bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interleukin-10 Has Different Effects on Proliferation ofListeria monocytogenesin Livers and Spleens of Mice
Authors: Samsom Janneke N. , Annema Akke , Geertsma Minke F. , Langermans Jan A. M. , Groeneveld Paul H. P. , de Heer Emile , van Furth Ralph 
Published: July 2002

ABSTRACTThe aim of this study was to investigate the effect of interleukin-10 (IL-10) on the course ofListeria monocytogenesinfection in naive and immune mice. Treatment with IL-10 during the course of a primary infection significantly decreased the number of bacteria in the spleen and did not affect the number in the liver. During a secondary infection in immune mice treated with IL-10, the number of bacteria was significantly lower in the spleen but significantly higher in the liver in comparison to mock-treated immune mice. IL-10 treatment during a primaryListeriainfection decreased the concentration of gamma interferon (IFN-γ) in plasma and the toxoplasmastatic activity of macrophages, whereas it increased the percentage of mildly CD3-positive T cells in the spleen. During a secondary infection, the concentration of IFN-γ in plasma was decreased on day 1 but remained unaffected during later days of infection. From these results, we conclude that IL-10 has different effects on the proliferation ofL. monocytogenesin the spleen and liver during primary and secondaryListeriainfections.
Immunohistochemical Study of Lymphocyte Populations Infiltrating the Gastric Mucosa of Beagle Dogs Experimentally Infected withHelicobacter pylori
Authors: Rossi Giacomo , Fortuna Damiano , Pancotto Laura , Renzoni Giacomo , Taccini Ennio , Ghiara Paolo , Rappuoli Rino , Del Giudice Giuseppe 
Published: July 2002

ABSTRACTExperimental infection of beagle dogs withHelicobacter pyloriinduces recruitment to the gastric mucosae of neutrophils at early stages and later of mononuclear cells that organize into lymphoid follicles. These structures become macroscopically evident and consist of peripheral CD4+T lymphocytes and central CD21+B lymphocytes. Furthermore, transient expression of interleukin-8 (IL-8) parallels the presence of neutrophils in the gastric mucosae, whereas expression of IL-6 tends to persist chronically.
Nonimmune Interaction of the SfbI Protein ofStreptococcus pyogeneswith the Immunoglobulin G F(ab′)2Fragment
Authors: Medina Eva , Schulze Kai , Chhatwal Gursharan Singh , Guzmán Carlos Alberto 
Published: July 2002

ABSTRACTFibronectin-binding protein I (SfbI) ofStreptococcus pyogenesbinds to mouse immunoglobulin G (IgG) but not to IgA or IgM in a nonimmune fashion. The fibronectin-binding domains of SfbI were responsible for this activity, which was targeted to the IgG F(ab′)2fragment. SfbI also binds to B cells but not to CD4+or CD8+lymphocytes.
Burkholderia pseudomallei
Induces Cell Fusion and Actin-Associated Membrane Protrusion: a Possible Mechanism for Cell-to-Cell Spreading
Authors: Kespichayawattana W. , Rattanachetkul S. , Wanun T. , Utaisincharoen P. , Sirisinha S. 
Published: July 2002

ABSTRACT

Burkholderia pseudomallei
, a facultative intracellular bacterium, is the causative agent of a broad spectrum of diseases collectively known as melioidosis. Its ability to survive inside phagocytic and nonphagocytic cells and to induce multinucleated giant cell (MNGC) formation has been demonstrated. This study was designed to assess a possible mechanism(s) leading to this cellular change, using virulent and nonvirulent strains of
B. pseudomallei
to infect both phagocytic and nonphagocytic cell lines. We demonstrated that when the cells were labeled with two different cell markers (CMFDA or CMTMR), mixed, and then infected with
B. pseudomallei
, direct cell-to-cell fusion could be observed, leading to MNGC formation. Staining of the infected cells with rhodamine-conjugated phalloidin indicated that immediately after the infection, actin rearrangement into a comet tail appearance occurred, similar to that described earlier for other bacteria. The latter rearrangement led to the formation of bacterium-containing, actin-associated membrane protrusions which could lead to a direct cell-to-cell spreading of
B. pseudomallei
in the infected hosts. Results from 4′,6′-diamidine-2-phenylindole dihydrochloride (DAPI) nuclear staining, poly-ADP ribose polymerase cleavage, staining of infected cells for phosphatidylserine exposure with annexin V, and electrophoresis of the DNA extracted from these infected cells showed that
B. pseudomallei
could kill the host cells by inducing apoptosis in both phagocytic and nonphagocytic cells.
Prevotella intermedia
Stimulates Expansion of Vβ-Specific CD4
+
T Cells
Authors: Leung K.-P. , Torres Barbara A. 
Published: July 2002

ABSTRACT

Recent evidence suggests that certain periodontal pathogens preferentially stimulate T cells expressing specific variable regions on the β chain (Vβ) of the T-cell receptor, which may indicate the presence of a superantigen. Superantigens are microbial proteins that activate large numbers of CD4
+
T cells in a Vβ-specific manner. The purpose of this study was to determine whether
Prevotella intermedia
, a putative periodontal pathogen, activates populations of specific Vβ on CD4
+
T cells. Among the bacterial strains tested,
P. intermedia
strain 17, a clinical isolate, induced the strongest proliferative response in peripheral blood mononuclear cells. Antibodies raised against whole cells of this organism blocked the proliferative activity.
P. intermedia
-induced proliferation was T-cell specific and required the presence of antigen-presenting cells. Flow cytometric analysis showed that CD4
+
T-cell subsets expressing Vβ8, Vβ12, and Vβ17 expanded in response to
P. intermedia
strain 17. The ability of
P. intermedia
to stimulate CD4
+
-T-cell proliferation was further supported by the production profiles of key T-cell cytokines, gamma interferon and interleukin-2. The data collectively suggest that certain strains of
P. intermedia
can activate Vβ-specific T cells in a manner similar to that of other known microbial superantigens.
Signaling via Interleukin-4 Receptor α Chain Is Required for Successful Vaccination against Schistosomiasis in BALB/c Mice
Authors: Mountford Adrian P. , Hogg Karen G. , Coulson Patricia S. , Brombacher Frank 
Published: July 2002

ABSTRACTAlthough protective immunity in C57BL/6 mice induced by a single dose of the radiation-attenuated schistosome vaccine is believed to be mediated by Th1-type immune responses, we here report that in BALB/c mice protection can also depend upon signaling via the interleukin-4 (IL-4) receptor which conventionally governs the development of Th2-type immune responses. We show that in BALB/c mice deficient for the IL-4 receptor α chain (IL-4Rα−/−), which are unresponsive to IL-4 and IL-13, vaccine-induced protection is abrogated compared with that in wild-type (WT) mice. In vaccinated IL-4Rα−/−mice, IL-12p40 production by cells from the skin exposure site was elevated, although gamma interferon (IFN-γ) production in draining lymphoid tissues was similar in WT and IL-4Rα−/−mice. Nevertheless, the effector response in IL-4Rα−/−mice was Th1 biased with elevated IFN-γ in the lungs and higher immunoglobulin G2a (IgG2a) and IgG2b titers but negligible quantities of Th2-associated IgG1 and IgE. Interestingly, levels of IL-4 were equivalent in WT and IL-4Rα−/−mice, indicating that Th2 responses were not dependent upon signaling by IL-4 or IL-13. No differences in the phenotype and composition of the pulmonary effector mechanism that might explain the failure to induce protection in IL-4Rα−/−mice were detected. However, passive transfer of partial protection to naive IL-4Rα−/−mice, using serum from vaccinated WT mice, indicates that Th2-associated antibodies such as IgG1 have a role in parasite elimination in BALB/c strain mice and that signaling via IL-4R can be an important factor in the generation of protection.
Synthesis and Surface Expression of CD14 by Human Endothelial Cells
Authors: Jersmann Hubertus P. A. , Hii Charles S. T. , Hodge Greg L. , Ferrante Antonio 
Published: July 2002

ABSTRACTPrevious studies have reported that human vascular endothelial cells lack the membrane-bound lipopolysaccharide (LPS) receptor, CD14 (mCD14). By optimizing assay conditions, including the selection of anti-CD14 monoclonal antibody, we now demonstrate that human umbilical vein endothelial cells (HUVEC) express CD14 on the cell surface. Single-passage HUVEC showed approximately 20 times less expression of CD14 than monocytes. Interestingly, there was significant loss of surface CD14 expression with increasing numbers of culture passages. Evidence for synthesis of CD14 by HUVEC was provided by the finding thatl-[35S]methionine was incorporated into CD14. In addition, the expression of CD14 on HUVEC was upregulated by LPS, lysophosphatidic acid, and tissue culture supplements, and this upregulation was dependent on protein synthesis. Furthermore, the results imply that mCD14 is required for LPS-induced activation of endothelial cells in the absence of serum and that it acts in concert with serum factors (soluble CD14). Our results provide evidence that CD14 is expressed by endothelial cells and suggest that the previous inability to observe expression of this molecule has been due to culture and staining conditions. This finding has important implications for the understanding of the mechanisms by which LPS stimulates endothelial cells and the management of sepsis caused by gram-negative bacteria.
Molecular Cloning of aBacteroides caccaeTonB-Linked Outer Membrane Protein Identified by an Inflammatory Bowel Disease Marker Antibody
Authors: Wei Bo , Dalwadi Harnisha , Gordon Lynn K. , Landers Carol , Bruckner David , Targan Stephan R. , Braun Jonathan 
Published: July 2002

ABSTRACTCommensal enteric bacteria are a required pathogenic factor in inflammatory bowel disease (IBD), but the identity of the pertinent bacterial species is unresolved. Using an IBD-associated pANCA monoclonal antibody, a 100-kDa protein was recently characterized from an IBD clinical isolate ofBacteroides caccae(p2Lc3). In this study, consensus oligonucleotides were designed from 100-kDa peptides and used to identify a single-copy gene from the p2Lc3 genome. Sequence analysis of the genomic clone revealed a 2,844-bp (948 amino acid) open reading frame encoding features typical of the TonB-linked outer membrane protein family. This gene, termedompW,was detected by Southern analysis only inB. caccaeand was absent in other species ofBacteroidesand gram-negative coliforms. The closest homologues of OmpW included the outer membrane proteins SusC ofBacteroides thetaiotaomicronand RagA ofPorphyromonas gingivalis. Recombinant OmpW protein was immunoreactive with the monoclonal antibody, and serum anti-OmpW immunoglobulin A levels were elevated in a Crohn's disease patient subset. These findings suggest that OmpW may be a target of the IBD-associated immune response and reveal its structural relationship to a bacterial virulence factor ofP. gingivalisand periodontal disease.
Shiga Toxins Induce, Superinduce, and Stabilize a Variety of C-X-C Chemokine mRNAs in Intestinal Epithelial Cells, Resulting in Increased Chemokine Expression
Authors: Thorpe Cheleste M. , Smith Wendy E. , Hurley Bryan P. , Acheson David W. K. 
Published: July 2002

ABSTRACT

Exposure of humans to Shiga toxins (Stxs) is a risk factor for hemolytic-uremic syndrome (HUS). Because Stx-producing
Escherichia coli
(STEC) is a noninvasive enteric pathogen, the extent to which Stxs can cross the host intestinal epithelium may affect the risk of developing HUS. We have previously shown that Stxs can induce and superinduce IL-8 mRNA and protein in intestinal epithelial cells (IECs) in vitro via a ribotoxic stress response. We used cytokine expression arrays to determine the effect of Stx1 on various C-X-C chemokine genes in IECs. We observed that Stx1 induces multiple C-X-C chemokines at the mRNA level, including interleukin-8 (IL-8), GRO-α, GRO-β, GRO-γ, and ENA-78. Like that of IL-8, GRO-α and ENA-78 mRNAs are both induced and superinduced by Stx1. Furthermore, Stx1 induces both IL-8 and GRO-α protein in a dose-response fashion, despite an overall inhibition in host cell protein synthesis. Stx1 treatment stabilizes both IL-8 and GRO-α mRNA. We conclude that Stxs are able to increase mRNA and protein levels of multiple C-X-C chemokines in IECs, with increased mRNA stability at least one mechanism involved. We hypothesize that ribotoxic stress is a pathway by which Stxs can alter host signal transduction in IECs, resulting in the production of multiple chemokine mRNAs, leading to increased expression of specific proteins. Taken together, these data suggest that exposing IECs to Stxs may stimulate a proinflammatory response, resulting in influx of acute inflammatory cells and thus contributing to the intestinal tissue damage seen in STEC infection.
HLA-B27 Expression Does Not Modulate IntracellularChlamydia trachomatisInfection of Cell Lines
Authors: Young J. L. , Smith L. , Matyszak M. K. , Gaston J. S. H. 
Published: July 2002

ABSTRACTChlamydia trachomatisis an obligate intracellular pathogen. Infection of susceptible individuals with this bacterium can trigger the development of reactive arthritis, an acute inflammation that is associated with the expression of the class I major histocompatibility antigen, HLA-B27. Other facultative intracellular pathogens, such asYersiniaandSalmonellaspp., are also known triggers of reactive arthritis. Previous studies report conflicting results concerning whether the presence of HLA-B27 modulates the infection of cells with these enteric pathogens. In the present study, we have examined whether the expression of HLA-B27 can influence the infection of cell lines withC. trachomatisand also whether the replication of these bacteria is altered in HLA-B27-expressing cell lines. To do this, we have used a sensitive flow cytometric approach. We fixed and permeabilized cells and used fluorescein isothiocyanate-conjugated monoclonal antibody specific for chlamydia lipopolysaccharide to detect intracellular bacteria. The staining pattern obtained closely resembled the intracellular life cycle of chlamydia, with the appearance of brightly staining cells correlating to the microscopic detection of mature inclusion bodies. Moreover, since the percentage of cells that stained with the antibody was proportional to the infectious inoculum used, we were able to use the technique to quantitate the number of infectious organisms recoverable from infected cell lines. An important component of our study was the use of heparin to prevent reinfection of cells and thus enable the infection to be followed from a discrete time point. Our results suggest that HLA-B27 influences neither the infection nor replication ofC. trachomatisserovar L2 within cell lines. Consequently, the role of HLA-B27 in the pathogenesis of reactive arthritis may lie downstream of the invasion and replication stages of the triggering pathogenic infection.
Sequence Analysis of Four
Shigella boydii
O-Antigen Loci: Implication for
Escherichia coli
and
Shigella
Relationships
Authors: Wang Lei , Qu Wenjia , Reeves Peter R. 
Published: July 2002

ABSTRACT

Shigella
strains are in reality clones of
Escherichia coli
and are believed to have emerged relatively recently (G. M. Pupo, R. Lan, and P. R. Reeves, Proc. Natl. Acad. Sci. USA 97:10567–10572, 2000). There are 33 O-antigen forms in these
Shigella
clones, of which 12 are identical to O antigens of other
E. coli
strains. We sequenced O-antigen gene clusters from
Shigella boydii
serotypes 4, 5, 6, and 9 and also studied the O53- and O79-antigen gene clusters of
E. coli
, encoding O antigens identical to those of
S. boydii
serotype 4 and
S. boydii
serotype 5, respectively. In both cases the
S. boydii
and
E. coli
O-antigen gene clusters have the same genes and organization. The clusters of both
S. boydii
6 and
S. boydii
9 O antigens have atypical features, with a functional insertion sequence and a
wzx
gene located in the orientation opposite to that of all other genes in
S. boydii
serotype 9 and an
rmlC
gene located away from other
rml
genes in
S. boydii
serotype 6. Sequences of O-antigen gene clusters from another three
Shigella
clones have been published, and two of them also have abnormal structures, with either the entire cluster or one gene being located on a plasmid in
Shigella sonnei
or
Shigella dysenteriae
, respectively. It appears that a high proportion of clusters coding for O antigens specific to
Shigella
clones have atypical features, perhaps indicating recent formation of these gene clusters.
Role of Glucan and Surface Protein BAD1 in Complement Activation byBlastomyces dermatitidisYeast
Authors: Zhang Mason X. , Brandhorst Tristan T. , Kozel Thomas R. , Klein Bruce S. 
Published: July 2002

ABSTRACTOur previous studies showed thatBlastomyces dermatitidisyeast activates the human complement system, leading to deposition of opsonic complement fragments onto the yeast surface. This report examines the influence of altered surface expression of glucan or BAD1 protein (formerly WI-1) on the yeast's ability to activate and bind C3. Compared to the wild type, a glucan-deficient mutant yeast delayed initiation of C3 deposition and reduced C3-binding capacity by 50%. Linkage of baker's-yeast β-glucan to the glucan-deficient yeast restored initial C3 deposition kinetics to the wild-type level and partially restored C3-binding capacity, suggesting that β-glucan is an initiator of complement activation and a C3 acceptor. The role of BAD1 inB. dermatitidisyeast-complement interaction was also assessed.BAD1knockout yeast initiated faster C3 deposition and increased C3-binding capacity compared to the wild-type yeast or aBAD1-reconstituted yeast, suggesting either a lack of an intrinsic ability in BAD1 or an inhibitory role of BAD1 in complement activation and binding. However, both complement activation and the capacity for C3 binding by the wild-type yeast were enhanced in normal human serum supplemented with an anti-BAD1 monoclonal antibody (MAb) or in immune sera from blastomycosis patients. Microscopic analysis revealed that more initial C3-binding sites were formed on yeast in the presence of both naturally occurring complement initiators and exogenous anti-BAD1 MAb, suggesting that anti-BAD1 antibody enhanced the ability ofB. dermatitidisyeast to interact with the host complement system. Thus, glucan and BAD1 have distinctly different regulatory effects on complement activation byB. dermatitidis.
Characterization ofChlamydia pneumoniaePersistence in HEp-2 Cells Treated with Gamma Interferon
Authors: Pantoja Laura G. , Miller Richard D. , Ramirez Julio A. , Molestina Robert E. , Summersgill James T. 
Published: July 2002

ABSTRACTInfection withChlamydia pneumoniaehas been implicated as a potential risk factor for atherosclerosis. This study demonstrated the effects of gamma interferon (IFN-γ)-mediated indoleamine 2,3-dioxygenase activity onC. pneumoniaepersistence in HEp-2 cells, inclusion morphology, and ultrastructure.C. pneumoniaereplication showed a dose-dependent decrease when treated with increasing concentrations of IFN-γ and a phenotypic switch resulting in a decrease in typical inclusions with an increase in smaller, less-dense atypical inclusions. Ultrastructural analysis of IFN-γ-treatedC. pneumoniaerevealed atypical inclusions containing large reticulatate-like aberrant bodies with no evidence of redifferentiation into elementary bodies.
Migration-Inhibitory Factor Gene-Deficient Mice Are Susceptible to CutaneousLeishmania majorInfection
Authors: Satoskar Abhay R. , Bozza Marcelo , Rodriguez Sosa Miriam , Lin Guoshing , David John R. 
Published: July 2002

ABSTRACTTo determine the role of endogenous migration-inhibitory factor (MIF) in the development of protective immunity against cutaneous leishmaniasis, we analyzed the course of cutaneousLeishmania majorinfection in MIF gene-deficient mice (MIF−/−) and wild-type (MIF+/+) mice. Following cutaneousL. majorinfection, MIF−/−mice were susceptible to disease and developed significantly larger lesions and greater parasite burdens than MIF+/+mice. Interestingly, antigen-stimulated lymph node cells from MIF−/−mice produced more interleukin-4 (IL-4) and gamma interferon (IFN-γ) than those from MIF+/+mice, although the differences were statistically not significant. IFN-γ-activated resting peritoneal macrophages from MIF−/−mice showed impaired macrophage leishmanicidal activity and produced significantly lower levels of nitric oxide and superoxide in vitro. The macrophages from MIF−/−mice, however, produced much more IL-6 than macrophages from wild-type mice. These findings demonstrate that endogenous MIF plays an important role in the development of protective immunity againstL. majorin vivo. Furthermore, they indicate that the susceptibility of MIF−/−mice toL. majorinfection is due to impaired macrophage leishmanicidal activity rather than dysregulation of Th1 and Th2 responses.
Protective Cytotoxic T Lymphocyte Responses Induced by DNA Immunization against Immunodominant and Subdominant Epitopes ofListeria monocytogenesAre Noncompetitive
Authors: Yamada Takashi , Uchiyama Hiroshi , Nagata Toshi , Uchijima Masato , Suda Takafumi , Chida Kingo , Nakamura Hirotoshi , Koide Yukio 
Published: July 2002

ABSTRACTTaking advantage of the fact that plasmid DNA encoding a single cytotoxic T lymphocyte (CTL) epitope can induce CTLs, we examined the influence of T-cell responses to dominant epitopes on those to a subdominant epitope derived fromListeria monocytogenes. Our data suggest that interaction between T cells against dominant and subdominant epitopes does not operate in the generation of the hierarchy. Furthermore, we found that a single dominant epitope is sufficient for the induction of protective immunity.
Safety and Immunogenicity of Oral Inactivated Whole-Cell
Helicobacter pylori
Vaccine with Adjuvant among Volunteers with or without Subclinical Infection
Authors: Kotloff Karen L. , Sztein Marcelo B. , Wasserman Steven S. , Losonsky Genevieve A. , DiLorenzo Susan C. , Walker Richard I. 
Published: July 2002

ABSTRACT

Helicobacter pylori
infection of the gastric mucosa can be found in approximately 50% of the world's population and is associated with a range of pathology, including peptic ulcer, atrophic gastritis, and gastric cancer. To explore immunization as a strategy for preventing and treating
H. pylori
-associated disease, we assessed the safety and immunogenicity in healthy adults of a formalin-inactivated, oral
H. pylori
whole-cell (HWC) vaccine, administered with or without mutant
Escherichia coli
heat-labile toxin (LT
R192G
) as a mucosal adjuvant. In a dose-response study, 23 subjects with or without
H. pylori
infection were vaccinated with either 2.5 × 10
6
HWC, 2.5 × 10
8
HWC, or 2.5 × 10
10
HWC, plus 25 μg of LT
R192G
. Thereafter, a randomized study was conducted in which 18
H. pylori
-infected subjects were assigned, in a double-blind fashion, to receive either 2.5 × 10
10
HWC plus placebo-adjuvant, placebo-vaccine plus 25 μg of LT
R192G
, placebo-vaccine plus placebo-adjuvant, or 2.5 × 10
10
HWC plus 25 μg of LT
R192G
. Diarrhea (six subjects), low-grade fever (five subjects), and vomiting (two subjects) were observed, usually after the first dose. Significant rises in geometric mean mucosal (fecal and salivary) anti-HWC immunoglobulin A antibodies occurred among
H. pylori
-infected and uninfected subjects following inoculation with 2.5 × 10
10
HWC plus 25 μg of LT
R192G
. Moreover, among
H. pylori
-negative volunteers, this regimen induced significant lymphoproliferative responses in 5 of 10 subjects and gamma interferon production responses to
H. pylori
sonicate in 7 of 10 subjects. There was no evidence that vaccination eradicated
H. pylori
in infected volunteers. These results suggest that it is possible to stimulate mucosal and systemic immune responses in humans to
H. pylori
antigens by using an HWC vaccine.