bluuebunny/crossref_metadata_2025_split huggingface dataset:
Attractiveness of single and multiple species flower patches to beneficial insects in agroecosystems
Authors: Pontin D.R. , Wade M.R. , Kehrli P. , Wratten S.D. 
Published: December 2005

AbstractThe provision of floral resources for the enhancement of beneficial insect populations has shown promise as a strategy to enhance biological control and pollination in agroecosystems. One approach involves the provision of a single flower species while a second involves the multiple flower species, but the two have never been compared experimentally. Here we examine the influence of single and multiple species flower treatments on the abundance and foraging behaviour of key beneficial insects in two agricultural agroecosystems (broccoli and lucerne crops). The five flower treatments comprised buckwheat only, phacelia only, a simple mixture of buckwheat and phacelia, a complex mixture of buckwheat, phacelia and a commercial seed blend or the existing crop as a control. The abundance of bumble‐bees (Bombus hortorum) and honey bees (Apis mellifera) was highest in the three treatments that contained phacelia, while hoverfly (Melanostoma fasciatum) numbers were high in all four flower treatments. Bumble‐bees and honey bees probed almost exclusively phacelia flowers, even when provided with a choice of other flower species in the simple and complex mixture treatments. In contrast, hoverflies probed the flowers of all plant species in single and multiple species treatments, with no apparent difference in acceptance. However, in mixture treatments, the majority of individual bumble‐bees, honey bees and hoverflies probed the flowers from only one species, despite the presence of alternative flower species. Our results illustrate how an appreciation of insect floral attractiveness can be used to customise the species composition of floral patches to potentially maximise biological control and pollination in targeted agroecosystems.
The
Brucella suis
Type IV Secretion System Assembles in the Cell Envelope of the Heterologous Host
Agrobacterium tumefaciens
and Increases IncQ Plasmid pLS1 Recipient Competence
Authors: Carle Anna , Höppner Christoph , Ahmed Aly Khaled , Yuan Qing , den Dulk-Ras Amke , Vergunst Annette , O'Callaghan David , Baron Christian 
Published: December 2005

ABSTRACT

Pathogenic
Brucella
species replicate within mammalian cells, and their type IV secretion system is essential for intracellular survival and replication. The options for biochemical studies on the
Brucella
secretion system are limited due to the rigidity of the cells and biosafety concerns, which preclude large-scale cell culture and fractionation. To overcome these problems, we heterologously expressed the
Brucella suis virB
operon in the closely related α
2
-proteobacterium
Agrobacterium tumefaciens
and showed that the VirB proteins assembled into a complex. Eight of the twelve VirB proteins were detected in the membranes of the heterologous host with specific antisera. Cross-linking indicated protein-protein interactions similar to those in other type IV secretion systems, and the results of immunofluorescence analysis supported the formation of VirB protein complexes in the cell envelope. Production of a subset of the
B. suis
VirB proteins (VirB3-VirB12) in
A. tumefaciens
strongly increased its ability to receive IncQ plasmid pLS1 in conjugation experiments, and production of VirB1 further enhanced the conjugation efficiency. Plasmid recipient competence correlated with periplasmic leakage and the detergent sensitivity of
A. tumefaciens
, suggesting a weakening of the cell envelope. Heterologous expression thus permits biochemical characterization of
B. suis
type IV secretion system assembly.
Sexual Dimorphism in the Control of Amebic Liver Abscess in a Mouse Model of Disease
Authors: Lotter Hannelore , Jacobs Thomas , Gaworski Iris , Tannich Egbert 
Published: December 2005

ABSTRACTAmebic liver abscess (ALA) is the most common extraintestinal manifestation of human infection by the enteric protozoan parasiteEntamoeba histolytica. In contrast to intestinal infection, ALA greatly predominates in males but is rare in females. Since humans are the only relevant host forE. histolytica, experimental studies concerning this sexual dimorphism have been hampered by the lack of a suitable animal model. By serial liver passage of culturedE. histolyticatrophozoites in gerbils and mice, we generated amebae which reproducibly induce ALA in C57BL/6 mice. Interestingly, all animals developed ALA, but the time courses of abscess formation differed significantly between the genders. Female mice were able to clear the infection within 3 days, whereas in male mice the parasite could be recovered for at least 14 days. Accordingly, male mice showed a prolonged time of recovery from ALA. Immunohistology of abscesses revealed that polymorphonuclear leukocytes and macrophages were the dominant infiltrates, but in addition, γ,δ-T cells, NK cells, and natural killer T (NKT) cells were also present at early times during abscess development, whereas conventional α,β-T cells appeared later, when female mice had already cleared the parasite. Interestingly, male and female mice differed in early cytokine production in response to ameba infection. Enzyme-linked immunospot assays performed with spleen cells of infected animals revealed significantly higher numbers of interleukin-4-producing cells in male mice but significantly higher numbers of gamma interferon (IFN-γ)-producing cells in female mice. Early IFN-γ production and the presence of functional NKT cells were found to be important for the control of hepatic amebiasis as application of an IFN-γ-neutralizing monoclonal antibody or the use of NKT knockout mice (Vα14iNKT, Jα 18−/−) dramatically increased the size of ALA in female mice. In addition,E. histolyticatrophozoites could be reisolated from liver abscesses of Jα18−/−mice on day 7 postinfection, when wild-type mice had already cleared the parasite. These data suggest that the sexual dimorphism in the control of ALA is due to gender-specific differences in early cytokine production mediated at least in part by NKT cells in response toE. histolyticainfection of the liver.
The Chemokines CXCL9 and CXCL10 Promote a Protective Immune Response but Do Not Contribute to Cardiac Inflammation following Infection withTrypanosoma cruzi
Authors: Hardison Jenny L. , Wrightsman Ruth A. , Carpenter Philip M. , Lane Thomas E. , Manning Jerry E. 
Published: December 2005

ABSTRACTThe expression of chemokines within the heart during experimental infection of susceptible mice with the Colombiana strain ofTrypanosoma cruziwas characterized in an attempt to determine a functional role for these molecules in both host defense and disease. Analysis of chemokine transcripts revealed that CXC chemokine ligand 9 (CXCL9) and CXCL10, as well as CC chemokine ligand 2 (CCL2) and CCL5, were prominently expressed during acute disease, whereas transcripts for CXCL9, CXCL10, and CCL5 remained elevated during chronic infection. Inflammatory macrophages present within the heart were the primary cellular source of these chemokines followingT. cruziinfection. Peak chemokine expression levels coincided with increased gamma interferon expression and inflammation within the heart, suggesting a role for these molecules in both host defense and disease. Indeed, simultaneous treatment ofT. cruzi-infected mice with neutralizing antibodies specific for CXCL9 and CXCL10 resulted in an increased parasite burden that was sustained out to 50 days p.i. Antibody targeting either CXCL10 or CCL5 did not change eitherT. cruziburden within the heart nor attenuate the severity of cardiac inflammation at any time point examined, while targeting CXCL9 in combination with CXCL10 resulted in increased parasite burden. Collectively, these studies imply that CXCL9 and CXCL10 signaling enhances immune responses following parasite infection. However, antibody targeting of CXCL9 and CXCL10, or CXCL10 alone, or CCL5 alone does not directly modulate the inflammatory response within the heart, suggesting that other proinflammatory factors are able to regulate inflammation in this tissue in response toT. cruziinfection.
The CC Chemokine Receptor 5 Is Important in Control of Parasite Replication and Acute Cardiac Inflammation following Infection withTrypanosoma cruzi
Authors: Hardison Jenny L. , Wrightsman Ruth A. , Carpenter Philip M. , Kuziel William A. , Lane Thomas E. , Manning Jerry E. 
Published: December 2005

ABSTRACTInfection of susceptible mice with the Colombiana strain ofTrypanosoma cruziresults in an orchestrated expression of chemokines and chemokine receptors within the heart that coincides with parasite burden and cellular infiltration. CC chemokine receptor 5 (CCR5) is prominently expressed during both acute and chronic disease, suggesting a role in regulating leukocyte trafficking and accumulation within the heart followingT. cruziinfection. To better understand the functional role of CCR5 and its ligands with regard to both host defense and/or disease, CCR5−/−mice were infected withT. cruzi, and the disease severity was evaluated. Infected CCR5−/−mice develop significantly higher levels of parasitemia (P≤ 0.05) and cardiac parasitism (P ≤ 0.01) during acute infection that correlated with reduced survival. Further, we show that CCR5 is essential for directing the migration of macrophages and T cells to the heart early in acute infection withT. cruzi. In addition, data are provided demonstrating that CCR5 does not play an essential role in maintaining inflammation in the heart during chronic infection. Collectively, these studies clearly demonstrate that CCR5 contributes to the control of parasite replication and the development of a protective immune response during acute infection but does not ultimately participate in maintaining a chronic inflammatory response within the heart.
Binding and Internalization of Glucuronoxylomannan, the Major Capsular Polysaccharide ofCryptococcus neoformans, by Murine Peritoneal Macrophages
Authors: Chang Zong Liang , Netski Dale , Thorkildson Peter , Kozel Thomas R. 
Published: December 2005

ABSTRACTGlucuronoxylomannan (GXM), the major component of the capsular polysaccharide ofCryptococcus neoformans, is essential to virulence of the yeast. Previous studies found that the interaction between GXM and phagocytic cells has biological consequences that may contribute to the pathogenesis of cryptococcosis. We found that GXM binds to and is taken up by murine peritoneal macrophages. Uptake is dose and time dependent. Examination of the sites of GXM accumulation by immunofluorescence microscopy showed that the pattern was discontinuous and punctate both on the surfaces of macrophages and at intracellular depots. Although resident macrophages showed appreciable accumulation of GXM, uptake was greatest with thioglycolate-elicited macrophages. A modest stimulation of GXM binding followed treatment of resident macrophages with phorbol 12-myristate 13-acetate, but treatment with lipopolysaccharide or gamma interferon alone or in combination had no effect. Accumulation of GXM was critically dependent on cytoskeleton function; a near complete blockade of accumulation followed treatment with inhibitors of actin. GXM accumulation by elicited macrophages was blocked by treatment with inhibitors of tyrosine kinase, protein kinase C, and phospholipase C, but not by inhibitors of phosphatidylinositol 3-kinase, suggesting a critical role for one or more signaling pathways in the macrophage response to GXM. Taken together, the results demonstrate that it is possible to experimentally enhance or suppress binding of GXM to macrophages, raising the possibility for regulation of the interaction between this essential virulence factor and binding sites on cells that are central to host resistance.
Trypanosoma cruzi
Infection Induces Proliferation of Vascular Smooth Muscle Cells
Authors: Hassan Ghada S. , Mukherjee Shankar , Nagajyothi Fnu , Weiss Louis M. , Petkova Stefka B. , de Almeida Cecilia J. , Huang Huan , Desruisseaux Mahalia S. , Bouzahzah Boumediene , Pestell Richard G. , Albanese Chris , Christ George J. , Lisanti Michael P. , Tanowitz Herbert B. 
Published: December 2005

ABSTRACT

Trypanosoma cruzi
infection causes cardiomyopathy and vasculopathy. Previous studies have demonstrated that infection of human umbilical vein endothelial and smooth muscle cells resulted in activation of extracellular signal-regulated kinase (ERK). In the present study, smooth muscle cells were infected with trypomastigotes, and immunoblot analysis revealed an increase in the expression of cyclin D1 and proliferating cell nuclear antigen (PCNA), important mediators of smooth muscle cell proliferation. Interestingly, after infection, the expression of caveolin-1 was reduced in both human umbilical vein endothelial cells and smooth muscle cells. Immunoblot and immunohistochemical analyses of lysates of carotid arteries obtained from infected mice revealed increased expression of PCNA, cyclin D1, its substrate, phospho-Rb (Ser780), and phospho-ERK1/2. The expression of the cyclin-dependent kinase inhibitor p21

Cip1/Waf1

, caveolin-1, and caveolin-3 was reduced in carotid arteries obtained from infected mice. There was an increase in the abundance of pre-pro-endothelin-1 mRNA in the carotid artery and aorta from infected mice. The ET
A
receptor was also elevated in infected arteries. ERK activates endothelin-1, which in turn exerts positive feedback activating ERK, and cyclin D1 is a downstream target of both endothelin-1 and ERK. There was significant incorporation of bromodeoxyuridine into smooth muscle cell DNA when treatment was with conditioned medium obtained from infected endothelial cells. Taken together, these data suggest that
T. cruzi
infection stimulates smooth muscle cell proliferation and is likely a result of the upregulation of the ERK-cyclin D1-endothelin-1 pathway.
Transcriptional Profiling of
Mycoplasma hyopneumoniae
during Heat Shock Using Microarrays
Authors: Madsen Melissa L. , Nettleton Dan , Thacker Eileen L. , Edwards Robert , Minion F. Chris 
Published: December 2005

ABSTRACT

Bacterial pathogens undergo stress during host colonization and disease processes. These stresses result in changes in gene expression to compensate for potentially lethal environments developed in the host during disease.
Mycoplasma hyopneumoniae
colonizes the swine epithelium and causes a pneumonia that predisposes the host to enhanced disease from other pathogens. How
M. hyopneumoniae
responds to changing environments in the respiratory tract during disease progression is not known. In fact, little is known concerning the capabilities of mycoplasmas to respond to changing growth environments. With limited genes, mycoplasmas are thought to possess only a few mechanisms for gene regulation. A microarray consisting of 632 of the 698 open reading frames of
M. hyopneumoniae
was constructed and used to study gene expression differences during a temperature shift from 37°C to 42°C, a temperature swing that might be encountered during disease. To enhance sensitivity, a unique hexamer primer set was employed for generating cDNA from only mRNA species. Our analysis identified 91 genes that had significant transcriptional differences in response to heat shock conditions (
P
< 0.01) with an estimated false-discovery rate of 4 percent. Thirty-three genes had a change threshold of 1.5-fold or greater. Many of the heat shock proteins previously characterized in other bacteria were identified as significant in this study as well. A proportion of the identified genes (54 of 91) currently have no assigned function.
Antigen Discovery: a Postgenomic Approach to Leprosy Diagnosis
Authors: Aráoz Romulo , Honoré Nadine , Cho Sungae , Kim Jong-Pill , Cho Sang-Nae , Monot Marc , Demangel Caroline , Brennan Patrick J. , Cole Stewart T. 
Published: December 2005

ABSTRACT

Leprosy is an infectious, neurodegenerative disease of humans caused by
Mycobacterium leprae
. Despite effective control programs, the incidence of leprosy remains stubbornly high, suggesting that transmission may be more common than expected. The rationale of this work was to use bioinformatics and comparative genomics to identify potentially antigenic proteins for diagnostic purposes. This approach defined three classes of proteins: those restricted to
M. leprae
(class I), those present in
M. leprae
with orthologues in other organisms besides mycobacteria (class II), and exported or surface-exposed proteins (class III). Twelve genes (two class I, four class II, and six class III proteins) were cloned in
Escherichia coli
, and their protein products were purified. Six of these proteins were detected in cell extracts of
M. leprae
by immunoblotting. The immunogenicity of each recombinant protein was then investigated in leprosy patients by measuring the reactivity of circulating antibody and gamma interferon (IFN-γ) responses in T-cell restimulation assays. Several class II and class III proteins were recognized by circulating antibodies. Importantly, most class II proteins elicited IFN-γ responses that were significantly stronger than those produced by previously identified antigens. Among them, two class II proteins, ML0308 and ML2498, showed marked humoral and cellular immunogenicity, therefore providing promising candidates for the diagnosis of both tuberculoid and lepromatous forms of leprosy.
Enterocyte Cytoskeleton Changes Are Crucial for Enhanced Translocation of NonpathogenicEscherichia coliacross Metabolically Stressed Gut Epithelia
Authors: Nazli Aisha , Wang Arthur , Steen Oren , Prescott David , Lu Jun , Perdue Mary H. , Söderholm Johan D. , Sherman Philip M. , McKay Derek M. 
Published: December 2005

ABSTRACTSubstantial data implicate the commensal flora as triggers for the initiation of enteric inflammation or inflammatory disease relapse. We have shown that enteric epithelia under metabolic stress respond to nonpathogenic bacteria by increases in epithelial paracellular permeability and bacterial translocation. Here we assessed the structural basis of these findings. Confluent filter-grown monolayers of the human colonic T84 epithelial cell line were treated with 0.1 mM dinitrophenol (which uncouples oxidative phosphorylation) and noninvasive, nonpathogenicEscherichia coli(strain HB101, 106CFU) with or without pretreatment with various pharmacological agents. At 24 h later, apoptosis, tight-junction protein expression, transepithelial resistance (TER; a marker of paracellular permeability), and bacterial internalization and translocation were assessed. Treatment with stabilizers of microtubules (i.e., colchicine), microfilaments (i.e., jasplakinolide) and clathrin-coated pit endocytosis (i.e., phenylarsine oxide) all failed to block DNP+E. coliHB101-induced reductions in TER but effectively prevented bacterial internalization and translocation. Neither the TER defect nor the enhanced bacterial translocations were a consequence of increased apoptosis. These data show that epithelial paracellular and transcellular (i.e., bacterial internalization) permeation pathways are controlled by different mechanisms. Thus, epithelia under metabolic stress increase their endocytotic activity that can result in a microtubule-, microfilament-dependent internalization and transcytosis of bacteria. We speculate that similar events in vivo would allow excess unprocessed antigen and bacteria into the mucosa and could evoke an inflammatory response by, for example, the activation of resident or recruited immune cells.
Implications for Induction of Autoimmunity via Activation of B-1 Cells byHelicobacter pyloriUrease
Authors: Yamanishi Shingo , Iizumi Tadasu , Watanabe Eri , Shimizu Masumi , Kamiya Shigeru , Nagata Kumiko , Kumagai Yoshihiro , Fukunaga Yoshitaka , Takahashi Hidemi 
Published: December 2005

ABSTRACTBesides various gastroduodenal diseases,Helicobacter pyloriinfection may be involved in autoimmune disorders like rheumatoid arthritis (RA) or idiopathic thrombocytopenic purpura. Such autoimmune disorders are often associated with autoreactive antibodies produced by B-1 cells, a subpopulation of B lymphocytes. These B-1 cells are mainly located in the pleural cavity or mucosal compartment. The existence ofH. pyloriurease-specific immunoglobulin A (IgA)-producing B cells in the mucosal compartment and of their specific IgM in the sera of acutely infected volunteers suggests the possibility that urease stimulates mucosal innate immune responses. Here, we show for the first time that purifiedH. pyloriurease predominantly stimulates the B-1-cell population rather than B-2 cells, which produce antigen-specific conventional antibodies among splenic B220+B cells. The fact that such stimulation of B-1 cells was not affected by the addition of polymyxin B indicates that the effect of purifiedH. pyloriurease was not due to the contamination with bacterial lipopolysaccharide. Furthermore, the production of various B-1-cell-related autoreactive antibodies such as IgM-type rheumatoid factor, anti-single-stranded DNA antibody, and anti-phosphatidyl choline antibody was observed when the splenic B cells were stimulated with purifiedH. pyloriurease in vitro. These findings suggest thatH. pyloricomponents, urease in particular, may be among the environmental triggars that initiate various autoimmune diseases via producing autoreactive antibodies through the activation of B-1 cells. The findings shown here offer important new insights into the pathogenesis of autoimmune disorders related toH. pyloriinfection.
Target Antigen, Age, and Duration of Antigen Exposure Independently Regulate Immunoglobulin G Subclass Switching in Malaria
Authors: Tongren J. Eric , Drakeley Christopher J. , McDonald Suzanna L. R. , Reyburn Hugh G. , Manjurano Alphaxard , Nkya Watoky M. M. , Lemnge Martha M. , Gowda Channe D. , Todd Jim E. , Corran Patrick H. , Riley Eleanor M. 
Published: December 2005

ABSTRACTThe isotype/subclass of immunoglobulin determines antibody function, but rather little is known about factors that direct class switching in vivo. To evaluate factors that might influence the maturation of the antibody response during infection, we conducted a seroepidemiological study of the immunoglobulin G (IgG) subclass response to four merozoite-associated antigens ofPlasmodium falciparumin a mountainous region of northeastern Tanzania, where malaria endemicity declines with increasing altitudes. We found that IgG1/IgG3 class switching is independently affected by the nature of the antigen, cumulative exposure to the antigen, and the maturity of the immune system (i.e., the age of the individual). These observations provide insights into the effects of immune system maturity, the duration and intensity of antigen exposure, and inherent characteristics of individual antigens on the process of class switching in human B cells. Our data also throw light on the consequences of class switch decisions on the gradual acquisition of antimalarial immunity.