https://www.cell.com/cell/pdf/S0092-8674(04)00661-0.pdf

Recognition of Commensal Microflora by Toll-Like Receptors Is Required for Intestinal Homeostasis

The gastrointestinal tract is a complex ecosystem that associates a resident microbiota and cells of various phenotypes lining the epithelial wall expressing complex metabolic activities. The resident microbiota in the digestive tract is a heterogeneous microbial ecosystem containing up to 1×1014 colony-forming units (CFUs) of bacteria. The intestinal microbiota plays an important role in normal gut function and maintaining host health. The host is protected from attack by potentially harmful microbial microorganisms by the physical and chemical barriers created by the gastrointestinal epithelium. The cells lining the gastrointestinal epithelium and the resident microbiota are two partners that properly and/or synergistically function to promote an efficient host system of defence. The gastrointestinal cells that make up the epithelium, provide a physical barrier that protects the host against the unwanted intrusion of microorganisms into the gastrointestinal microbiota, and against the penetration of harmful microorganisms which usurp the cellular molecules and signalling pathways of the host to become pathogenic. One of the basic physiological functions of the resident microbiota is that it functions as a microbial barrier against microbial pathogens. The mechanisms by which the species of the microbiota exert this barrier effect remain largely to be determined. There is increasing evidence that lactobacilli and bifidobacteria, which inhabit the gastrointestinal microbiota, develop antimicrobial activities that participate in the host's gastrointestinal system of defence. The objective of this review is to analyze the in vitro and in vivo experimental and clinical studies in which the antimicrobial activities of selected lactobacilli and bifidobacteria strains have been documented.

Antagonistic activities of lactobacilli and bifidobacteria against microbial pathogens

Typically, pathogen-associated molecular patterns (PAMPs) are considered to be conserved throughout classes of microbes and to contribute to general microbial fitness, whereas effectors are species, race, or strain specific and contribute to pathogen virulence. Both types of molecule can trigger plant immunity, designated PAMP-triggered and effector-triggered immunity (PTI and ETI, respectively). However, not all microbial defense activators conform to the common distinction between PAMPs and effectors. For example, some effectors display wide distribution, while some PAMPs are rather narrowly conserved or contribute to pathogen virulence. As effectors may elicit defense responses and PAMPs may be required for virulence, single components cannot exclusively be referred to by one of the two terms. Therefore, we put forward that the distinction between PAMPs and effectors, between PAMP receptors and resistance proteins, and, therefore, also between PTI and ETI, cannot strictly be maintained. Rather, as illustrated by examples provided here, there is a continuum between PTI and ETI. We argue that plant resistance is determined by immune receptors that recognize appropriate ligands to activate defense, the amplitude of which is likely determined by the level required for effective immunity.

Of PAMPs and Effectors: The Blurred PTI-ETI Dichotomy

Some of the more important evidence is presented which supports the view that accumulation of phytoalexins at the site of attempted infection in plants. The accumulation of phytoalexins represents only one of a number of disease-resistance mechanisms in plants. Experiments are described demonstrating that the enzymes that catalyze the synthesis of phytoalexins are themselves synthesized de novo when plant cells are exposed to microbes of other effective stimuli. Evidence is also presented showing that phytoalexins, once accumulated, are catabolized or detoxified by many microorganisms as well as by the plants themselves. Elicitors are the major concern of this review. The literature is summarized in which elicitors are shown to be not only constituents of some microbes but also to be present in the cell walls of plants. A hypothesis is presented that suggests that all of the abiotic and some of the biotic elicitors stimulate phytoalexin accumulation by causing the release of an endogenous elicitor from the cell walls of plants. 108 references, 9 figures.

PHYTOALEXINS AND THEIR ELICITORS-A Defense Against Microbial Infection in Plants

INTRODUCTION .. . . . . . . . . . . ..... . . . . . . . . . . . . . . . . . . . . . . . ..... . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . ... . . 340 SIGNALS FOR THE ESTABLISHMENT OF INFECTION.. . . . . . . . . . . . . ..... .. . . . . . . . . . . . . 340 MICROBIAL DETERMINANTS OF A VIRULENCE..... . . . . . . . . . . . . . ..... . . . . . . . . . . . . . ..... 341 PLANT DISEASE-RESISTANCE GENES . . . . . ... . . . . . . . . . . . . . ..... . . . . . . . . . . . . . . ..... . . . . . . . . . 344 ELICITORS AND ELICITOR RECEPTORS . . . . . . ..... . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . 346 Race-Specific Elicitors . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . .. . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . .. . . 346 S tructure-Function Rela tionship s . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 347 Elicitor-Bindin g Sites...... . .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . .... . . . . . . . . . . .. ..... . . . . . . . . . . 347 Multiple Signal Functions . . . . . . . ... . . . . . . . . . . . . ... . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . . . . . . . . . . . 348 Elicitor Release. Modification, and Turnover . . . ..... . . . . . . . . . . . . . .. . . . . . . . . . . . . . .... . . . . . . . 348 Signal Interactions . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..... ... . . . . . . .. . . ....... . . . . . . . . . . 349 DEFENSE GENE REGULATION: IMPLICATIONS FOR SIGNALING . . . . . . . . . . . . . . . . . 351 Defense Mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..... . . . . . . . . . . ... . . . . . . . . . . . . . . ... . . . . . . . . . . 35 1 Defense Gene Activation: Signal Complexity . . . ......... .. . . ... . . . . . . . . . . . . . . .... . . . . . . . . . .. 352 Developmental Regulation of Defense Genes...... . . . . . . . . ........ . . . . . . . .... ...... . ... . .... 353 Defense Gene Regulatory Elemen ts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 355

Molecular Communication in Interactions Between Plants and Microbial Pathogens

The biochemical basis for the ability of the pterocarpan phytoalexin glycinol (3,6a,9-trihydroxypterocarpan) to inhibit the growth of bacteria was examined. Glycinol at bacteriostatic concentrations ( e.g. 50 micrograms per milliliter) inhibits the ability of Erwinia carotovora to incorporate [ 3 H]leucine, [ 3 H]thymidine, or [ 3 H]uridine into biopolymers. Exposure of Escherichia coli membrane vesicles to glycinol at 20 micrograms per milliliter results in inhibition of respiration-linked transport of [ 14 C]lactose and [ 14 C]glycine into the vesicles when either d-lactate or succinate is supplied as the energy source. The ability of E. coli membrane vesicles to transport [ 14 C]α-methyl glucoside, a vectorial phosphorylation-mediated process, is also inhibited by glycinol at 20 micrograms per milliliter. Furthermore, exposure of membrane vesicles to glycinol (50 micrograms per milliliter) at 20°C results in the leakage of accumulated [ 14 C]α-methyl glucoside-6-phosphate. The effects of the phytoalexins glyceollin, capsidiol, and coumestrol, and daidzein, a compound structurally related to glycinol but without antibiotic activity, upon the E. coli membrane vesicle respiration-linked transport of [ 14 C]glycine and of [ 14 C]α-methyl glucoside was also examined. Glyceollin and coumestrol (50 micrograms per milliliter), but not daidzein, inhibit both membrane-associated transport processes. These data imply that the antimicrobial activity of glycinol, glyceollin, and coumestrol are due to a general interaction with the bacterial membrane. Capsidiol (50 micrograms per milliliter) inhibits d-lactate-dependent transport of [ 14 C]glycine but not vectorial phosphorylation-mediated transport of [ 14 C]α-methyl glucoside. Thus, capsidiol9s mechanism of antimicrobial action seems to differ from that of the other phytoalexins examined.

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Host-Pathogen Interactions : XXIII. The Mechanism of the Antibacterial Action of Glycinol, a Pterocarpan Phytoalexin Synthesized by Soybeans.

Wild type Bacillus subtilis, when grown on beet araban, secretes into its culture medium an endo-arabanase and two arabinosidases. An alternate procedure to one previously described (Kaji A, T Saheki 1975 Biochim Biophys Acta 410: 354-360) has been developed for the purification of the endo-arabanase. The purified endo-arabanase is shown to be homogeneous by sodium dodecyl sulfate-urea disc gel electrophoresis (molecular weight approximately 32,000) and by isoelectric focusing (pI = 9.3). The endo-arabanase, acting on a branched araban substrate, has maximal activity at pH 6.0 and preferentially cleaves 5-linked arabinosyl residues. One of the arabinosidases (molecular weight approximately 65,000, pI = 5.3) has been purified to the point that it contains only one quantitatively minor contaminant, as shown by sodium dodecyl sulfate-urea disc gel electrophoresis and isoelectric focusing. The purified arabinosidase, acting on p-nitrophenyl-alpha-l-arabinofuranoside, has maximal activity at pH 6.5, and, when acting on a branched araban substrate, preferentially attacks nonreducing terminal arabinosyl residues linked to the 2 or 3 position of other arabinosyl residues. Neither of the two purified enzymes is capable of hydrolyzing a variety of carbohydrate substrates which lack arabinosidic linkages. The purified endo-arabinase is shown to be capable of releasing arabinosyl oligomers from the walls of suspension-cultured sycamore cells, thereby suggesting its usefulness as a probe in studying the structure of the araban component of primary cell walls.

/pdf/structure-of-plant-cell-walls-ix-purification-and-partial-56dq8lz0gn.pdf

Structure of Plant Cell Walls IX. Purification and Partial Characterization of a Wall-degrading Endo-Arabanase and an Arabinosidase from Bacillus subtilis

A previously unrecognized phytoalexin has been isolated from soybean cotyledons that had been infected with bacteria or exposed to ultraviolet light. The phytoalexin has been purified to homogeneity by silica gel flash chromatography and high pressure liquid chromatography. It has been structurally characterized by its ultraviolet, circular dichroism and nuclear magnetic resonance spectra, polarimetry, and its mass spectrometric fragmentation pattern. The phytoalexin, (6aS,11aS)-3,6a,9-trihydroxypterocarpan, is a compound that had previously been detected in CuCl2-treated soybeans and is structurally related to the previously identified soybean phytoalexins glycerollins I to IV. It is proposed that the trivial name glycinol be used for this phytoalexin. Glycinol is a broad spectrum antibiotic capable of prolonging the lag phase of growth of all six bacteria examined, namely Erwinia carotovora, Pseudomonas glycinea (races 1 and 3), Escherichia coli, Xanthomonas phaseoli, and Bacillus subtilis. Glycinol also inhibits the growth of the fungi Phytophthora megasperma f. sp. glycinea (race 1), Saccharomyces cerevisiae, and Cladosporium cucumerinum. Glycinol is a static agent against the six bacterial species listed above and against S. cerevisiae, and appears to be static against the other fungi examined. As with other phytoalexins, there is no correlation between the pathogenicity of a microorganism and its sensitivity to glycinol.

/pdf/host-pathogen-interactions-xviii-isolation-and-biological-5fvhg3hjwt.pdf

Lawrence I. Weinstein

Papers

Host-Pathogen Interactions : XXIII. The Mechanism of the Antibacterial Action of Glycinol, a Pterocarpan Phytoalexin Synthesized by Soybeans.

Structure of Plant Cell Walls IX. Purification and Partial Characterization of a Wall-degrading Endo-Arabanase and an Arabinosidase from Bacillus subtilis

Host-Pathogen Interactions : XVIII. ISOLATION AND BIOLOGICAL ACTIVITY OF GLYCINOL, A PTEROCARPAN PHYTOALEXIN SYNTHESIZED BY SOYBEANS