bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gamma Interferon Expression in CD8+T Cells Is a Marker for Circulating Cytotoxic T Lymphocytes That Recognize an HLA A2-Restricted Epitope of Human Cytomegalovirus Phosphoprotein pp65
Authors: Ghanekar Smita A. , Nomura Laurel E. , Suni Maria A. , Picker Louis J. , Maecker Holden T. , Maino Vernon C. 
Published: July 2002

ABSTRACTAntigen-specific CD8+T cells with cytotoxic activity are often critical in immune responses to infectious pathogens. To determine whether gamma interferon (IFN-γ) expression is a surrogate marker for cytotoxic T lymphocytes (CTL), human cytomegalovirus-specific CTL responses were correlated with CD8+T-cell IFN-γ expression determined by cytokine flow cytometry. A strong positive correlation was observed between specific lysis of peptide-pulsed targets in a51Cr release assay and frequencies of peptide-activated CD8+T cells expressing IFN-γ at 6 h (r2= 0.72) or 7 days (r2= 0.91). Enumeration of responding cells expressing perforin, another marker associated with CTL, did not improve this correlation. These results demonstrate that IFN-γ expression can be a functional surrogate for identification of CTL precursor cells.
Comparison of Hepatitis C Viral Loads in Patients with or without Human Immunodeficiency Virus
Authors: Matthews-Greer Janice M. , Caldito Gloria C. , Adley Sharon D. , Willis Regina , Mire Angela C. , Jamison Richard M. , McRae Kenny L. , King John W. , Chang Wun-Ling 
Published: July 2002

ABSTRACT

A better understanding of how human immunodeficiency virus (HIV) coinfection affects the course of hepatitis C virus (HCV) infection is required to select patients with HIV who would benefit from current HCV therapy. Between June 1996 and March 2000, HCV RNA levels were quantified for 1,279 patients at the Louisiana State University Health Sciences Center; 28 of these patients were coinfected with HIV. HCV loads were quantified by the Bayer branched-DNA assay with a lower limit of detection of 0.2 Meq/ml. We compared the median HCV RNA levels of for patients coinfected with HIV and HCV and patients infected only with HCV who were in the same age range (23 to 55 years). The median HCV load for the 28 patients coinfected with HCV and HIV (17.8 Meq/ml) was significantly greater (
P
< 0.05) than that for similarly aged patients infected only with HCV (6.1 Meq/ml). The HCV load did not correlate with age or sex for either group of patients. A significant (
R
= −0.4;
P
< 0.05) negative correlation was observed between HCV load and CD4 count in the coinfected group, for whom the CD4 counts at the time of HCV load analysis ranged from 6 to 1,773/mm
3
. The increased HCV load in patients coinfected with HCV and HIV compared to that in patients infected only with HCV and the inverse relationship of the HCV load to the CD4 count indicate that immunosuppression results in decreased control of HCV replication. In addition, we report significantly higher HCV loads among coinfected African Americans than Caucasians.
Excretory-Secretory Antigens of
Trypanosoma cruzi
Are Potentially Useful for Serodiagnosis of Chronic Chagas' Disease
Authors: Nakazawa Mineo , Rosa Daniela S. , Pereira Valéria R. A. , Moura Milena O. , Furtado Veridiana C. , Souza Wayner V. , Barros Maria Das Neves D. S. , Abath Frederico G. C. , Gomes Yara M. 
Published: July 2002

ABSTRACT

The reactivities of sera from chronic chagasic patients against the trypomastigote excreted-secreted antigens (TESA) of
Trypanosoma cruzi
strains with different biodemes were analyzed by TESA-blot and TESA–enzyme-linked immunosorbent assay (ELISA). Although both tests presented high sensitivity and specificity, TESA-ELISA is more appropriate for screening a larger number of samples.
Prevalence of Hepatitis E Virus Antibodies in Canadian Swine Herds and Identification of a Novel Variant of Swine Hepatitis E Virus
Authors: Yoo Dongwan , Willson Philip , Pei Yanlong , Hayes M. Anthony , Deckert Anne , Dewey Catherine E. , Friendship Robert M. , Yoon Yungho , Gottschalk Marcelo , Yason Carmencita , Giulivi Antonio 
Published: July 2002

ABSTRACT

Swine hepatitis E virus is a newly identified potentially zoonotic virus from pigs of particular concern for possible direct transmission to a human xenotransplant recipient by organ transplantation. In the present study, prevalence of serum antibodies to hepatitis E virus was examined in Canadian swine herds. A total of 998 serum samples collected from 6-month-old healthy slaughter hogs were examined by enzyme immunoassay and Western blot analysis for antibodies to the recombinant open reading frame 3 (ORF3) protein of hepatitis E virus expressed in
Escherichia coli
. These samples represented more than 80 different swine production units from five major swine-producing provinces across Canada. From this study, 594 samples (59.4%) were found to be positive for hepatitis E virus antibody. The seroprevalence was higher in Quebec (88.8%) and Ontario (80.1%) than in Alberta and Saskatchewan (38.3%). By PCR using a pair of oligonucleotide primers deduced from the ORF2 sequence of human hepatitis E virus, a specific hepatitis E virus sequence was recovered from feces of pigs. The nucleotide sequence identity between the U.S. swine hepatitis E virus and the Canadian isolate (SK3) was only 85.8%, suggesting that genotypic variations may exist in swine hepatitis E virus in North America. Among 165 serum samples collected from humans in Saskatchewan, 2.4% were found to be positive for antibodies to the hepatitis E virus ORF3 protein. Our data indicate that hepatitis E virus is highly prevalent in commercial swine populations in Canada and support the suggestion that the swine hepatitis E virus may be an important zoonotic agent for humans.
Wound Microbiology and Associated Approaches to Wound Management
Authors: Bowler P. G. , Duerden B. I. , Armstrong D. G. 
Published: July 2002

SUMMARYThe majority of dermal wounds are colonized with aerobic and anaerobic microorganisms that originate predominantly from mucosal surfaces such as those of the oral cavity and gut. The role and significance of microorganisms in wound healing has been debated for many years. While some experts consider the microbial density to be critical in predicting wound healing and infection, others consider the types of microorganisms to be of greater importance. However, these and other factors such as microbial synergy, the host immune response, and the quality of tissue must be considered collectively in assessing the probability of infection. Debate also exists regarding the value of wound sampling, the types of wounds that should be sampled, and the sampling technique required to generate the most meaningful data. In the laboratory, consideration must be given to the relevance of culturing polymicrobial specimens, the value in identifying one or more microorganisms, and the microorganisms that should be assayed for antibiotic susceptibility. Although appropriate systemic antibiotics are essential for the treatment of deteriorating, clinically infected wounds, debate exists regarding the relevance and use of antibiotics (systemic or topical) and antiseptics (topical) in the treatment of nonhealing wounds that have no clinical signs of infection. In providing a detailed analysis of wound microbiology, together with current opinion and controversies regarding wound assessment and treatment, this review has attempted to capture and address microbiological aspects that are critical to the successful management of microorganisms in wounds.
Adjuvant Activity of Monophosphoryl Lipid A for Nasal and Oral Immunization with Soluble or Liposome-Associated Antigen
Authors: Childers Noel K. , Miller Keri L. , Tong Giang , Llarena Juan Carlos , Greenway Terrance , Ulrich J. Terry , Michalek Suzanne M. 
Published: July 2002

ABSTRACTThe effectiveness of monophosphoryl lipid A (MPL) as a mucosal adjuvant was investigated following oral or intranasal (i.n.) administration of an aqueous adjuvant formulation of MPL (MPL-AF) added to soluble antigen or liposomal antigen or incorporated into liposomal antigen membranes. Groups of BALB/c female mice were immunized with 50 to 100 μg of free or liposomalStreptococcus mutanscrude glucosyltransferase (C-GTF) with or without MPL-AF added to the vaccine or incorporated into the liposomal membrane. Plasma, saliva, vaginal wash, and fecal extract samples were collected biweekly following immunization and assessed for antigen-specific antibody activity by enzyme-linked immunosorbent assay (ELISA). Mice immunized by the i.n. route had higher levels of salivary, plasma, and vaginal immunoglobulin A (IgA) anti-C-GTF responses and higher levels of plasma IgG anti-C-GTF than the orally immunized groups. A second administration of the vaccine 14 weeks after the initial immunization resulted in an anamnestic response to C-GTF resulting in 10- and 100-fold increases in saliva and plasma IgA and plasma IgG, respectively (in the i.n. immunized groups). Mice receiving a second i.n. immunization with liposomal antigen and MPL-AF had higher salivary IgA anti-C-GTF responses than mice immunized with antigen plus MPL-AF or liposomal antigen (P< 0.05). Plasma IgG anti-C-GTF activity was highest in mice immunized by the i.n. route with antigen formulations containing MPL-AF (P< 0.05). These results demonstrate the effectiveness of MPL-AF as an adjuvant for potentiating mucosal and systemic immune responses to liposomal C-GTF following i.n. immunization.
Comparison of Abilities of
Salmonella enterica
Serovar Typhimurium
aroA aroD
and
aroA htrA
Mutants To Act as Live Vectors
Authors: Roberts Mark , Chatfield Steven , Pickard Derek , Li Jingli , Bacon Andrew 
Published: July 2002

ABSTRACT

We compared the ability of
Salmonella enterica
serovar Typhimurium SL1344
aroA aroD
(BRD509) and
aroA htrA
(BRD807) mutants to act as live vectors for delivery of fragment C of tetanus toxin (FrgC). FrgC was expressed in these strains from either pTETnir15 or pTEThtrA1. BRD509FrgC
+
strains elicited ∼2-log-higher serum anti-FrgC antibody titers than BRD807FrgC
+
strains. All mice immunized with BRD807pTEThtrA1, BRD509pTEThtrA1, and BRD509pTETnir15 (but not BRD807pTETnir15) were protected against tetanus.
Activation of Nuclear Factor κB and Induction of Inducible Nitric Oxide Synthase byUreaplasma urealyticumin Macrophages
Authors: Li Y.-H. , Yan Z.-Q. , Jensen J. Skov , Tullus K. , Brauner A. 
Published: July 2002

ABSTRACTChronic lung disease (CLD) of prematurity is an inflammatory disease with a multifactorial etiology. The importance ofUreaplasma urealyticumin the development of CLD is debated, and steroids produce some improvement in neonates with this disease. In the present study, the capability ofU. urealyticumto stimulate rat alveolar macrophages to produce nitric oxide (NO), express inducible nitric oxide synthase (iNOS), and activate nuclear factor κB (NF-κB) in vitro was characterized. The effect of NO on the growth ofU. urealyticumwas also investigated. In addition, the impact of dexamethasone and budesonide on these processes was examined. We found thatU. urealyticumantigen (≥4 × 107color-changing units/ml) stimulated alveolar macrophages to produce NO in a dose- and time-dependent manner (P< 0.05). This effect was further enhanced by gamma interferon (100 IU/ml;P< 0.05) but was attenuated by budesonide and dexamethasone (10−4to 10−6M) (P< 0.05). The mRNA and protein levels of iNOS were also induced in response toU. urealyticumand inhibited by steroids.U. urealyticumantigen triggered NF-κB activation, a possible mechanism for the induced iNOS expression, which also was inhibited by steroids. NO induced byU. urealyticumcaused a sixfold reduction of its own growth after infection for 10 h. Our findings imply thatU. urealyticummay be an important factor in the development of CLD. The host defense response againstU. urealyticuminfection may also be influenced by NO. The down-regulatory effect of steroids on NF-κB activation, iNOS expression, and NO production might partly explain the beneficial effect of steroids in neonates with CLD.
Disruption of the Genes Encoding Antigen 85A and Antigen 85B of
Mycobacterium tuberculosis
H37Rv: Effect on Growth in Culture and in Macrophages
Authors: Armitige Lisa Y. , Jagannath Chinnaswamy , Wanger Audrey R. , Norris Steven J. 
Published: July 2002

ABSTRACT

The mechanism of pathogenesis of
Mycobacterium tuberculosis
is thought to be multifactorial. Among the putative virulence factors is the antigen 85 (Ag85) complex. This family of exported fibronectin-binding proteins consists of members Ag85A, Ag85B, and Ag85C and is most prominently represented by 85A and 85B. These proteins have recently been shown to possess mycolyl transferase activity and likely play a role in cell wall synthesis. The purpose of this study was to generate strains of
M. tuberculosis
deficient in expression of the principal members of this complex in order to determine their role in the pathogenesis of
M. tuberculosis
. Constructs of
fbpA
and
fbpB
disrupted with the kanamycin resistance marker ΩKm and containing varying amounts of flanking gene and plasmid vector sequences were then introduced as linear fragments into H37Rv by electroporation. Southern blot and PCR analyses revealed disruption of the homologous gene locus in one
fbpA
::ΩKm transformant and one
fbpB
::ΩKm transformant. The
fbpA
::ΩKm mutant, LAa1, resulted from a double-crossover integration event, whereas the
fbpB
::ΩKm variant, LAb1, was the product of a single-crossover type event that resulted in insertion of both ΩKm and plasmid sequences. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis confirmed that expression of the disrupted gene was not detectable in the
fbpA
and
fbpB
mutants. Analysis of growth rates demonstrated that the
fbpB
mutant LAb1 grew at a rate similar to that of the wild-type parent in enriched and nutrient-poor laboratory media as well as in human (THP-1) and mouse (J774.1A) macrophage-like cell lines. The
fbpA
mutant LAa1 grew similarly to the parent H37Rv in enriched laboratory media but exhibited little or no growth in nutrient-poor media and macrophage-like cell lines. The targeted disruption of two genes encoding mycolyl transferase and fibronectin-binding activities in
M. tuberculosis
will permit the systematic determination of their roles in the physiology and pathogenesis of this organism.
Activated T Cells Induce Macrophages To Produce NO and ControlLeishmania majorin the Absence of Tumor Necrosis Factor Receptor p55
Authors: Nashleanas Michelle , Scott Phillip 
Published: July 2002

ABSTRACTThe ability to activate macrophages in vitro for nitric oxide production and killing ofLeishmania majorparasites is dependent on tumor necrosis factor, althoughL. major-infected mice lacking the TNF receptor p55 (TNFRp55−/−mice) or both the TNFRp55 and TNFRp75 (TNFRp55p75−/−mice) are able to produce NO in vivo and eliminate the parasites. Here we report that activated T cells cocultured with macrophages results in TNFR-independent activation sufficient to control parasites and that both CD40/CD40L and LFA-1 contribute to T-cell-mediated macrophage activation. Thus, anti-CD3-stimulated T cells activated TNFR-deficient macrophages, while T cells from CD40L−/−mice were partially defective in triggering NO production by TNFRp55p75−/−macrophages. Moreover, in the presence of gamma interferon, anti-CD40 monoclonal antibody (MAb) activated TNFR-deficient macrophages. Finally, MAb blockade of LFA-1 completely inhibited macrophage NO production. Our data indicate that T cells can activate macrophages in the absence of TNF, thus providing a mechanism for how TNFR-deficient mice can control intracellular pathogens.
CXC Chemokine Receptor CXCR2 Is Essential for Protective Innate Host Response in MurinePseudomonas aeruginosaPneumonia
Authors: Tsai Wan C. , Strieter Robert M. , Mehrad Borna , Newstead Michael W. , Zeng Xianying , Standiford Theodore J. 
Published: July 2002

ABSTRACTPulmonary infection due toPseudomonas aeruginosahas emerged as a leading cause of mortality. A vigorous host response is required to effectively clear the organisms from the lungs. This host defense is dependent on the recruitment and activation of neutrophils and macrophages. A family of chemotactic cytokines (chemokines) has been shown to participate in this protective response. In this study, we assessed the role of the ELR+(glutamic acid-leucine-arginine motif positive) CXC chemokines and their CXC chemokine receptor (CXCR2) in lung antibacterial host defense. The intratracheal administration ofPseudomonasto mice resulted in the time-dependent influx of neutrophils to the lung, peaking at 12 to 24 h after inoculation. The influx of neutrophils was associated with a similar time-dependent expression of the ELR+CXC chemokines, KC, macrophage inflammatory protein 2 (MIP-2), and lipopolysaccharide-induced CXC chemokine (LIX). Selective neutralization of MIP-2 or KC resulted in modest changes in neutrophil influx but no change in bacterial clearance or survival. However, neutralization of CXCR2 resulted in a striking increase in mortality, which was associated with a marked decrease in neutrophil recruitment and bacterial clearance. Conversely, the site-specific transgenic expression of KC resulted in enhanced clearance of bacteria afterPseudomonaschallenge. This study indicates that ELR+CXC chemokines are critical mediators of neutrophil-mediated host defense inPseudomonaspneumonia.
Cl
−
Secretion in Colonic Epithelial Cells Induced by the
Vibrio parahaemolyticus
Hemolytic Toxin Related to Thermostable Direct Hemolysin
Authors: Takahashi Akira , Kenjyo Noriko , Imura Kinichi , Myonsun Yoh , Honda Takeshi 
Published: July 2002

ABSTRACT

A hemolytic toxin related to thermostable direct hemolysin (TDH), TDH-related hemolysin (TRH), produced by Kanagawa-phenomenon-negative
Vibrio parahaemolyticus
is suspected of playing an important, but yet-to-be-elucidated role in diarrhea caused by this organism. In cultured human colonic epithelial cells, TRH increases Cl
−
secretion, followed by elevation of intracellular calcium.
Human T- and B-Cell Responses toSchistosoma mansoniRecombinant Glyceraldehyde 3-Phosphate Dehydrogenase Correlate with Resistance to Reinfection withS. mansoniorSchistosoma haematobiumafter Chemotherapy
Authors: El Ridi Rashika , Shoemaker Charles B. , Farouk Faten , El Sherif Naglaa H. , Afifi Ahmed 
Published: July 2002

ABSTRACTRecently we reported that human T- and B-cell recognition of a 42-kDa protein (p42) in soluble extracts of adultSchistosoma mansoniworms correlates with resistance to reinfection withS. mansoniorS. haematobium. Amino acid microsequencing of p42 revealed that it consists predominantly of schistosome glyceraldehyde 3-phosphate dehydrogenase (SG3PDH). We have expressed SG3PDH inEscherichia coliand purified the recombinant protein in a soluble and enzymatically active form. Recombinant SG3PDH (rSG3PDH) reacted with human monospecific antibodies to p42. Lymphoproliferation and production of interleukin-4 and gamma interferon (IFN-γ) after in vitro stimulation with rSG3PDH and serum isotype responses to rSG3PDH were examined in individuals with extremes of resistance and susceptibility to reinfection after treatment of previousS. mansoniorS. haematobiuminfection. Lymphoproliferation and IFN-γ production in response to rSG3PDH and the presence of serum immunoglobulin G1 (IgG1), IgG3, and IgA antibodies to rSG3PDH generally characterized individuals who are resistant to reinfection after chemotherapy. The data indicate that T- and B-cell immune reactivity to rSG3PDH correlates with resistance to reinfection, confirming previous studies identifying SG3PDH as a target of protective immunity in humans, and suggest that SG3PDH should be investigated as a possible vaccine for human schistosomiasis.
Legionella pneumophilaEntry GenertxAIs Involved in Virulence
Authors: Cirillo Suat L. G. , Bermudez Luiz E. , El-Etr Sahar H. , Duhamel Gerald E. , Cirillo Jeffrey D. 
Published: July 2002

ABSTRACTSuccessful parasitism of host cells by intracellular pathogens involves adherence, entry, survival, intracellular replication, and cell-to-cell spread. Our laboratory has been examining the role of early events, adherence and entry, in the pathogenesis of the facultative intracellular pathogenLegionella pneumophila. Currently, the mechanisms used byL. pneumophilato gain access to the intracellular environment are not well understood. We have recently isolated three loci, designatedenh1,enh2, andenh3, that are involved in the ability ofL. pneumophilato enter host cells. One of the genes present in theenh1locus,rtxA, is homologous to repeats in structural toxin genes (RTX) found in many bacterial pathogens. RTX proteins from other bacterial species are commonly cytotoxic, and some of them have been shown to bind to β2integrin receptors. In the current study, we demonstrate that theL. pneumophila rtxAgene is involved in adherence, cytotoxicity, and pore formation in addition to its role in entry. Furthermore, anrtxAmutant does not replicate as well as wild-typeL. pneumophilain monocytes and is less virulent in mice. Thus, we conclude that the entry genertxAis an important virulence determinant inL. pneumophilaand is likely to be critical for the production of Legionnaires' disease in humans.
EnteropathogenicEscherichia coliInfection Induces Expression of the Early Growth Response Factor by Activating Mitogen-Activated Protein Kinase Cascades in Epithelial Cells
Authors: de Grado Myriam , Rosenberger Carrie M. , Gauthier Annick , Vallance Bruce A. , Finlay B. Brett 
Published: July 2002

ABSTRACTEnteropathogenicEscherichia coli(EPEC) is an extracellular bacterial pathogen that infects the human intestinal epithelium and is a major cause of infantile diarrhea in developing countries. EPEC belongs to the group of attaching and effacing (A/E) pathogens. It uses a type III secretion system to deliver proteins into the host cell that mediate signal transduction events in host cells. We used gene array technology to study epithelial cell responses to EPEC infection at the level of gene expression. We found that EPEC induces the expression of several genes in infected HeLa cells by a lipopolysaccharide (LPS)-independent mechanism, including cytokines and early growth response factor 1 (Egr-1). The transcription factor Egr-1 is an immediate-early-induced gene that is activated in most cell types in response to stress. EPEC-induced upregulation ofegr-1is mediated by the activation of the MEK/extracellular signal-regulated kinase signal transduction pathway and is dependent on the type III secretion system.egr-1is also induced during infection of mice by the A/E pathogenCitrobacter rodentium, suggesting that both Egr-1 and the activation of this mitogen-activated protein kinase signal transduction pathway may play a role in disease.