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PubMed2003

Scaling up: the next challenge in environmental microbiology.

Great strides have recently been made in identifying and characterizing the staggering diversity of microorganisms conducting primary and secondary production, nutrient transformation and mineralization processes that underlie ecosystem and regional biogeochemical, trophodynamic and ecological change. We are now faced with the challenge of assigning and coupling function to structure in highly complex and interactive microbial communities mediating such change. Previous and ongoing ecophysiological work has shown that microbial processes controlled by environmental variables and limiting resources are highly specific in terms of what, when, where and why they are active, not to mention how they impact ecosystem dynamics. As such, it is imperative that we assess the activities and roles of key microbial 'players' along the appropriate environmental scales and gradients catalysing ecological change. Here, we discuss conceptual and technical challenges for some key microbially mediated environmental processes, problems and extremes that require synthesizing our growing knowledge of microbial community structure with emerging knowledge of function in aquatic ecosystems. We emphasize the importance of assessing ecological change over a range of relevant time scales that vary from minutes to millennia and spatial scales that range from microscale aggregates to ocean basins.

Biodiversity↗

PubMed2001

Inhibitory effect of acetosyringone on two aflatoxin biosynthetic genes.

AIMS: The objective of this study was to determine if acetosyringone affected the expression of aflatoxin biosynthetic genes. METHODS AND RESULTS: Two genes, nor1 and ver1, representing genes whose products are involved in early and late steps in aflatoxin biosynthesis, were examined. Two GUS (beta-glucuronidase) reporter constructs, nor1:GUS (pGAP12) and ver1:GUS (pGAP13), were used to study the effect of acetosyringone on expression of aflatoxin biosynthetic (AF) genes, nor1 and ver1. The product of nor1 is involved in the formation of norsolorinic acid, the first stable intermediate in the aflatoxin pathway. The ver1 gene codes for the enzyme catalyzing the formation of demethylsterigmatocystin, an intermediate late in the AF pathway. GUS activities of these two reporter constructs were inhibited by 80% in the presence of 2 m mol l-1 acetosyringone. CONCLUSION: Aflatoxin production in a toxigenic strain 42-12 was also shown to be inhibited by acetosyringone to the same level. The levels of inhibition in aflatoxin production and gene transcription are congruous in these three strains. SIGNIFICANCE AND IMPACT OF THE STUDY: Recent studies have indicated that some phenolics act as signal molecules in plant microbial interactions. Concentration of acetosyringone is shown to increase about ten fold when certain metabolically active plant tissues are wounded. The knowledge gained can be applied to develop strategies in plant breeding programs. The compound may be useful for studying molecular mechanism of modulating aflatoxin biosynthesis.

Acetophenones↗

PubMed1999

Dynamics of Helicobacter pylori colonization in relation to the host response.

The dynamics of Helicobacter pylori colonization from its acquisition through the development of steady-state are examined through a mathematical model that includes the host response. The model encompasses both host and microbiological variation. The individual capacity of the host response is shown to be a key model parameter, leading to either transient or persistent colonization, whereas the growth rate of that response has little effect. Analyses of competing strains indicate that each must occupy a specific niche, otherwise exclusion occurs. The model implies that there exists a lower bound on the host response to the indigenous microflora that is consistent with current biological views of H. pylori. Parallel models may be useful in understanding other persistent host-microbial interactions.

Cell Division↗

PubMed1997

Examining the role of Paneth cells in the small intestine by lineage ablation in transgenic mice.

The Paneth cell lineage is one of four epithelial lineages derived from the adult mouse small intestine's multipotent stem cell. Mature Paneth cells secrete antimicrobial peptides (cryptdins), growth factors, as well as two gene products, a secreted phospholipase A2 and matrilysin, that has been implicated as modifiers of adenoma formation in mice containing a mutation in the tumor suppressor Apc. Immature Paneth cells are located just above and below the cell layer, in intestinal crypts, that has been proposed to contain the multipotent stem cell. Paneth cells differentiate during a downward migration to the crypt base. The location and direction of Paneth cell migration, their high density and long residency time at the crypt base, and the nature of their secreted gene products, suggest that they may influence the structure and/or function of the stem cell niche. Paneth cell ablation can therefore be viewed as an experimental manipulation of the cellular microenvironment that purportedly contains the stem cell and its immediate descendants. Two types of ablation experiments were performed in transgenic mice. Nucleotides -6500 to +34 of the mouse cryptdin-2 gene (CR2) were used to express an attenuated diphtheria toxin A fragment. Light and electron microscopic immunohistochemical analyses of several pedigrees of postnatal day 28 to 180 animals established that ablation of Paneth cells is accompanied by an increase in the proportion of undifferentiated crypt base columnar cells. These cells normally co-exist with Paneth cells. The ablation does not produce a detectable effect on the proliferation or terminal differentiation programs of the other three lineages or on host-microbial interactions. The last conclusion is based on the ability of crypts to remain free of microbes detectable by Gram and Warthin-Starry stains and by retention of the normal crypt-villus distribution of components of the diffuse gut-associated lymphoid tissue. CR2-directed expression of simian virus 40 large T antigen also results in a loss of mature Paneth cells but produces a marked amplification of crypt cells having a morphology intermediate between Paneth and granule goblet cells. EM immunohistochemical analyses suggest that intermediate cells can differentiate to mature goblet cells but not to Paneth cells, as they migrate up the crypt-villus axis. Our findings suggest that (i) stemness in the crypt is not defined by instructive interactions involving the Paneth cell; (ii) expressing a Paneth cell fate may require that precursors migrate to the crypt base; (iii) antimicrobial factors produced by Paneth cells are not required to prevent colonization of small intestinal crypts; and (iv) this lineage does not function to maintain the asymmetric crypt-villus distribution of components of the diffuse gut-associated lymphoid tissue.

Animals↗

PubMed1995

Omega-3 fatty acids in respiratory diseases: a review.

The health benefits of dietary omega-3 fatty acids have been investigated in a variety of conditions but there have been few studies of their effects in human respiratory diseases. Although many of the physiological changes associated with omega-3 polyunsaturate ingestion have been attributed to alterations in endogenous eicosanoid production, effects on blood rheology, host-microbial interactions and lung surfactant production have also been described. In reviewing the literature, there is little evidence that these polyunsaturates have beneficial effects in allergic disorders, but they may have potential as modulators of respiratory diseases involving chronic inflammatory and infectious processes or impaired pulmonary blood flow. Further work on the effects of omega-3 fatty acids in several chronic pulmonary syndromes, for which there are currently no effective therapies, appears to be warranted.

Asthma↗

PubMed2026

Gut microbiota and metabolic alterations in participants with flatulence identify Faecalibacterium prausnitzii as a key microbial target for clinical intervention.

Flatulence is closely associated with gut dysbiosis, yet the characteristic microbial signatures, metabolic alterations, and actionable intervention targets remain unclear. This limited mechanistic understanding has hindered the development of precise microbiota-based strategies for managing flatulence. Here, we found that participants with flatulence exhibited marked shifts in gut microbial functions and fecal metabolic profiles compared with healthy controls, characterized by enhanced abnormal fermentation, enrichment of oxidative stress-related functions, elevated low-grade inflammatory signatures, and reduced anti-inflammatory and mucosal-protective metabolic features. Faecalibacterium prausnitzii was significantly negatively associated with the high-gas-producing phenotype. In vitro replenishment experiments further validated the role of F. prausnitzii in reducing gas production, promoting butyrate generation, and remodeling butyrate-associated microbial communities. Based on microbial interaction analysis, we identified Bifidobacterium longum CCFM1319 as a candidate strain for targeting F. prausnitzii. In a double-blind, randomized, placebo-controlled clinical trial, supplementation with B. longum CCFM1319 significantly increased intestinal F. prausnitzii abundance and improved flatulence-related symptoms. Collectively, these findings reveal the microbiota and metabolic dysbiosis underlying flatulence, highlight the key regulatory role of F. prausnitzii, and lays the foundation for targeted microbiota-based intervention strategies for flatulence.

Humans↗

PubMed2001

Environmental and food safety aspects of Escherichia coli O157:H7 infections in cattle.

The presence of E. coli O157:H7 in cattle illustrates the complex, interrelated nature of the environment, livestock production practices, food safety, and the science of microbiology, particularly microbial ecology. Enterohemorrhagic E. coli, including E. coli O157:H7, can cause severe human diseases that can be debilitating and life threatening. Cattle are currently considered to be the definitive source for E. coli O157:H7 in the food supply, but this view may be simplistic and incomplete. E. coli O157:H7, appears widespread among U.S. cattle herds, while individual animal prevalence is low and transient. Most individual animals appear to be a transient reservoir for E. coli O157:H7 although the issue of carrier animals still remains unresolved. Epidemiological studies of the cattle production system have not clearly identified risk factors or management practices that affect E. coli O157:H7 prevalence in cattle feces. The problem of E. coli O157:H7 increases during the summer and fall months, but the environmental factors that contribute to this increase are poorly understood. Possible environmental factors that may influence E. coli O157:H7 shedding in cattle include livestock feed and waste handling practices as well as insects and microbial interactions in soil and water. Studies of E. coli O157:H7 ecology in cattle and the environment have been limited, but they suggest that a consideration of other independent, environmental sources of this microbe seems appropriate. The natural ecology of cholera may serve as a useful environmental model for pursuing additional environmental research on the occurrence and transmission of E. coli O157:H7 in nature.

Animals↗

PubMed1995

The PapG-adhesin at the tip of P-fimbriae provides Escherichia coli with a competitive edge in experimental bladder infections of cynomolgus monkeys.

Human urinary tract infection is an infectious disease that depends on a series of host-microbial interactions. The bacteria first colonize the colon and then the periurethral/vaginal areas; they ascend to and infect first the bladder and then the kidneys. Expression of Escherichia coli P-fimbriae constitutes the strongest correlation to renal pathogenicity, but is also related to first-time cystitis in children. The role of P-fimbriae in the preceding steps in the infectious process is unknown. To examine this, we constructed, from a P-fimbriated E. coli strain with a class II G-adhesin preferentially binding to globoside, one isogenic mutant lacking the G-adhesin and another isogenic mutant in which we replaced the papG class II allele with a class III adhesin preferentially binding to the Forssman antigen. We report here the comparison of the adhesin knockout mutant (DS17-8) and the class-switch mutant (DS17-1) with the wild-type (DS17) for in vivo colonization of the gut, vagina, and bladder of cynomolgus monkeys. It was recently shown that the class II tip G-adhesin is a prerequisite for acute pyelonephritis to occur in the monkey model in the absence of other kidney-specific adhesins or obstruction of the urinary flow. Here we show that it is not required for bladder infection but gives a competitive advantage in mixed infections. In the vagina and colon, the G-adhesin gives no competitive advantage.

Adhesins, Escherichia coli↗

PubMed2005

Lipopolysaccharide: an endotoxin or an exogenous hormone?

Conventional models of the pathogenesis of sepsis assume that microorganisms or their products are necessarily injurious to the host. In contrast, an evolutionary perspective suggests that host-microbial interactions are a symbiotic model and that disease results from the disruption of a mutually beneficial homeostatic state. Lipopolysaccharide (LPS) from gram-negative bacteria is a prototypical trigger of sepsis and a target for the development of novel therapeutics. The biological mechanisms underlying the recognition of, and response to, LPS are more characteristic of a hormone than of a toxin. All mammals carry endogenous stores of LPS and express dedicated carrier proteins, a cellular receptor complex, and mechanisms that specifically antagonize the response to LPS. Disruption of any component of this complex recognition system jeopardizes host defenses against infection with exogenous microorganisms. Thus, LPS is not less an endotoxin than an exohormone, and its neutralization may potentially result in either benefit or harm.

Animals↗

PubMed2006

Interplay between Helicobacter pylori and host gene polymorphisms in inducing oxidative DNA damage in the gastric mucosa.

Infection by Helicobacter pylori is the most important risk factor for gastric cancer. However, only a small fraction of colonized individuals, representing at least half of the world's population, develop this malignancy. In order to shed light on host-microbial interactions, gastric mucosa biopsies were collected from 119 patients suffering from dyspeptic symptoms. 8-Hydroxy-2'-deoxyguanosine (8-oxo-dG) levels in the gastric mucosa were increased in carriers of H.pylori, detected either by cultural method or by polymerase chain reaction, and were further increased in subjects infected with strains positive for the cagA gene, encoding the cytotoxin-associated protein, cagA. Oxidative DNA damage was more pronounced in males, in older subjects, and in H.pylori-positive subjects suffering from gastric dysplasia. Moreover, 8-oxo-dG levels were significantly higher in a small subset of subjects having a homozygous variant allele of the 8-oxoguanosine-glycosylase 1 (OGG1) gene, encoding the enzyme removing 8-oxo-dG from DNA. Conversely, they were not significantly elevated in glutathione S-transferase M1 (GSTM1)-null subjects. Thus, both bacterial and host gene polymorphisms affect oxidative stress and DNA damage, which is believed to represent a key mechanism in the pathogenesis of gastric cancer. The interplay between bacterial and host gene polymorphisms may explain why gastric cancer only occurs in a small fraction of H.pylori-infected individuals.

8-Hydroxy-2'-Deoxyguanosine↗

PubMedDate not supplied

Oral candidiasis: pathogenesis and host defense.

Oral candidiasis is a common problem, frequently presenting as a chronic recurring infection. Oral infection is a potential reservoir of organisms for severe, spreading, local disease and systemic disease in the compromised host. Nonspecific local oral factors in host defense include the epithelial barrier, flow or saliva, microbial interactions, antimicrobial constituents of saliva, lysozyme, lactoferrin, the lactoperoxidase system, levels of iron, and salivary glycoproteins. Immunoglobins are present in saliva, but their role is poorly understood. The activity of antibody against Candida on oral mucosal surfaces may not be mediated by complement and phagocyte activity. Specific antibodies against Candida may function by aggregating the organisms and preventing mucosal adherence of the fungi.

Animals↗

PubMed2003

Default biosynthesis pathway for blood group-related glycolipids in human small intestine as defined by structural identification of linear and branched glycosylceramides in a group O Le(a-b-) nonsecretor.

Glycoconjugates of the GI tract are important for microbial interactions. The expression of histo-blood group glycosyltransferases governs both the expression of blood group determinants and in part the structure and size of the glycoconjugates. Using neutral glycolipids isolated from the small intestine of a rare blood group O Le(a-b-) ABH secretor-negative (nonsecretor) individual we were able to map the "default" pathway of the individual lacking ABO, Lewis, and secretor glycosyltransferases. Structures were deduced with combined analysis of mass spectrometry (MALDI-TOF and ESI-MS/MS), and 1H NMR (500 and 600 MHz). All structures present at a level >5% were structurally resolved and included two extended structures: Galbeta4(Fucalpha3)GlcNAcbeta3(Galbeta4[Fucalpha3]GlcNAcbeta6)Galbeta4GlcNAcbeta3Galbeta4Glcbeta1Cer and Galbeta3GlcNAcbeta3(Galbeta4[Fucalpha3]GlcNAcbeta6)Galbeta3GlcNAcbeta3Galbeta4Glcbeta1Cer. The first, a novel component, is based on a type 2 chain and bears the Lex glycotopes on both its branches. The second, a major component, is based on a type 1 chain, which bears a 3-linked type 1 precursor (Lec) glycotope and a 6-linked Lex glycotope on its branches. This latter structure is identical to that previously isolated from plasma and characterized by MS and GC-MS but not by NMR. Structural resolution of these structures was supported by reanalysis of the blood group H-active decaosylceramides previously isolated from rat small intestine. Other minor linear monofucosylated penta-, hepta-, and difucosylated octaosylceramides, some bearing blood group determinants, were also identified. The cumulative data were used to define a default biosynthesis pathway where it can be seen that carbohydrate chain extension, in the absence of blood group glycosyltransferases, is controlled and regulated by non-blood group fucosylation and branching with type 2 Galbeta4GlcNAc branches.

Animals↗

PubMed2026

Penicillium melinii promotes root growth through subtle host reprogramming across model and crop species.

Root development is highly responsive to microbial interactions, yet the mechanisms by which beneficial fungi promote root growth remain incompletely understood. Here, we identified Penicillium melinii 'isolate 2' through a screen of endophytic fungi isolated from Arabidopsis and characterized it as a promoter of root development in both Arabidopsis and crop species. We combined phenotyping in vitro, rhizotron, greenhouse and field assays with reporter and mutant analyses, transcriptomics, phytohormone profiling and sequencing and annotation of the fungal genome to investigate the basis of this interaction. P. melinii consistently stimulated root growth and modified root architecture across experimental systems and host species. These effects were associated with subtle but reproducible host transcriptional reprogramming, supporting a model in which the fungus fine-tunes endogenous developmental programmes rather than broadly perturbing stress or growth pathways. Genetic and reporter analyses further suggested that this interaction modulates root branching through localized developmental reprogramming. Genomic analysis provided a framework for understanding the fungal traits associated with this beneficial interaction. The conservation of the response across model and crop species supports the relevance of P. melinii as both a useful experimental system to study beneficial plant-fungus interactions and a promising candidate for improving root traits and crop performance.

Penicillium melinii↗

PubMed2025

Multi-ancestry genome-wide and transcriptome-wide association analyses identified new risk loci and genes for inflammatory bowel disease.

To advance genetic understanding of inflammatory bowel disease (IBD), we conducted genome-wide association meta-analyses of 63,415 IBD cases of European and East Asian descendants and identified 90 previously unknown risk loci. Integrating multi-ancestry transcriptome-wide association studies (TWAS), cell type-specific TWAS, alternative splicing (AS-WAS), and alternative polyadenylation (APA-WAS) analyses using RNA-seq data from normal colon tissues of 707 European and 364 East Asian individuals, we uncovered 506 high-confidence IBD risk genes, including 384 not previously reported. These genes converge on immune regulation, microbial interaction, and other pathways central to IBD pathogenesis, with over half showing transcriptional dysregulation supported by single-cell and spatial omics analyses. Notably, 46 risk genes are targeted by 225 drugs that have been approved or in Phase II/III trials, including sulfasalazine already used in IBD therapy. Our study findings deepen the understanding of IBD genetics and support the development of precision medicine for its prevention and treatment.

GWAS↗

PubMed2005

Experimental models of inflammatory bowel disease reveal innate, adaptive, and regulatory mechanisms of host dialogue with the microbiota.

There are now many experimental models of inflammatory bowel disease (IBD), most of which are due to induced mutations in mice that result in an impaired homeostasis with the intestinal microbiota. These models can be clustered into several broad categories that, in turn, define the crucial cellular and molecular mechanisms of host microbial interactions in the intestine. The first of these components is innate immunity defined broadly to include both myeloid and epithelial cell mechanisms. A second component is the effector response of the adaptive immune system, which, in most instances, comprises the CD4+ T cell and its relevant cytokines. The third component is regulation, which can involve multiple cell types, but again particularly involves CD4+ T cells. Severe impairment of a single component can result in disease, but many models demonstrate milder defects in more than one component. The same is true for both spontaneous models of IBD, C3H/HeJBir and SAMPI/Yit mice. The thesis is advanced that 'multiple hits' or defects in these interacting components is required for IBD to occur in both mouse and human.

Animals↗

PubMed2004

The microbial synergy of Peptostreptococcus micros and Prevotella intermedia in a murine abscess model.

This study characterized the microbial interaction of Peptostreptococcus micros and Prevotella intermedia, the major pathogens of dentoalveolar infection, using a murine model. Subcutaneous injection of P. micros cells in the dorsum of the mouse together with living cells of P. intermedia resulted in a significantly larger abscess when compared with single injection of the organisms (P < 0.02). The abscess size was also significantly increased (P < 0.05) when the plate-cultured cell suspension of P. micros was injected into mouse with the culture filtrate of P. intermedia. The heat-treated culture filtrate of P. intermedia also enhanced the virulence of P. micros. P. micros culture filtrate did not affect the virulence of P. intermedia. Interestingly, the virulence of P. micros appeared to be enhanced even when the culture filtrate of P. intermedia was injected at separate sites in the mouse. These results suggest that a heat-stable product or products of P. intermedia increase the virulence of P. micros indirectly by altering the host condition, whereas living cells of P. micros can directly enhance virulence of P. intermedia.

Abscess↗

PubMed1983

Effect of inoculation sequence and nutrients upon Streptococcus mutans BHT and Streptococcus mitior LPA-1 growing on human teeth in an artificial mouth.

Human teeth in an artificial mouth were inoculated with Streptococcus mutans BHT, Streptococcus mitior LPA-1, or sequentially with both organisms. Incubation was continued for 90 h. Mixed populations were largest when a nutrient supplement containing 5.0% (w/v) sucrose was supplied. Fewer organisms were recovered from experiments with synthetic saliva only, or when a supplement containing 0.05% (w/v) glucose was available. The inoculation sequence determined the total viable count and a larger population resulted when Strep. mutans was the initial colonizer (P less than 0.01). Strep. mutans was always able to become established even when super-infected on to a 24 h plaque of Strep. mitior. The final proportion of Strep mutans was lower when it was the superinfecting organism and the sucrose (P less than 0.01) or glucose (P less than 0.05) nutrient supplement was provided. This work confirms the importance of inoculation sequence and presence of sugars in plaque accumulation and demonstrates the fundamental role of microbial interactions in this process.

Ecology↗

PubMed1987

The effect of sucrose on the colonization of acrylic by Candida albicans in pure and mixed culture in an artificial mouth.

The roles of sucrose and microbial interactions in the colonization of acrylic by Candida albicans in an artificial mouth were investigated. The acrylic was colonized by pure cultures of the organism but a visible plaque was not produced whether or not sucrose was present. Salivary bacteria had no effect in the absence of sucrose but when sucrose was present the numbers of C. albicans were significantly increased. It is suggested that this phenomenon is related to the production of extracellular polysaccharides by salivary streptococci in the presence of sucrose. In mixed culture of C. albicans and Streptococcus salivarius CJ2, growth of the latter was inhibited in the presence of sucrose. This inhibition was due to factors other than pH, although no such antagonism could be demonstrated on solid media.

Candida albicans↗