SEARCH · Search PubMed

Results for “microbial interaction network”

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.

SourceResearch connectionFrom yearThrough year

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

At least 55 records · Page 3Linked to original sources

PubMedDate not supplied

Single-cell optical imaging of the phagocyte NADPH oxidase.

The phagocyte NADPH oxidase is a key component of the innate immune response against invading microorganisms, because the generation of superoxide (O(2)(-)) inside the phagocytic vacuole by this enzyme is responsible for microbial killing by mechanisms that are directly or indirectly dependent on reactive oxygen species (ROS) formation. Most of what is known about the membrane-embedded and cytosolic NADPH oxidase subunits and their intricate network of interactions on assembly and activation has been derived from biochemical and biophysical studies involving subcellular fractionation or reconstituted cell-free systems. Such investigations can be complemented by single-cell microscopy on phagocytes, which may reveal spatial and/or temporal details about NADPH oxidase assembly that cannot be obtained from fractionated-cell assays. In recent years, we have investigated the NADPH oxidase in neutrophils using two complementary optical imaging techniques: Raman microscopy, a vibrational spectroscopic technique that does not require protein labeling, and live-cell fluorescence microscopy, which sheds light on the dynamics of NADPH oxidase assembly in individual cells. Here, we briefly introduce these techniques, compare their characteristics, and show their potential for studying NADPH oxidase at the single-cell level. New microscopy data are presented to illustrate the versatility of Raman and fluorescence microscopy on intact neutrophils.

Adult↗

PubMed2007

Zea mays: benzoxazolinone detoxification under sulfur deficiency conditions--a complex allelopathic alliance including endophytic Fusarium verticillioides.

Benzoxazolinone detoxification is similar in plants grown under sulfur deficiency conditions and in control plants grown with an optimal S supply. However, when S-deficient plants were treated with metolachlor before benzoxazolin-2(3H)-one (BOA) incubation, detoxification was reduced, as indicated by a lower accumulation of the detoxification products BOA-6-O-glucoside and glucoside carbamate and by a loss of BOA-6-OH glucosyltransfease activity. Root colonizing microorganisms and the endophytic fungus Fusarium verticillioides participated in benzoxazolinone detoxification by converting the compound to 2-acetamidophenol (AAP) or O-hydroxyphenyl malonamic acid (OHPMA), a process accompanied by the appearance of phenoxazinone. Maize roots, however, absorbed AAP and OHPMA only in traces. Absorbed traces of OHPMA stimulated maize radicle growth, and traces of AAP stimulated cress. Phenoxazinone inhibited the growth of cress radicles at concentrations higher than 500 microM, whereas maize radicles were hardly affected. F. verticillioides did not convert benzoxazolinone to any known microbial degradation product when the medium of maize seedlings was inoculated with the fungus under sterile condition. Plant-fungus interactions seem to be important in plant survival of allelopathic attacks. This study points to a complicated network of allelopathic interactions that are influenced by biotic and abiotic factors, including herbicides.

Acetamides↗

PubMed2007

Translational mini-review series on Toll-like receptors: networks regulated by Toll-like receptors mediate innate and adaptive immunity.

The Toll-like receptor (TLR) family provide key components of mammalian immunity and are part of the earliest surveillance mechanisms responding to infection. Their activation triggers the innate immune response, and is crucial to the successful induction of Th1/Th2-phenotyped adaptive immunity. Innate immunity was long considered to be non-specific and somewhat simple compared to adaptive immunity, mediated via the engulfment and lysis of microbial pathogens by phagocytic cells such as macrophages and neutrophils, and involving no complex protein-protein interactions. The emergence of the TLR field has contributed to a revision of our understanding, and innate immunity is now viewed as a highly complex process, in line with adaptive immunity. This review will give a brief overview of our current knowledge of TLR biology, and will focus on TLRs as key components in complex networks that activate, integrate and select the appropriate innate and adaptive immune responses in the face of immunological danger.

Animals↗

PubMed2025

Depth-dependent multi-kingdom microbial interactions and biogeochemical cycling genes in eutrophic shallow lake sediments.

Microorganisms are pivotal to lake ecosystem biogeochemical cycles, yet existing research often focuses on single microbial kingdoms or surface sediments, neglecting multi-kingdom interactions and depth-resolved dynamics. To address these gaps, we used metagenomic sequencing to characterize microbial communities and their functional associations across overlying water and 0-45 cm sediments in four shallow lakes of the middle Yangtze River basin, China. Despite increasing bacterial and fungal diversity with depth, the 0-9 cm surface sediments exhibited the strongest multi-kingdom network connectivity and the greatest microbial stability. Functional genes exhibited clear depth-dependent patterns: nitrogen cycling genes, including those involved in dissimilatory nitrate reduction to ammonium, were most enriched in the upper 0-9 cm of sediment; methane cycling genes were positively correlated with depth; phosphorus cycling genes and some sulfur cycling genes, such as assimilatory sulphate reduction, declined with depth. Sediment microbial assembly was dominated by deterministic processes, in which the vertical distribution of functional genes was primarily dictated by heavy metals and conventional environmental indicators. These findings highlight depth-specific multi-kingdom microbial interactions and their associations with biogeochemical cycling, advancing lacustrine microbial ecology understanding and providing references for lake conservation under environmental change.

Lakes↗

PubMed2004

[Cytological characteristics of the human periodontal fibroblasts].

This review examines current concepts of functional morphology and molecular biology of periodontal fibroblasts. These cells appear to be the major cellular elements of human periodontium that realize its functions. Recent evidence on fibroblast structure, regeneration, synthetic and secretory activity, adhesion to various matrix components, migration, response to hormones, cytokines, growth factors and microbial products as well as on their interaction with other cellular elements of periodontium, is reviewed. On the basis of the newest findings on cellular and molecular biology, the concept of the central role of fibroblasts in the local network of cytokine regulation that controls the integrated function of periodontal cells, is formulated.

Cytokines↗

PubMed2004

Bugs and the gut: an unstable marriage.

There is a symbiotic relationship between the gastrointestinal microflora and the human host. Commensal bacteria provide essential nutrients to the epithelium and promote healthy immune responses in the gut. Commensal bacteria such as Escherichia coli can, however, transform into pathogens when they acquire genetic material encoding virulence factors such as adhesins, enterotoxins, invasins and cytotoxins. Enterovirulent organisms 'communicate' with the host by a variety of diverse mechanisms; these underpin the pathogenic processes that are essential for the expression of diarrhoeal disease. Many of these mechanisms involve the activation of signal transduction pathways in epithelial cells. Classical pathways include activation of adenylate or guanylate cyclases to produce chloride secretion, and subversion of cytoskeletal functions to effect intimate attachment with or without invasion of epithelial cells. Other systems are also involved, including inflammatory cells and local neuroendocrine networks. Understanding the complex interactions between the human gastrointestinal tract and the commensals and pathogens which it encounters will hopefully help us to exploit further the beneficial effects of the 'marriage' and to find new ways of preventing and treating microbial disease of the intestine which occurs when the symbiotic arrangement breaks down.

Biological Evolution↗

PubMed2026

Optimizing eco-engineering pedogenesis of bauxite residues: Synergistic effects of humus and FeSO4/sulfur on microbial community and function.

Eco-engineered pedogenesis represents a promising approach for soil amelioration of bauxite residues (BRs) through exogenous organic matter. However, the role of humus in mediating this process remains poorly understood, significantly impeding the eco-engineering rehabilitation of BRs. In this study, we conducted pot experiments and subsequent microbial analysis to evaluate the individual improvement of humic acid (HA), fulvic acid (FA), and corn straw (SWZ) on the BRs' pedogenesis. High-throughput sequencing analysis revealed that both FA and SWZ were more effective than HA in steering microbial community assembly, as community diversity, dominant taxa enrichment, and species' interaction were all significantly higher (p < 0.05) in the FA/SWZ treatments than in HA treatments. Notably, the combination of FA with FeSO4 specifically enriched halophilic taxa, while FA coupled with sulfur (S) significantly improved the connectivity and complexity of the microbial network, as the average connection degree increasing from 1.008 to 1.113. Hydrolytic enzyme activity assays further indicated that FA, especially when combined with S, was the most effective treatment in restoring microbial function during BR pedogenesis. These findings highlight FA as a critical driver of microbial restructuring and functional recovery in BRs. Moreover, its efficacy can be enhanced by co-amendment with FeSO4 or S. This study provides important theoretical and practical insights for optimizing organic-inorganic amendment strategies to accelerate the eco-engineering pedogenesis of bauxite residues.

Humic Substances↗

PubMed2006

Carbohydrate recognition systems in autoimmunity.

The immune system is a complex functional network of diverse cells and soluble molecules orchestrating innate and adaptive immunity. Biological information, to run these intricate interactions, is not only stored in protein sequences but also in the structure of the glycan part of the glycoconjugates. The spatially accessible carbohydrate structures that contribute to the cell's glycome are decoded by versatile recognition systems in order to maintain the immune homeostasis of an organism. Microbial carbohydrate structures are recognized by pathogen associated molecular pattern (PAMP) receptors of innate immunity including C-type lectins such as MBL, the tandem-repeat-type macrophage mannose receptor, DC-SIGN or dectin-1 of dendritic cells, certain TLRS or the TCR of NKT cells. Natural autoantibodies, a long known effector branch of this network-based operation, are effective to home in on non-self and self-glycosylation also. The recirculating pool of mammalian immune cells is recruited to inflammatory sites by a reaction pathway involving the self-carbohydrate-binding selectins as initial recognition step. Galectins, further key sensors reading the high-density sugar code, exert regulatory functions on activated T cells, among other activities. Autoimmune diseases are being associated with defined changes of glycosylation. This correlation deserves to be thoroughly studied on the levels of structural mimicry and dysregulation as well as effector molecules to devise innovative anti-inflammatory strategies. This review briefly summarizes data on sensor systems for carbohydrate epitopes and implications for autoimmunity.

Animals↗

PubMed2026

Functional analysis of Candida albicans protein kinases identifies Crk1 as a modulator of epithelial cell damage.

UNLABELLED: The commensal and pathogenic lifestyles of the opportunistic fungal pathogen Candida albicans require complex signaling networks regulated by protein kinases. To investigate the role of C. albicans protein kinases at the intestinal epithelial interface, we screened a comprehensive protein kinase deletion library for the capacity of the mutants to damage intestinal epithelial cells (IEC). Mutants showing altered IEC cytotoxicity relative to the wild type were further analyzed for their growth and morphology, focusing on hyper-damaging strains to identify kinases that rather prevent host cell damage. Deletion of CRK1 caused increased IEC-specific damage, despite slower growth, reduced hyphal length, and reduced adhesion as compared to wild-type cells. While tissue invasion levels and the formation of transcellular tunnels of the crk1Δ/Δ mutant were increased, the translocation capacity through the IEC barrier was reduced. Transcriptional and metabolic profiling suggested a role for Crk1 in metabolic adaptation to carbon and nitrogen sources, which was validated by showing that high glucose and amino acids are required for crk1Δ/Δ to cause increased IEC damage. Deletion of CRK1 rendered C. albicans more susceptible to cell wall and membrane stressors, but caused higher resistance to a catalase-specific and histidine biosynthesis inhibitor. This phenotypic pattern of medium- and epithelial cell type-specific cytotoxicity displayed by a C. albicans protein kinase mutant suggests that Crk1 regulates processes linked to carbon and amino acid metabolism that are relevant to interactions with intestinal epithelial cells. IMPORTANCE: Microbial signal transduction pathways regulate adaptation to changing environmental conditions and facilitate the success of many microbes during interactions with their hosts. The fungal pathobiont Candida albicans exists as a harmless commensal on mucosal surfaces of most humans but can also cause superficial and invasive infections under certain circumstances. Both lifestyles require complex signaling networks, predominantly regulated by protein kinases. The C. albicans genome was predicted to encode 108 protein kinases, yet nearly 50% remain uncharacterized. We aimed to dissect the role of C. albicans protein kinases during the transition from commensal to pathogen. We showed that multiple protein kinase genes are involved in epithelial cell damage. Particularly, the protein kinase gene Crk1 was of interest because deletion of CRK1 caused increased damage to intestinal epithelial cells under distinct conditions. Our study links Crk1 with regulation of metabolic processes relevant for commensalism and pathogenicity of C. albicans.

Candida albicans↗

PubMed2005

Polyamines regulate expression of E-cadherin and play an important role in control of intestinal epithelial barrier function.

Epithelial cells line the gastrointestinal mucosa and form an important barrier that protects the subepithelial tissue against a wide array of noxious substances, allergens, viruses and luminal microbial pathogens. Restoration of mucosal integrity following injury and various environmental stresses requires epithelial cell decisions that regulate signaling networks controlling gene expression, survival, migration and proliferation. Recently, it has been shown that polyamines play an important role in the regulation of cell-cell interactions and are critical for maintenance of intestinal epithelial integrity. Both the function of polyamines in expression of adherens junction proteins and their possible mechanisms, especially in implication of intracellular Ca2+ and c-Myc transcription factor, are the subject of this review article.

Animals↗

PubMed2005

Molecular communication through stochastic synchronization induced by extracellular fluctuations.

We model a synthetic gene regulatory network in a microbial cell, and investigate the effect of noises on cell-cell communication in a well-mixed multicellular system. A biologically plausible model is developed for cellular communication in an indirectly coupled multicellular system. Without extracellular noises, all cells, in spite of interaction among them, behave irregularly due to independent intracellular noises. On the other hand, extracellular noises that are common to all cells can induce collective dynamics and stochastically synchronize the multicellular system by actively enhancing the integrated interchange of signaling molecules.

Aliivibrio fischeri↗

PubMed2006

Using the topology of metabolic networks to predict viability of mutant strains.

Understanding the relationships between the structure (topology) and function of biological networks is a central question of systems biology. The idea that topology is a major determinant of systems function has become an attractive and highly disputed hypothesis. Although structural analysis of interaction networks demonstrates a correlation between the topological properties of a node (protein, gene) in the network and its functional essentiality, the analysis of metabolic networks fails to find such correlations. In contrast, approaches utilizing both the topology and biochemical parameters of metabolic networks, e.g., flux balance analysis, are more successful in predicting phenotypes of knockout strains. We reconcile these seemingly conflicting results by showing that the topology of the metabolic networks of both Escherichia coli and Saccharomyces cerevisiae are, in fact, sufficient to predict the viability of knockout strains with accuracy comparable to flux balance analysis on large, unbiased mutant data sets. This surprising result is obtained by introducing a novel topology-based measure of network transport: synthetic accessibility. We also show that other popular topology-based characteristics such as node degree, graph diameter, and node usage (betweenness) fail to predict the viability of E. coli mutant strains. The success of synthetic accessibility demonstrates its ability to capture the essential properties of the metabolic network, such as the branching of chemical reactions and the directed transport of material from inputs to outputs. Our results strongly support a link between the topology and function of biological networks and, in agreement with recent genetic studies, emphasize the minimal role of flux rerouting in providing robustness of mutant strains.

Algorithms↗

PubMed2003

Helicobacter pylori.

PURPOSE OF REVIEW: Helicobacter pylori is an important human pathogen, responsible for most peptic ulcer disease, gastritis and gastric malignancies. H. pylori has several unique features: it is highly adapted for gastric colonization, yet it produces clinical consequences in a small minority, its genome is known, and it is the only bacterium strongly associated with cancer. H. pylori is therefore of great interest to clinicians and researchers of many, often disparate, disciplines. We highlight recent advances in this fast changing field from many different areas. RECENT FINDINGS: The major contentious clinical issues relate to the synergistic gastrotoxic interactions of H. pylori with non-steroidal anti-inflammatory drugs, and a possible association of H. pylori with atherosclerotic events. Accumulating evidence implicates genetic variation in the inflammatory response to H. pylori in the etiology of the increased risk of gastric cancer after H. pylori infection. Studies of pathogenesis have been aided by increasingly sophisticated murine models. The effects in gastric epithelial cells of two of the major virulence factors (genes within the cag pathogenicity island and the vacuolating cytotoxin, VacA) of H. pylori illustrate the complex network of cellular reactions activated by H. pylori. The metabolism of H. pylori is dependent on the availability of hydrogen. SUMMARY: Basic science research into H. pylori continues to elucidate the mechanisms by which H. pylori infection causes disease. These findings have implications for the design of novel therapies and for improving clinical strategies to identify at-risk individuals. Many are also worthy of consideration for other epithelial-microbial interactions.

Animals↗

PubMed2001

The antioxidant network of the stratum corneum.

Many studies have demonstrated beneficial health effects of topical antioxidant application; however, the underlying mechanisms are not well understood. To better understand the protective mechanism of oxogenous anti-oxidants, it is important to clarify the physiological distribution, activity and regulation of antioxidants. Also, the generation of ROS by the resident and transient microbial flora and their interaction with cutaneous antioxidants appears to be of relevance for the redox properties of skin. Our studies have demonstrated that alpha-tocopherol is, relative to the respective levels in the epidermis, the major antioxidant in the human SC, that alpha-tocopherol depletion is a very early and sensitive biomarker of environmentally induced oxidation and that a physiological mechanism exists to transport alpha-tocopherol to the skin surface via sebaceous gland secretion. Furthermore, there is conclusive evidence that the introduction of carbonyl groups into human SC keratins is inducible by oxidants and that the levels of protein oxidation increase towards outer SC layers. The demonstration of specific redox gradients within the human SC may contribute to a better understanding of the complex biochemical processes of keratinization and desquamation. Taken together, the presented data suggest that, under conditions of environmentally challenged skin or during prooxidative dermatological treatment, topical and/or systemic application of antioxidants could support physiological mechanisms to maintain or restore a healthy skin barrier. Growing experimental evidence should lead to the development of more powerful pharmaceutical and cosmetic strategies involving antioxidant formulations to prevent UV-induced carcinogenesis and photoaging as well as to modulate desquamatory skin disorders.

Aging↗

PubMed2026

Conserved protein folds underpin the diversification of secreted proteins in a fungal pathogen.

BACKGROUND: During host colonization, fungal plant pathogens secrete effector-like proteins that alter host cell physiology and target plant-associated microbes. However, rapid evolution and low sequence conservation hinder the study and characterization of these proteins. The fungus Zymoseptoria passerinii infects Hordeum spp. and includes lineages adapted to wild and domesticated barley. To date, the evolution of effector-like proteins in this species has not been addressed. RESULTS: We combined multiple structure-based and network analyses to unravel the secretome of Z. passerinii. We first compared AlphaFold2 and ESMFold predictions to establish the baseline for structural analyses. We identified 72 structural clusters in the secretome, revealing fold-level relationships across divergent sequences. We showed that effector-like proteins with predicted host immune-interfering functions evolved from a limited group of protein folds, whereas proteins with predicted antimicrobial properties were distributed across fold groups. Physicochemical comparisons indicate that putative antimicrobial effectors predominantly emerged through amino acid replacements on common effector-enriched scaffolds in Z. passerinii, reconfiguring surface charge and electrostatics. We analyzed intra- and interspecific variation in selected effector-enriched families by comparing Z. passerinii proteins and homologs across the genus Zymoseptoria. We describe constrained core folds, with local variation in loop and surface-exposed regions, consistent with fold stability while still enabling protein diversification. We further report that putative antimicrobial effector homologs are broadly distributed across the genus despite sequence divergence. CONCLUSIONS: The secretome of Z. passerinii is organized around common structural folds that support diverse biological roles, including host manipulation and host-associated microbial interactions. Conserved scaffolds combined with surface and physicochemical variation likely contribute to rapid adaptive evolution of effector-like proteins in Z. passerinii.

Fungal Proteins↗

PubMed2001

Coevolutionary networks: a novel approach to understanding the relationships of humans with the infectious agents.

Human organism is interpenetrated by the world of microorganisms, from the conception until the death. This interpenetration involves different levels of interactions between the partners including trophic exchanges, bi-directional cell signaling and gene activation, besides genetic and epigenetic phenomena, and tends towards mutual adaptation and coevolution. Since these processes are critical for the survival of individuals and species, they rely on the existence of a complex organization of adaptive systems aiming at two apparently conflicting purposes: the maintenance of the internal coherence of each partner, and a mutually advantageous coexistence and progressive adaptation between them. Humans possess three adaptive systems: the nervous, the endocrine and the immune system, each internally organized into subsystems functionally connected by intraconnections, to maintain the internal coherence of the system. The three adaptive systems aim at the maintenance of the internal coherence of the organism and are functionally linked by interconnections, in such way that what happens to one is immediately sensed by the others. The different communities of infectious agents that live within the organism are also organized into functional networks. The members of each community are linked by intraconnections, represented by the mutual trophic, metabolic and other influences, while the different infectious communities affect each other through interconnections. Furthermore, by means of its adaptive systems, the organism influences and is influenced by the microbial communities through the existence of transconnections. It is proposed that these highly complex and dynamic networks, involving gene exchange and epigenetic phenomena, represent major coevolutionary forces for humans and microorganisms.

Adaptation, Physiological↗

PubMed2001

Metabolic modeling of microbial strains in silico.

The large volume of genome-scale data that is being produced and made available in databases on the World Wide Web is demanding the development of integrated mathematical models of cellular processes. The analysis of reconstructed metabolic networks as systems leads to the development of an in silico or computer representation of collections of cellular metabolic constituents, their interactions and their integrated function as a whole. The use of quantitative analysis methods to generate testable hypotheses and drive experimentation at a whole-genome level signals the advent of a systemic modeling approach to cellular and molecular biology.

Genome↗

PubMed2026

Lesion-specific oral microbiome signatures and predicted carcinogenic pathways in oral squamous cell carcinoma: a paired-site study in Pakistan.

BACKGROUND: Oral squamous cell carcinoma accounts for over 90% of oral neoplasms. Despite therapeutic advances, the lack of reliable, non-invasive biomarkers and delayed diagnosis continues to impede effective clinical management. By combining paired lesion and non-lesion sampling with predictive metagenomics analysis, our study addresses this gap and advances the current understanding of microbiome‒tumor interactions. METHODS: We analyzed 92 buccal swab samples from 39 OSCC patients and 14 healthy controls using 16S rRNA gene (V3-V4) sequencing. Taxonomic profiling was conducted using QIIME2 and SILVA/eHOMD databases, functional pathways were predicted using PICRUSt2, and hub taxa were identified through co-abundance network analysis. RESULTS: Microbial community structure differed significantly across lesion, non-lesion, and healthy sites (PERMANOVA, p = 0.001). Lesions were enriched with Selenomonas infelix and Treponema vincentii, while healthy controls harbored Streptococcus oralis and Gemella haemolysans. Co-abundance network analysis revealed lesion-specific hub species, notably T. vincentii, strongly correlated with predicted activation of pyrimidine biosynthesis pathways (r = 0.69, q < 1E-6), suggesting predicted metabolic alterations in the tumor microenvironment. Non-lesion sites were also characterized by two hub species, Prevotella melaninogenica and Segatella oulorum. CONCLUSION: Our findings define a lesion-specific microbial signature of OSCC characterized by the depletion of health-associated taxa, enrichment of pro-inflammatory pathobionts, and predicted associations with metabolic pathways implicated in carcinogenesis. These alterations reflect a predicted functionally altered tumor microenvironment.

16S rRNA gene↗