bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Polysaccharide Portion of Lipopolysaccharide Regulates Antigen-Specific T-Cell Activation via Effects on Macrophage-Mediated Antigen Processing
Authors: Zirk Nicole M. , Hashmi Saira F. , Ziegler H. Kirk 
Published: December 2019

ABSTRACTThe lipopolysaccharide (LPS) structure ofSalmonella typhimuriumhas been correlated with the virulence of wild-type strain LT2. Mutants of LT2 with truncated polysaccharide portions of LPS are less virulent than strains with a complete LPS structure. Polyclonal T cells and monoclonal T-cell hybridomas were more reactive to heat-killed rough mutants than to heat-killed smooth strains, as measured by interleukin-2 (IL-2) production. Using a large panel of strains with truncated LPS molecules, we found that T-cell reactivity decreased with certain lengths of polysaccharide. The decreased response was not due to differential phagocytic uptake, IL-12 production, or major histocompatibility complex class II surface expression by macrophages. Also, LT2 did not mediate any global suppression since addition of LT2 did not diminish the response of T cells specific for antigens unrelated toSalmonella. In an experiment in which processing times were varied, we found that antigens from rough strains were processed and presented more quickly than those associated with smooth strains. At longer processing times, epitopes from LT2 were presented well. We hypothesize that the slower antigen processing and presentation of wild-typeSalmonellamay be caused by masking of surface antigens by the longer polysaccharide portion of smooth LPS. This blocking of effective antigen presentation may contribute to the virulence ofSalmonella.
Helicobacter pyloriInfection in Immunized Mice Lacking Major Histocompatibility Complex Class I and Class II Functions
Authors: Pappo Jacques , Torrey Deirdre , Castriotta Lillian , Savinainen Anneli , Kabok Zita , Ibraghimov Alexander 
Published: December 2019

ABSTRACTThe role of major histocompatibility complex (MHC) class I- and class II-restricted functions inHelicobacter pyloriinfection and immunity upon oral immunization was examined in vivo. Experimental challenge withH. pyloriSS1 resulted in significantly greater (P≤ 0.025) colonization of MHC class I and class II mutant mice than C57BL/6 wild-type mice. Oral immunization withH. pyloriwhole-cell lysates and cholera toxin adjuvant significantly reduced the magnitude ofH. pyloriinfection in C57BL/6 wild-type (P= 0.0083) and MHC class I knockout mice (P= 0.0048), but it had no effect on theH. pyloriinfection level in MHC class II-deficient mice. Analysis of the anti-H. pyloriantibody levels in serum showed a dominant serum immunoglobulin G1 (IgG1) response in immunized C57BL/6 wild-type and MHC class I mutant mice but no detectable serum IgG response in MHC class II knockout mice. Populations of T-cell-receptor (TCR) αβ+CD4+CD54+cells localized to gastric tissue of immunized C57BL/6 wild-type and MHC class I knockout mice, but TCRαβ+CD8+cells predominated in the gastric tissue of immunized MHC class II-deficient mice. These observations show that CD4+T cells engaged after mucosal immunization may be important for the generation of a protective anti-H. pyloriimmune response and that CD4+CD8−and CD4−CD8+T cells regulate the extent ofH. pyloriinfection in vivo.
Specificity of Infection-Induced Immunity amongBorrelia burgdorferiSensu Lato Species
Authors: Barthold Stephen W. 
Published: December 2019

ABSTRACTThe specificity of infection-induced immunity in mice infected with cultured or host-adaptedBorrelia burgdorferisensu lato, the agent of Lyme disease, was examined. Sera obtained from mice following infection with high and low doses of culturedB. burgdorferisensu stricto, transplantation of infected tissue (host-adapted spirochetes), or tick-borne inoculation all showed protective activity in passive immunization assays. Infection and disease were similar in mice infected with cultured spirochetes or by transplantation. Thus, the adaptive form of inoculated spirochetes did not influence the immune response during active infection. Mice infected withB. burgdorferisensu stricto and then cured of infection with an antibiotic during early or late stages of infection were resistant to challenge with high doses of homologous cultured spirochetes for up to 1 year. In contrast, actively immune mice infected with differentBorreliaspecies (B. burgdorferisensu lato,B. burgdorferisensu stricto cN40,Borrelia afzeliiPKo, andBorrelia gariniiPBi) and then treated with an antibiotic were resistant to challenge with cultured homologous but not heterologous spirochetes. Similar results were achieved for actively immune mice challenged by transplantation and by passive immunization with sera from mice infected with each of theBorreliaspecies and then challenged with cultured spirochetes. Arthritis and carditis in mice that had immunizing infections withB. afzeliiandB. gariniiand then challenged by transplantation withB. burgdorferisensu stricto were equivalent in prevalence and severity to those in nonimmune recipient mice. These results indicate that protective immunity and disease-modulating immunity that develop during active infection are universal among species related toB. burgdorferisensu lato but are species specific.
Increased Levels of Soluble CD14 in Sera of Periodontitis Patients
Authors: Hayashi Joichiro , Masaka Tamami , Ishikawa Isao 
Published: December 2019

ABSTRACTSoluble CD14 (sCD14) mediates the response to lipopolysaccharide (LPS) in cells lacking membrane-bound CD14. We determined sCD14 concentrations in the sera of 38 periodontitis patients and 25 healthy controls by enzyme-linked immunosorbent assay. The sCD14 levels in the sera of patients with periodontitis were significantly higher than those of healthy subjects and decreased after treatment. Enhanced levels of sCD14 in serum may contribute to the host response to LPS in periodontitis. Furthermore, we showed in vitro that addition of LPS enhanced the release of sCD14 by monoblastic U937 cells treated with 1α,25-dihydroxyvitamin D3. Thus, increased sCD14 levels in periodontitis patients may be due to chronic exposure to LPS.
Virulence Properties of
Escherichia coli
83972, a Prototype Strain Associated with Asymptomatic Bacteriuria
Authors: Hull Richard A. , Rudy Delbert C. , Donovan William H. , Wieser Inge E. , Stewart Colleen , Darouiche Rabih O. 
Published: December 2019

ABSTRACT

Little is known about bacteria associated with asymptomatic bacteriuria (ABU) with regard to urinary tract colonization mechanisms. In this study, virulence properties of
Escherichia coli
83972, a strain that was isolated from a clinical ABU episode, were examined. The genetic potential for expression of P and type 1 pili was demonstrated, and DNA sequences related to type 1C and G (UCA) pilus genes were also detected. However,
E. coli
83972 did not express
d
-mannose-resistant or
d
-mannose-sensitive hemagglutination after growth under standard conditions in vitro or upon isolation from the urine of colonized test subjects. Limited uroepithelial cell adherence was observed in vivo, and weak
d
-mannose-sensitive hemagglutination was detected after extended growth in urine in vitro.
Nonrestricted Differential Intoxication of Cells by Pertussis Toxin
Authors: el Bayâ Ali , Brückener Kerstin , Schmidt M. Alexander 
Published: December 2019

ABSTRACT

After uptake and retrograde transport pertussis toxin acts by ADP-ribosylating α-G
i
proteins. We show that uptake via many different receptor proteins followed by retrograde transport and intoxication is not restricted to a particular cell type. The efficiency of cellular intoxication, however, was found to be cell type dependent.
γδ T-Cell Function in Pathogenesis of Cerebral Malaria in Mice Infected withPlasmodium bergheiANKA
Authors: Yañez D. M. , Batchelder J. , van der Heyde H. C. , Manning D. D. , Weidanz W. P. 
Published: December 2019

ABSTRACTMice depleted of γδ T cells by monoclonal antibody treatment and infected withPlasmodium bergheiANKA did not develop cerebral malaria (CM). In striking contrast, δ0/0mice infected withP. bergheideveloped CM despite their γδ T-cell deficiency. γδ T cells appear to be essential for the pathogenesis of CM in mice having experienced normal ontogeny but not in mice genetically deprived of γδ T cells from the beginning of life.
Binding of
Actinobacillus pleuropneumoniae
Lipopolysaccharides to Glycosphingolipids Evaluated by Thin-Layer Chromatography
Authors: Abul-Milh Maan , Paradis Sonia-Élaine , Dubreuil J. Daniel , Jacques Mario 
Published: December 2019

ABSTRACT

The binding profile of
Actinobacillus pleuropneumoniae
serotypes 1 and 2 to various glycosphingolipids was evaluated by using thin-layer chromatogram overlay.
A. pleuropneumoniae
whole cells recognized glucosylceramide (Glcβ1Cer), galactosylceramide (Galβ1Cer) with hydroxy and nonhydroxy fatty acids, sulfatide (SO
3
-3Galβ1Cer), lactosylceramide (Galβ1-4Glcβ1Cer), gangliotriaosylceramide GgO
3
(GalNAcβ1-4Galβ1-4Glcβ1Cer), and gangliotetraosylceramide GgO
4
(Galβ1-3GalNAcβ1-4Galβ1-4Glcβ1Cer) glycosphingolipids. We observed no binding to globoseries, globotriaosylceramide Gb
3
, globoside Gb
4
, or Forssman Gb
5
glycosphingolipids or to gangliosides GM1, GM2, GM3, GD1a, GD1b, GD3, and GT1b. The
A. pleuropneumoniae
strains tested also failed to detect phosphatidylethanolamine or ceramide. Interestingly, extracted lipopolysaccharide (LPS) of serotype 1 and serotype 2 as well as detoxified LPS of serotype 1 showed binding patterns similar to that of whole bacterial cells. Binding to GlcCer, GalCer, sulfatide, and LacCer, but not to GgO
3
and GgO
4
glycosphingolipids, was inhibited after incubation of the bacteria with monoclonal antibodies against LPS O antigen. These findings indicate the involvement of LPS in recognition of three groups of glycosphingolipids: (i) GlcCer and LacCer, where glucose is probably an important saccharide sequence required for LPS binding; (ii) GalCer and sulfatide glycosphingolipids, where the sulfate group is part of the binding epitope of the isoreceptor; and (iii) GgO
3
and GgO
4
, where GalNacβ1-4Gal disaccharide represents the minimal common binding epitope. Taken together, our results indicate that
A. pleuropneumoniae
LPS recognize various saccharide sequences found in different glycosphingolipids, which probably represents a strong virulence attribute.
Limited Interleukin-18 Response inSalmonella-Infected Murine Macrophages and inSalmonella-Infected Mice
Authors: Elhofy Adam , Bost Kenneth L. 
Published: December 2019

ABSTRACTOptimal immune responses against an intracellular bacterial pathogen, such asSalmonella, involve the production of gamma interferon (IFN-γ), which activates macrophages. It has recently been suggested that, interleukin-18 (IL-18), in addition to IL-12, contributes to the induction of IFN-γ following infection. Given this hypothesis, an optimal host immune response against intracellular bacterial pathogens would include the induction of IL-18 secretion by macrophages due toSalmonellainfection. We questioned whetherSalmonellacould induce macrophages to upregulate their expression of IL-18 mRNA and secretion of IL-18. With cultures of murine macrophages, we were surprised to find that infection by wild-typeSalmonella dublinresulted in decreased expression of IL-18 mRNA and IL-18 secretion rather than an increase. Reduction of macrophage-derived IL-18 expression by wild-typeSalmonellaoccurred early in the response, suggesting a direct effect. Furthermore, mice orally inoculated with wild-typeSalmonellawere shown to have reduced IL-18 mRNA expression at mucosal sites within hours postinoculation. Together these studies demonstrateSalmonella-induced reductions in IL-18 expression, suggesting that this intracellular pathogen may be capable of limiting a potentially protective immune response.
Modulation of Cytokine Response of Pneumonic Foals by VirulentRhodococcus equi
Authors: Giguère Steeve , Wilkie Bruce N. , Prescott John F. 
Published: December 2019

ABSTRACTThe ability ofRhodococcus equito induce pneumonia in foals depends on the presence of an 85- to 90-kb plasmid. In this study, we evaluated whether plasmid-encoded products mediate virulence by modulating the cytokine response of foals. Foals infected intrabronchially with a virulence plasmid-containing strain ofR. equihad similar gamma interferon (IFN-γ) and interleukin-12 (IL-12) p35 but significantly higher IL-1β, IL-10, IL-12 p40, and tumor necrosis factor alpha (TNF-α) mRNA expression in lung tissue compared to foals infected with the plasmid-cured derivative. IFN-γ mRNA expression levels in CD4+T lymphocytes isolated from bronchial lymph nodes (BLN) were similar for the two groups ofR. equi-infected foals on day 3 postinfection. However, on day 14, in association with pneumonia and marked multiplication of virulentR. equibut with complete clearance of the plasmid-cured derivative, IFN-γ mRNA expression in BLN CD4+T lymphocytes was significantly (P< 0.001) higher in foals infected with the plasmid-cured derivative. These results suggests an immunomodulating role forR. equivirulence plasmid-encoded products in downregulating IFN-γ mRNA expression by CD4+T lymphocytes.
Molecular Cloning and Characterization of the
afa-7
and
afa-8
Gene Clusters Encoding Afimbrial Adhesins in
Escherichia coli
Strains Associated with Diarrhea or Septicemia in Calves
Authors: Lalioui Lila , Jouve Mabel , Gounon Pierre , Le Bouguenec Chantal 
Published: December 2019

ABSTRACT

The
afa
gene clusters, which encode proteins involved in adhesion to epithelial cells, from
Escherichia coli
strains associated with urinary and intestinal infections in humans have been characterized. Pathogenic isolates of bovine and porcine origin that possess
afa
-related sequences have recently been described. We report in this work the cloning and characterization of the
afa-7
and
afa-8
gene clusters from bovine isolates. Hybridization and sequencing experiments revealed that despite similarity in genetic organization, the
afa-7
and
afa-8
genes, and the well-characterized
afa-3
operon expressed by human-pathogenic isolates, correspond to three different members of the
afa
family of gene clusters. However, like the
afa-3
gene cluster, both the
afa-7
and
afa-8
gene clusters were found to encode an afimbrial adhesin (AfaE) and an invasin (AfaD). The AfaD peptides encoded by the three gene clusters were only 45% identical, but functional complementation experiments indicated that they belong to the same family of invasins. Hemagglutination and adhesion assays demonstrated that the AfaE-VII and AfaE-VIII adhesins bind to different receptors and that these receptors are not the human decay-accelerating factor recognized to be the receptor of all previously described AfaE adhesins. The AfaE-VIII adhesin is very similar to the M agglutinin of human-uropathogenic strains. We used PCR assays to screen 25 bovine strains for
afaD
and
afaE
genes of either the
afa-7
or
afa-8
gene cluster. The
afa-8
gene cluster was highly prevalent in bovine isolates previously reported to carry
afa
-related sequences (23 of 24 strains), particularly in strains producing cytotoxic necrotizing factors (16 of 16 strains). The location of the
afa-8
gene cluster on the plasmids or chromosome of these isolates suggests that it could be carried by a mobile element, facilitating its dissemination among bovine-pathogenic
E. coli
strains.
Mycobacterium avium
Infection of Epithelial Cells Results in Inhibition or Delay in the Release of Interleukin-8 and RANTES
Authors: Sangari Felix J. , Petrofsky Mary , Bermudez Luiz E. 
Published: December 2019

ABSTRACT

Mycobacterium avium
is an opportunistic pathogen in AIDS patients, who acquire the infection mainly through the gastrointestinal tract. Previous studies in vitro have shown that
M. avium
invades epithelial cells of both intestinal and laryngeal origin. In addition,
M. avium
enters the intestinal mucosa of healthy mice. Because
M. avium
invasion of the intestinal mucosa in vivo initially is not accompanied by significant influx of inflammatory cells, we sought to determine whether
M. avium
would trigger chemokine release upon entry into epithelial cells by using HT-29 intestinal and HEp-2 laryngeal epithelial cell lines. Chemokine synthesis was measured both by the presence of specific mRNA and protein secretion in the cell culture supernatant as determined by enzyme-linked immunosorbent assay. Infection of HT-29 intestinal cells with
M. avium
did not induce the release of interleukin-8 (IL-8) or RANTES for up to 7 days postinfection. However, infection of HEp-2 cells resulted in the release of IL-8 and RANTES at 72 h. Similar findings were observed with other AIDS
M. avium
isolates belonging to different serovars. Secretion of IL-8 by HEp-2 cells was dependent upon bacterial uptake. In addition, prior infection with
M. avium
suppressed IL-8 production by HT-29 cells infected with
Salmonella typhimurium
. Our results suggest that
M. avium
infection of epithelial cells is associated with a delay in IL-8 and RANTES production which, in the case of HT-29, is prolonged up to 1 week. These findings may explain the weak inflammatory response after intestinal mucosa invasion in mice and are probably related with the ability of the bacterium to evade the host’s immune response.
Differential Transcription of the
tcpPH
Operon Confers Biotype-Specific Control of the
Vibrio cholerae
ToxR Virulence Regulon
Authors: Murley Yvette M. , Carroll Patricia A. , Skorupski Karen , Taylor Ronald K. , Calderwood Stephen B. 
Published: December 2019

ABSTRACT

Epidemic strains of
Vibrio cholerae
O1 are divided into two biotypes, classical and El Tor. In both biotypes, regulation of virulence gene expression depends on a cascade in which ToxR activates expression of ToxT, and ToxT activates expression of cholera toxin and other virulence genes. In the classical biotype, maximal expression of this ToxR regulon in vitro occurs at 30°C at pH 6.5 (ToxR-inducing conditions), whereas in the El Tor biotype, production of these virulence genes only occurs under very limited conditions and not in response to temperature and pH; this difference between biotypes is mediated at the level of
toxT
transcription. In the classical biotype, two other proteins, TcpP and TcpH, are needed for maximal
toxT
transcription. Transcription of
tcpPH
in the classical biotype is regulated by pH and temperature independently of ToxR or ToxT, suggesting that TcpP and TcpH couple environmental signals to transcription of
toxT
. In this study, we show a near absence of
tcpPH
message in the El Tor biotype under ToxR-inducing conditions of temperature and pH. However, once expressed, El Tor TcpP and TcpH appear to be as effective as classical TcpP and TcpH in activating
toxT
transcription. These results suggest that differences in regulation of virulence gene expression between the biotypes of
V. cholerae
primarily result from differences in expression of
tcpPH
message in response to environmental signals. We present an updated model for control of the ToxR virulence regulon in
V. cholerae
.
Serological Investigation of
Chlamydia trachomatis
Heat Shock Protein 10
Authors: Betsou Fotini , Sueur Jean Marie , Orfila Jeanne 
Published: December 2019

ABSTRACT

The humoral immune response to
Chlamydia trachomatis
10-kDa heat shock protein (Chsp10) in populations of Russian and French origin was studied by using a recombinant Chsp10 enzyme-linked immunosorbent assay. A physiological but not a serological correlation of Chsp10 exposure with Chsp60 exposure was observed in the Russian population. In the French population studied, there was a significant association between detection of anti-r-Chsp10 immunoglobulin G (IgG) antibodies and chronic genital tract infections. Chsp10 residues 50 to 67 were found to contain an immunodominant although not universal B epitope. Cross-reactions with
Chlamydia pneumoniae
or
Escherichia coli
GroES protein are limited but may occur. Our study suggests that detection of anti-Chsp10 IgG antibodies is associated with chronicity of
C. trachomatis
genital tract infection and does not parallel that of anti-Chsp60 IgG antibodies.
Differential Regulation of Macrophage Interleukin-1 (IL-1), IL-12, and CD80-CD86 by Two Bacterial Toxins
Authors: Foss Dennis L. , Zilliox Michael J. , Murtaugh Michael P. 
Published: December 2019

ABSTRACTThe ability of innate immune cells to differentially respond to various bacterial components provides a mechanism by which the acquired immune response may be tailored to specific pathogens. The response of innate immune cells to bacterial components provides regulatory signals to cognate immune cells. These signals include secreted cytokines and costimulatory molecules, and to a large extent they determine the quantitative and qualitative nature of the immune response. In order to determine if innate immune cells can differentially respond to bacterial components, we compared the responses of macrophages to two bacterially derived molecules, cholera toxin (CT) and lipopolysaccharide (LPS). We found that CT and LPS differentially regulated the expression of interleukin-12 (IL-12) and CD80-CD86 but not that of IL-1β. LPS and CT each induced IL-1β expression in macrophages, while only LPS induced IL-12 and only CT induced CD80-CD86. These differences were markedly potentiated in gamma interferon (IFN-γ)-treated macrophages, in which LPS potently induced IL-12 and CD80-CD86 expression. In contrast, IFN-γ treatment had no effect on the expression of IL-1β. These results define a molecular basis for the differential pathogenicities of bacterial toxins and are relevant to the design of vaccine adjuvants able to selectively induce desired types of immunity.
Involvement of the Enteroaggregative
Escherichia coli
Plasmid-Encoded Toxin in Causing Human Intestinal Damage
Authors: Henderson Ian R. , Hicks Susan , Navarro-Garcia Fernando , Elias Waldir P. , Philips Alan D. , Nataro James P. 
Published: December 2019

ABSTRACT

Enteroaggregative
Escherichia coli
(EAEC) strains have been shown to adhere to human intestinal tissue in an in vitro organ culture (IVOC) model, and certain strains manifest mucosal toxicity. We have recently described the EAEC plasmid-encoded toxin (Pet), a member of a specific serine protease subclass of the autotransporter proteins. When injected into rat ileal loops, Pet both elicited fluid accumulation and had cytotoxic effects on the mucosa. Furthermore, the Pet protein caused rises in short circuit current from rat jejunal tissue mounted in a Ussing chamber and rounding of intestinal epithelial cells in culture. We therefore hypothesized that the mucosal pathology induced by EAEC strains in the IVOC model was related to expression of the Pet protein. Here, we have examined the effects of EAEC strain 042 and its isogenic
pet
mutant in the IVOC model. 042-infected colonic explants exhibited dilation of crypt openings, increased cell rounding, development of prominent intercrypt crevices, and absence of apical mucus plugs. Colonic tissue incubated with the
pet
mutant exhibited significantly fewer mucosal abnormalities both subjectively and as quantitated morphometrically by measurement of crypt aperture diameter. Mucosal effects were restored upon complementation of the
pet
mutation in
trans
. Interestingly, we found that the ability of 042 to damage T84 cells was not dependent upon Pet. The data suggest that the Pet toxin is active on the human intestinal mucosa but that EAEC may have other mechanisms of eliciting mucosal damage.