bluuebunny/crossref_metadata_2025_split huggingface dataset:
Physical and Metabolic Interactions of
Pseudomonas
sp. Strain JA5-B45 and
Rhodococcus
sp. Strain F9-D79 during Growth on Crude Oil and Effect of a Chemical Surfactant on Them
Authors: Van Hamme Jonathan D. , Ward Owen P. 
Published: July 2002

ABSTRACT

Methods to enhance crude oil biodegradation by mixed bacterial cultures, for example, (bio)surfactant addition, are complicated by the diversity of microbial populations within a given culture. The physical and metabolic interactions between
Rhodococcus
sp. strain F9-D79 and
Pseudomonas
sp. strain JA5-B45 were examined during growth on Bow River crude oil. The effects of a nonionic chemical surfactant, Igepal CO-630 (nonylphenol ethoxylate), also were evaluated. Strain F9-D79 grew attached to the oil-water interface and produced a mycolic acid-containing capsule. Crude oil emulsification and surface activity were associated with the cellular fraction. Strain JA5-B45 grew in the aqueous phase and was unable to emulsify oil, but cell-free supernatants mediated kerosene-water emulsion formation. In coculture, stable emulsions were formed and strain JA5-B45 had an affinity for the capsule produced by strain F9-D79. Igepal CO-630 inhibited F9-D79 cells from adhering to the interface, and cells grew dispersed in the aqueous phase as 0.5-μm cocci rather than 2.5-μm rods. The surfactant increased total petroleum hydrocarbon removal by strain JA5-B45 from 4 to 22% and included both saturated compounds and aromatics. In coculture, TPH removal increased from 13 to 40% following surfactant addition. The culture pH normally increased from 7.0 to between 7.5 and 8.5, although addition of Igepal CO-630 to F9-D79 cultures resulted in a drop to pH 5.5. We suggest a dual role for the nonylphenol ethoxylate surfactant in the coculture: (i) to improve hydrocarbon uptake by strain JA5-B45 through emulsification and (ii) to prevent strain F9-D79 from adhering to the oil-water interface, indirectly increasing hydrocarbon availability. These varied effects on hydrocarbon biodegradation could explain some of the known diversity of surfactant effects.
Assessment of the Genetic Diversity among Strains of
Xanthomonas cynarae
by Randomly Amplified Polymorphic DNA Analysis and Development of Specific Characterized Amplified Regions for the Rapid Identification of
X. cynarae
Authors: Trébaol Gaëlle , Manceau Charles , Tirilly Yves , Boury Stéphane 
Published: July 2002

ABSTRACT

The randomly amplified polymorphic DNA (RAPD) method was used to investigate the genetic diversity in
Xanthomonas cynarae
, which causes bacterial bract spot disease of artichoke. This RAPD analysis was also intended to identify molecular markers characteristic of this species, in order to develop PCR-based markers which can be used to detect this pathogenic bacterium in artichoke fields. Among the 340 RAPD primers tested, 40 were selected on their ability to produce reproducible and reliable fingerprints in our genetic background. These 40 primers produced almost similar patterns for the 37
X. cynarae
strains studied, different from the fingerprints obtained for other
Xanthomonas
species and other xanthomonad-like bacteria isolated from artichoke leaves. Therefore,
X. cynarae
strains form a homogeneous genetic group. However, a little DNA polymorphism within this species was observed and the collection of
X. cynarae
isolates was divided into two groups (one containing three strains, the second one including all other strains). Out of seven RAPD markers characteristic of
X. cynarae
that were cloned, four did not hybridize to the genomic DNA of strains belonging to other
Xanthomonas
species. These four RAPD markers were converted into PCR markers (specific characterized amplified regions [SCARs]); they were sequenced, and a PCR primer pair was designed for each of them. Three derived SCARs are good candidates to develop PCR-based tests to detect
X. cynarae
in artichoke fields.
Interception of Small Particles by Flocculent Structures, Sessile Ciliates, and the Basic Layer of a Wastewater Biofilm
Authors: Eisenmann Heinrich , Letsiou Ioanna , Feuchtinger Anette , Beisker Wolfgang , Mannweiler Ernst , Hutzler Peter , Arnz Patrik 
Published: July 2002

ABSTRACT

We investigated attachment processes of hydrophobic and hydrophilic particles (diameter = 1 μm) to mature biofilms grown on clay marbles in a sequencing batch biofilm reactor. During a treatment cycle with filtered wastewater containing different fluorescent beads, the progression of particle density in various biofilm compartments (carrier biofilm, basic biofilm layer, biofilm flocs, and sessile ciliates) was determined by flow cytometry, confocal laser scanning microscopy and automated image analysis. Particles were almost completely removed from wastewater by typical processes of particle retention: up to 58% of particles attached to clay marbles, up to 15% were associated with suspended flocs, and up to 10% were ingested by sessile ciliates. Ingestion of particles by ciliates was exceptionally high immediately after wastewater addition (1,200 particles grazer
−1
h
−1
) and continued until approximately 14% of the water had been cleared by ciliate filter feeding. Most probably, ciliate bioturbation increases particle sorption to the basic biofilm. Backwashing of the reactor detached pieces of biofilm and thus released approximately 50% of the particles into rinsing water. Clay marbles in the upper part of the reactor were more efficiently abraded than in the lower part. No indications for selective attachment of the applied hydrophobic and hydrophilic beads were found. As a consequence of interception patterns, organisms at elevated biofilm structures are probably major profiteers of wastewater particles; among them, ciliates may be of major importance because of their highly active digestive food vacuoles.
Standardization ofNeisseria meningitidisSerogroup B Colorimetric Serum Bactericida Assay
Authors: Rodríguez Tamara , Lastre Miriam , Cedré Barbara , Campo Judith del , Bracho Gustavo , Zayas Caridad , Taboada Carlos , Díaz Miriam , Sierra Gustavo , Pérez Oliver 
Published: July 2002

ABSTRACTThe correlate of protection for serogroup B meningococci is not currently known, but for serogroup C it is believed to be the serum bactericidal assay (SBA). The current SBAs are labor intensive and the variations in protocols among different laboratories make interpretation of results difficult. A colorimetric SBA (cSBA), based on the ability ofNeisseria meningitidisserogroup B to consume glucose, leading to acid production, was standardized by using group B strain Cu385-83 as the target. The cSBA results were compared to those obtained for a traditional colony-counting microassay (mSBA). Glucose and bromocresol purple pH indicator were added to the medium in order to estimate growth of cSBA target cell survivors through color change. Different variants of the assay parameters were optimized: growth of target cells (Mueller Hinton agar plates), target cell number (100 CFU/per well), and human complement source used at a final concentration of 25%. After the optimization, three other group B strains (H44/76, 490/91, and 511/91) were used as targets for the cSBA. The selection of the assay parameters and the standardization of cSBA were done with 13 sera from vaccinated volunteers. The titers were determined as the higher serum dilution that totally inhibited the bacterial growth marked by the color invariability of the pH indicator. This was detected visually as well as spectrophotometrically and was closely related to a significant difference in the growth of target cell survivors determined using Student’sttest. Intralaboratory reproducibility was ±1 dilution. The correlation between bactericidal median titers and specific immunoglobulin G serum concentration by enzyme immunoassay was high (r= 0.910,P< 0.01). The bactericidal titers generated by the cSBA and the mSBA were nearly identical, and there was a high correlation between the two assays (r= 0.974,P< 0.01). The standardized cSBA allows easy, fast, and efficient evaluation of samples.
Resected Human Colonic Tissue: New Model for Characterizing Adhesion of Lactic Acid Bacteria
Authors: Ouwehand Arthur C. , Salminen Seppo , Tölkkö Satu , Roberts Peter , Ovaska Jari , Salminen Eeva 
Published: July 2002

ABSTRACT
Adhesion to the intestinal mucosa is one of the main selection criteria for probiotic strains. The adhesion of commonly used probiotic strains to human intestinal tissue pieces and mucus was assessed. The strains tested adhered to the intestinal tissue at low levels and adhered to the intestinal mucus at higher levels.
Inclusion Fluorescent-Antibody Test as a Screening Assay for Detection of Antibodies toChlamydia pneumoniae
Authors: Tapia Olga , Slepenkin Anatoly , Sevrioukov Evgueni , Hamor Kathi , de la Maza Luis M. , Peterson Ellena M. 
Published: July 2002

ABSTRACTA study was conducted to determine the ability of the inclusion immunofluorescence assay (inclusion IFA) to act as a screening test to detect samples with antibodies toChlamydia pneumoniae; microimmunofluorescence (MIF) was used as the “gold standard.” In addition, the inclusion IFA was compared using HEp-2 cells infected with eitherC. pneumoniaeCM-1 orChlamydia trachomatisserovar E. A total of 331 serum samples representing a range of MIF titers were evaluated. The sensitivities of the inclusion IFA for detecting samples withC. pneumoniaeMIF titers of ≥16 were 96.9 and 74.8% withC. pneumoniae-andC. trachomatis-infected cells, respectively. For samples with an elevatedC. pneumoniaeMIF titer of ≥512, the sensitivities of theC. pneumoniae-andC. trachomatis-based inclusion IFA were 97.0 and 8.8%, respectively. These results suggest that the inclusion IFA is not a genus-specific test, as evidenced by the failure of theC. trachomatis-infected cells to detect a significant number of samples withC. pneumoniaeantibodies. Samples that had elevatedC. pneumoniaeinclusion IFA and MIF titers but that were found negative (titer, <16) by theC. trachomatisinclusion IFA were further tested by an in vitro neutralization assay for functional antibodies that might not have been detected by the serological assays. The in vitro neutralization results corroborated the serological results in that all seven sera tested had a neutralization titer forC. pneumoniae(range, 20 to 225), while all but one failed to have any effect on the infectivity ofC. trachomatisserovar E. While theC. pneumoniaeinclusion IFA had a high sensitivity for detecting chlamydial antibodies, depending on whether it was used as a screening test for detecting samples with low (≥16) or elevated (≥512) MIF titers, its specificity ranged from 53.4 to 77.1%. In conclusion, the inclusion IFA withC. pneumoniae-infected cells was best suited as a sensitive screening test for identifying specimens with elevated MIF titers (those associated with a possible acute infection withC. pneumoniae).
Vitamin A Levels and Immunity in Humans
Authors: Jason Janine , Archibald Lennox K. , Nwanyanwu Okey C. , Sowell Anne L. , Buchanan Ian , Larned Joshua , Bell Michael , Kazembe Peter N. , Dobbie Hamish , Jarvis William R. 
Published: July 2002

ABSTRACTIn animal studies, vitamin A deficiency induces a shift from type 2 (humoral) to type 1 (cellular) cytokines; there are no similar data for humans. Control of human immunodeficiency virus (HIV) andMycobacterium tuberculosisinfections requires type 1 cytokine (cellular) immunity. These infections and vitamin A deficiency are highly prevalent in Africa. We therefore examined the interactions among serum vitamin A levels, immune parameters, HIV infection status,Mycobacterium bovisBCG vaccine scarring (as an indicator of a type 1 cytokine profile), and clinical findings for 70 hospitalized children in Malawi, Africa. Directly conjugated monoclonal antibodies and flow cytometry were used to assess cell-specific cytokine production by peripheral blood monocytes and lymphocyte subpopulations. The statistical techniques employed included nonparametric statistics and logistic regression analyses. Thirty percent of the participants had severe vitamin A deficiency (<10 μg/dl), 34% had moderate deficiency (10 to <20 μg/dl), and 36% had normal levels (≥20 μg/dl). Vitamin A levels were lower for HIV-positive than for HIV-negative children (median, 10 and 17 μg/dl, respectively). Vitamin A-deficient children (<20 μg/dl) were more likely than non-vitamin A-deficient children to have higher proportions of natural killer (NK) cells (median, 8.3 and 5.2%, respectively) and lower ratios of interleukin-10-producing monocytes to tumor necrosis factor alpha-producing monocytes after induction (median, 1.0 and 2.3, respectively). Vitamin A-deficient children were also more likely than non-vitamin A-deficient children to exhibit respiratory symptoms (47% versus 12%) and visible BCG vaccine scars (83% versus 48%), which are indicative of a type 1 response to vaccination. Vitamin A status did not vary with gender, age, incidence of malaria parasitemia, blood culture positivity, or rates of mortality (6% of vitamin A-deficient children died versus 20% of non-vitamin A-deficient children). Lower vitamin A levels were associated with a relative type 1 cytokine dominance and proportionately more NK cells, both of which may be somewhat beneficial to persons who are exposed to HIV,M. tuberculosis, or other type 1 pathogens.
Increased Levels of Soluble CD30 in Plasma of Patients withPlasmodium falciparumMalaria
Authors: Kemp Kåre , Kurtzhals Jørgen A. L. , Akanmori Bartholomew D. , Adabayeri Victoria , Goka Bamenla Q. , Behr Charlotte , Hviid Lars 
Published: July 2002

ABSTRACTLevels of soluble CD30 (sCD30) in serum were elevated in patients withPlasmodium falciparummalaria but showed decline following treatment. The levels of sCD30 in serum were correlated significantly with the expression of gamma interferon by peripheral T cells. These data suggest that CD30+cells are upregulated during a malaria attack and that they may play a regulating role at the site of inflammation.
Identification of Attenuated
Yersinia pseudotuberculosis
Strains and Characterization of an Orogastric Infection in BALB/c Mice on Day 5 Postinfection by Signature-Tagged Mutagenesis
Authors: Mecsas Joan , Bilis Inna , Falkow Stanley 
Published: July 2002

ABSTRACT

Yersinia pseudotuberculosis
localizes to the distal ileum, cecum, and proximal colon of the gastrointestinal tract after oral infection. Using signature-tagged mutagenesis, we isolated 13
Y. pseudotuberculosis
mutants that failed to survive in the cecum of mice after orogastric inoculation. Twelve of these mutants were also attenuated for replication in the spleen after intraperitoneal infection, whereas one strain, mutated the gene encoding invasin, replicated as well as wild-type bacteria in the spleen. Several mutations were in operons encoding components of the type III secretion system, including components involved in translocating Yop proteins into host cells. This indicates that one or more Yops may be necessary for survival in the gastrointestinal tract. Three mutants were defective in O-antigen biosynthesis; these mutants were also unable to invade epithelial cells as efficiently as wild-type
Y. pseudotuberculosis
. Several other mutations were in genes that had not previously been associated with growth in a host, including
cls, ksgA
, and
sufl
. In addition, using Y.
pseudotuberculosis
strains marked with signature tags, we counted the number of different bacterial clones that were present in the cecum, mesenteric lymph nodes, and spleen 5 days postinfection. We find barriers in the host animal that limit the number of bacteria that succeed in reaching and/or replicating in the mesenteric lymph nodes and spleen after breaching the gut mucosa.
Correlation of Susceptibility of Immature Mice to Fungal Infection (Blastomycosis) and Effector Cell Function
Authors: Ganer Ari , Brummer Elmer , Stevens David A. 
Published: July 2002

ABSTRACTImmature mice are highly susceptible to blastomycosis, which is similar to other mycoses and has parallels in humans. The murine susceptibility is noteworthy in that it persists beyond the development of resistance to other, nonfungal pathogens and the maturation of most immune functions. As the susceptibility to blastomycosis appeared to be related to an early event after infection, primary effector cell function was studied. We found that peritoneal inflammatory cells, enriched for neutrophils, from immature (3-week-old) mice killed nonphagocytizableBlastomyces dermatitidiscells less (25%) than did cells from mature (8-week) mice (70%) (P< 0.01), a defect intrinsic to the neutrophils. This correlated with an impaired immature cell oxidative burst. Killing of phagocytizableCandida albicanswas not significantly different, 73 versus 87%. Thioglycolate-elicited cells were more impaired; killing ofB. dermatitidiswas insignificant, and killing ofC. albicanswas more impaired in immature (16% killing) than in mature (45%) cells (P< 0.02). Peripheral blood neutrophils from mature animals killedB. dermatitidis(41%) more than did those from immature animals (10%) (P< 0.02);C. albicanswas killed efficiently by both. Resting or activated peritoneal macrophages from both types of animals showed no differences inB. dermatitidiskilling. These results suggest that the susceptibility of immature mice is related at least in part to the depressed capacity of their neutrophils to killB. dermatitidis.
Development of an In Vivo Model for Study of Intestinal Invasion bySalmonella entericain Chickens
Authors: Aabo S. , Christensen J. P. , Chadfield M. S. , Carstensen B. , Jensen T. K. , Bisgaard M. , Olsen J. E. 
Published: July 2002

ABSTRACTAn in vivo loop test model for the investigation of the invasiveness ofSalmonella entericain chickens was developed. Ten jejunal loops were made in 10- to 12-week-old Lohman Brown chickens under isofluoran anaesthesia.Salmonellaat 5.0 × 107CFU was inoculated into each loop and left for 2 h, followed by a 1-h incubation with gentamicin in order to kill noninvading bacteria. After euthanasia,Salmonellainvasiveness was measured as tissue-associated counts relative to a reference strain. The ability ofSalmonellainvasion was 1 log10CFU higher per 42-mm2mucosal tissue in the anterior than in the posterior part of jejunum. A statistically significant (P< 0.001) sixfold difference in invasiveness was observed between a wild-typeS. entericaserotype Typhimurium strain and the correspondinginvHmutant. The model was shown to be able to show small differences in invasive capability and allows for comparison of strains tested in different animals, provided that the same reference strain is present in all animals.
Reduced Th1, but Not Th2, Cytokine Production by Lymphocytes after In Vivo Exposure of Healthy Subjects to Endotoxin
Authors: Lauw Fanny N. , ten Hove Tessa , Dekkers Pascale E. P. , de Jonge Evert , van Deventer Sander J. H. , van der Poll Tom 
Published: July 2002

ABSTRACTEndotoxin (lipopolysaccharide [LPS]) tolerance is characterized by a reduced capacity of monocytes to produce proinflammatory cytokines upon restimulation in vitro. To determine whether LPS exposure induces a change in lymphocyte cytokine production and whether this results in a shift in the T-helper 1 (Th1)/Th2 balance, whole blood obtained from seven healthy subjects before and after an intravenous injection of LPS (4 ng/kg) was stimulated in vitro with the T-cell stimulus anti-CD3/CD28 or staphylococcal enterotoxin B. Whole-blood production of the Th1 cytokines gamma interferon (IFN-γ) and interleukin-2 (IL-2) was markedly reduced at 3 and 6 h, while the production of the Th2 cytokines IL-4 and IL-5 was not influenced or was slightly increased. The IFN-γ/IL-4 ratio was strongly decreased at 6 h. Serum obtained after LPS exposure could slightly inhibit the release of IFN-γ but increased IL-4 production during stimulation of blood drawn from subjects not previously exposed to LPS. Normal serum also inhibited IFN-γ production, albeit to a lesser extent. LPS exposure influences lymphocyte cytokine production, resulting in a shift toward a Th2 cytokine response, an effect that may be mediated in part by soluble factors present in serum after LPS administration in vivo.
Synergistic Epithelial Responses to Endotoxin and a Naturally Occurring Muramyl Peptide
Authors: Flak Tod A. , Heiss Linda N. , Engle Jacquelyn T. , Goldman William E. 
Published: July 2002

ABSTRACTWe have investigated the synergistic interactions of a naturally occurring peptidoglycan fragment (muramyl peptide) and bacterial endotoxin in the induction of inflammatory processes within respiratory epithelial cells, at the levels of both signal transduction events and ultimate cellular metabolic effects. The source of the muramyl peptide isBordetella pertussis, the causative agent of the respiratory disease pertussis. During log-phase growth,B. pertussisreleases the muramyl peptide tracheal cytotoxin (TCT), which has the structureN- acetylglucosaminyl - 1,6 - anhydro -N- acetylmuramyl - (l) - alanyl - γ - (d) - glutamyl -meso- diaminopimelyl - (d) - alanine, equivalent to a monomeric subunit of gram-negative bacterial peptidoglycan. When applied to hamster trachea epithelial (HTE) cells, TCT and endotoxin were found to be highly synergistic in the induction of interleukin-1α (IL-1α), type II (inducible) nitric oxide synthase (iNOS), nitric oxide production, and inhibition of DNA synthesis. Neither molecule alone significantly triggered these responses. The serine/threonine protein kinase inhibitor H7 blocked induction of both IL-1α and iNOS. More selective inhibitors of protein kinase C, cyclic AMP-dependent protein kinase, and cyclic GMP-dependent protein kinase were not capable of blocking the effects of TCT and endotoxin, suggesting that the H7-inhibited component in this pathway is not among the commonly described kinase targets of H7. Treatment of HTE cells with exogenous IL-1 reproduced the induction of iNOS and DNA synthesis inhibition caused by TCT and endotoxin. H7 was not capable of interfering with effects caused by exogenous IL-1, implying that the H7-sensitive step in the pathway is upstream of IL-1 protein production. Similar assays with the phorbol ester phorbol myristate acetate indicate that it could effectively synergize with endotoxin but not with TCT, suggesting that TCT and endotoxin induce different signal transduction events that combine synergistically. The synergy observed with TCT and endotoxin in epithelial cells is significantly different from their interaction with other cell types, revealing a unique inflammatory response by epithelial cells to these natural bacterial products.