mediators in tissue destruction.

Colonization or emergence of microbial pathogens may result in tissue destruction by activation of one or more of five distinct host degradative pathways (matrix metalloproteinase pathway, plasminogen-dependent pathway, phagocytic pathway, PMN-serine proteinase pathway and osteoclastic bone resorption) or by direct cleavage of extracellular matrix constituents by microbial proteinases. Activation of endogenous destructive pathways may be mediated by immune responses resulting in expression of degradative cellular phenotypes among both immigrant and resident cell populations. In addition, expression of degradative phenotypes may be triggered by direct influences on host cells of microbial products (LPS, enzymes, toxins). A body of evidence suggests that each of these mechanisms involves local production of proinflammatory cytokines and growth factors. The matrix metalloproteinase pathway is centrally involved in dissolution of all unmineralized connective tissues and perhaps in resorption of bone as well. The matrix metalloproteinase family consists of nine or more genetically distinct Zn++ endopeptidases which collectively cleave all of the constituents of the extracellular matrix. Recent studies have uncovered many essential elements of a complex, but still incomplete, regulatory network that governs tissue destruction. Proinflammatory cytokines and growth factors induce signalling pathways several of which are dependent on protein kinase C and result in transient expression of the transcription factors c-jun and c-fos. Initiation of transcription of most matrix metalloproteinase genes requires binding of the transcription factor AP-1 (c-jun/c-fos) to a specific promoter sequence but attainment of maximal transcription rates is dependent on interaction with other promoter elements as well. Several matrix metalloproteinases have been detected in crevicular fluids and tissues of inflamed human gingiva as have the proinflammatory cytokines (IL-1 and TNF-alpha) which regulate their transcription. Although the mere presence of enzymes and cytokines does not necessarily impart function per se, these observations suggest that some level of spatial or temporal linkage exists between metalloproteinase/cytokine expression and gingival inflammation.

Aggregatibacter actinomycetemcomitans↗
PubMed2003

Intelligent infrastructure for sustainable potable water: a roundtable for emerging transnational research and technology development needs.

PROBLEM STATEMENT: Recent commercial and residential development have substantially impacted the fluxes and quality of water that recharge the aquifers and discharges to streams, lakes and wetlands and, ultimately, is recycled for potable use. Whereas the contaminant sources may be varied in scope and composition, these issues of urban water sustainability are of public health concern at all levels of economic development worldwide, and require cheap and innovative environmental sensing capabilities and interactive monitoring networks, as well as tailored distributed water treatment technologies. To address this need, a roundtable was organized to explore the potential role of advances in biotechnology and bioengineering to aid in developing causative relationships between spatial and temporal changes in urbanization patterns and groundwater and surface water quality parameters, and to address aspects of socioeconomic constraints in implementing sustainable exploitation of water resources. WORKSHOP OUTCOMES: An interactive framework for quantitative analysis of the coupling between human and natural systems requires integrating information derived from online and offline point measurements with Geographic Information Systems (GIS)-based remote sensing imagery analysis, groundwater-surface water hydrologic fluxes and water quality data to assess the vulnerability of potable water supplies. Spatially referenced data to inform uncertainty-based dynamic models can be used to rank watershed-specific stressors and receptors to guide researchers and policymakers in the development of targeted sensing and monitoring technologies, as well as tailored control measures for risk mitigation of potable water from microbial and chemical environmental contamination. The enabling technologies encompass: (i) distributed sensing approaches for microbial and chemical contamination (e.g. pathogens, endocrine disruptors); (ii) distributed application-specific, and infrastructure-adaptive water treatment systems; (iii) geostatistical integration of monitoring data and GIS layers; and (iv) systems analysis of microbial and chemical proliferation in distribution systems. IMPACT: This operational framework is aimed at technology implementation while maximizing economic and public health benefits. The outcomes of the roundtable will further research agendas in information technology-based monitoring infrastructure development, integration of processes and spatial analysis, as well as in new educational and training platforms for students, practitioners and regulators. The potential for technology diffusion to emerging economies with limited financial resources is substantial.

Conservation of Natural Resources↗
PubMed2006

Bacterial tolerances to metals and antibiotics in metal-contaminated and reference streams.

Anthropogenic-derived sources of selection are typically implicated as mechanisms for maintaining antibiotic resistance in the environment. Here we report an additional mechanism for maintaining antibiotic resistance in the environment through bacterial exposure to metals. Using a culture-independent approach, bacteria sampled along a gradient of metal contamination were more tolerant of antibiotics and metals compared to bacteria from a reference site. This evidence supports the hypothesis that metal contamination directly selects for metal tolerant bacteria while co-selecting for antibiotic tolerant bacteria. Additionally, to assess how antibiotic and metal tolerance may be transported through a stream network, we studied antibiotic and metal tolerance patterns over three months in bacteria collected from multiple stream microhabitats including the water column, biofilm, sediment and Corbicula fluminea (Asiatic clam) digestive tracts. Sediment bacteria were the most tolerant to antibiotics and metals, while bacteria from Corbicula were the least tolerant. Differences between microhabitats may be important for identifying reservoirs of resistance and for predicting how these genes are transferred and transported in metal-contaminated streams. Temporal dynamics were not directly correlated to a suite of physicochemical parameters, suggesting that tolerance patterns within microhabitats are linked to a complex interaction of the physicochemical characteristics of the stream.

Animals↗
PubMed2001

Connectivity patterns in tuberculosis and leprosy patients are indistinguishable from that of healthy donors.

Connectivity, the self-defined interactions between antigen-recognising molecules in a network system can in part be assessed by measuring the reactivity of a given serum against an ordered set of immunoglobulin (Ig)G F(ab')2 fractions, separated by means of isoelectric focusing so that, the serum reactivity against the whole set of fractions defines a characteristic pattern of connectivity. Deviations from the normal condition (healthy donors) have so far been documented for two autoimmune diseases: systemic lupus erythematosus (SLE) and pemphigus vulgaris, as well as for human immunodeficiency virus (HIV)-1 infection. We tested here if bacterial infections lead to alterations in connectivity. In addition, we wanted to test if two antigenically related bacteria would produce similar or otherwise distinctive connectivity patterns. Connectivity analysis was applied on the sera from tuberculosis and leprosy patients and the sera from healthy donors were used as control. No statistically significant differences between the three groups studied were found. These results have implications for theories that set the origin of autoimmune diseases in microbial infections. To the best of our knowledge, this is the first attempt to analyze the connectivity status in bacterial infections.

Adult↗
PubMed2004

Intestinal epithelial tight junctions as targets for enteric bacteria-derived toxins.

The application of a multidisciplinary approach to study bacterial pathogenesis, along with the recent sequencing of entire microbial genomes have made possible discoveries that are changing the way scientists view the bacterium-host interaction. Today, research on the molecular basis of the pathogenesis of infectious diarrheal diseases of necessity transcends established boundaries between microbiology, cell biology, intestinal pathophysiology, and immunology. Novel multidisciplinary approaches led to the discovery of new bacteria-host cell interactions involving signals regulating intestinal permeability through the modulation of cell cytoskeleton and intercellular tight junctions (TJ). A century ago, TJ were conceptualized as a secreted extracellular cement forming an absolute and unregulated barrier within the paracellular space. Biological studies of the past several decades have shown that TJ are dynamic structures subjected to structural changes that dictate their functional status under a variety of developmental, physiological, and pathological circumstances. To meet the many diverse physiological challenges to which the intestinal epithelial barrier is subjected, TJ must be capable of rapid and coordinated responses. This requires the presence of a complex regulatory system that orchestrates the state of assembly of the TJ multiprotein network. Many pathogenic bacteria exploit this system to accomplish their pathogenic strategies by ultimately modulating intestinal permeability.

Animals↗