bluuebunny/crossref_metadata_2025_split huggingface dataset:
Repression of Hyphal Proteinase Expression by the Mitogen-Activated Protein (MAP) Kinase Phosphatase Cpp1p of
Candida albicans
Is Independent of the MAP Kinase Cek1p
Authors: Schröppel Klaus , Sprößer Katrin , Whiteway Malcolm , Thomas David Y. , Röllinghoff Martin , Csank Csilla 
Published: July 2002

ABSTRACT

Cpp1p is a putative mitogen-activated protein (MAP) kinase phosphatase that suppresses
Candida albicans
hyphal formation at 25°C through its probable substrate, the Cek1p filamentation MAP kinase. Here we report that expression of the serum-induced genes
SAP4-6
and
HYR1
increased several fold in hyphal forms of a
cpp1/cpp1
null mutant, while the rate and extent of hyphal development up to 5 h were normal. Therefore, we provide evidence that Cpp1p represses hyphal gene expression by acting through a Cek1p-independent mechanism.
SAP4-6
and
HYR1
transcripts were undetectable in a null mutant of another key regulator of filamentation, Efg1p; thus, Efg1p and Cpp1p oppose each other during the expression of these genes in hyphal forms.
Molecular Characterization of
Mycoplasma arthritidis
Membrane Lipoprotein MAA1
Authors: Washburn Leigh Rice , Miller Elizabeth J. , Weaver Keith E. 
Published: July 2002

ABSTRACT

Genes encoding the
Mycoplasma arthritidis
surface-exposed lipoprotein MAA1 were cloned and sequenced from MAA1-expressing strains 158p10p9 and PG6, from a low-adherence (LA) variant derived from 158p10p9 that expresses a truncated version of MAA1 (MAA1Δ) and from two MAA1-negative strains, 158 and H39. The deduced amino acid sequences of
maa1
from 158p10p9 and PG6 predicted, respectively, 86.5- and 86.4-kDa basic, largely hydrophilic lipoproteins with 29-amino-acid signal peptides and predicted cleavage sites for signal peptidase II (Ala-Ala-Ala↓Cys). The truncation in the LA variant resulted from a G→T substitution at nucleotide 695, which created a premature stop codon. This, in turn, generated a predicted 26.6-kDa prolipoprotein (23.6 kDa after processing), consistent with an
M
r
of ∼24,000 calculated for MAA1Δ. Similarly, absence of MAA1 expression in H39 and 158 resulted from C→A substitutions at nucleotide 208, generating premature stop codons at that site in both strains.
Candida albicans-Derived β-1,2-Linked Mannooligosaccharides Induce Desensitization of Macrophages
Authors: Jouault Thierry , Fradin Chantal , Trinel Pierre-André , Poulain Daniel 
Published: July 2002

ABSTRACTCandida albicansβ-1,2-oligomannosides stimulate macrophage tumor necrosis factor alpha (TNF-α) but not NO release. This stimulation desensitized macrophages by altering β-1,2-oligomannoside-dependent TNF-α production and lipopolysaccharide-dependent TNF-α and NO secretion. Desensitization was not related to tyrosine phosphorylation signal transduction but was transferred by culture supernatants in which arachidonic acid derivatives were evidenced.
Differential Bacterial Survival, Replication, and Apoptosis-Inducing Ability ofSalmonellaSerovars within Human and Murine Macrophages
Authors: Schwan William R. , Huang Xiao-Zhe , Hu Lan , Kopecko Dennis J. 
Published: July 2002

ABSTRACTSalmonellaserovars are associated with human diseases that range from mild gastroenteritis to host-disseminated enteric fever. Human infections bySalmonella entericaserovar Typhi can lead to typhoid fever, but this serovar does not typically cause disease in mice or other animals. In contrast,S. entericaserovar Typhimurium andS. entericaserovar Enteritidis, which are usually linked to localized gastroenteritis in humans and some animal species, elicit a systemic infection in mice. To better understand these observations, multiple strains of each of several chosen serovars ofSalmonellawere tested for the ability in the nonopsonized state to enter, survive, and replicate within human macrophage cells (U937 and elutriated primary cells) compared with murine macrophage cells (J774A.1 and primary peritoneal cells); in addition, death of the infected macrophages was monitored. The serovar Typhimurium strains all demonstrated enhanced survival within J774A.1 cells and murine peritoneal macrophages, compared with the significant, almost 100-fold declines in viable counts noted for serovar Typhi strains. Viable counts for serovar Enteritidis either matched the level of serovar Typhi (J774A.1 macrophages) or were comparable to counts for serovar Typhimurium (murine peritoneal macrophages). Apoptosis was significantly higher in J774A.1 cells infected with serovar Typhimurium strain LT2 compared to serovar Typhi strain Ty2. On the other hand, serovar Typhi survived at a level up to 100-fold higher in elutriated human macrophages and 2- to 3-fold higher in U937 cells compared to the serovar Typhimurium and Enteritidis strains tested. Despite the differential multiplication of serovar Typhi during infection of U937 cells, serovar Typhi caused significantly less apoptosis than infections with serovar Typhimurium. These observations indicate variability in intramacrophage survival and host cytotoxicity among the various serovars and are the first to show differences in the apoptotic response of distinctSalmonellaserovars residing in human macrophage cells. These studies suggest that nonopsonized serovar Typhimurium enters, multiplies within, and causes considerable, acute death of macrophages, leading to a highly virulent infection in mice (resulting in death within 14 days). In striking contrast, nonopsonized serovar Typhi survives silently and chronically within human macrophages, causing little cell death, which allows for intrahost dissemination and typhoid fever (low host mortality). The type of disease associated with any particular serovar ofSalmonellais linked to the ability of that serovar both to persist within and to elicit damage in a specific host's macrophage cells.
Peripheral Cytokine Responses toTrichuris murisReflect Those Occurring Locally at the Site of Infection
Authors: Taylor Matthew D. , Betts Catherine J. , Else Kathryn J. 
Published: July 2002

ABSTRACTThe study of human cellular immune responses to parasite infection under field conditions is very complex. Often, the only practical site from which to sample the cellular responses is the peripheral blood. Sampling peripheral blood lymphocytes (PBL) relies on the assumption that these peripheral responses accurately reflect the immune responses acting locally at the site of infection. This is a particularly important point for the human intestinal helminthTrichuris trichiura, which solely inhabits the cecum and large intestine and so will stimulate a localized immune response. Using the well-defined model ofT. trichiura,T. murisin the mouse, we have demonstrated that the dominant cytokine responses of the mesenteric lymph nodes (MLN) can be detected by sampling PBL. Resistant mice which mount a type 2 cytokine response in their MLN had PBL producing interleukin-4 (IL-4), IL-5, and IL-9, with negligible levels of gamma interferon (IFN-γ). Conversely, susceptible mice which mount a type 1 cytokine response in their MLN had PBL producing IFN-γ and negligible levels of type 2 cytokines. We have also shown that the PBL are capable of mounting a functional immune response againstT. muris. PBL from immune mice were capable of transferring immunity toT. muris-infected severe combined immunodeficient (C.B-17scid/scid) mice. Sampling PBL responses is therefore a viable option for monitoring human intestinal immune responses duringT. trichiurainfection in the field.
Drastic Reduction of a Filarial Infection in Eosinophilic Interleukin-5 Transgenic Mice
Authors: Martin Coralie , Le Goff Laëtitia , Ungeheuer Marie-Noelle , Vuong Phat N. , Bain Odile 
Published: July 2002

ABSTRACTIn order to establish the role of eosinophils in destroying parasites, transgenic mice have been used in experimental helminthiases but not in filariasis.Litomosoides sigmodontisoffers a good opportunity for this study because it is the only filarial species that completes its life cycle in mice. Its development was compared in transgenic CBA/Ca mice overexpressing interleukin-5 (IL-5) and in wild-type mice following subcutaneous inoculation of 40 infective larvae. An acceleration of larval growth was observed in the IL-5 transgenic mice. However, the recovery rate of adult worms was considerably reduced in these mice, as evidenced 2 months postinoculation (p.i.). The reduction occurs between days 10 and 30 p.i. in the coelomic cavities. As early as day 10, spherical aggregates of eosinophils and macrophages are seen attached on live developing larvae (always similarly localized on the worm) in both wild-type and transgenic mice. However, on day 60 p.i., granulomas were found in the transgenic mice only, probably because of the higher density of eosinophils. Furthermore, on day 30 p.i., young filariae are seen trapped in granulomas, some of them surrounded by Splendore-Hoeppli deposits, which illustrates the release of the major basic protein by eosinophils. The high protection rate obtained (65%) is similar to that observed previously in BALB/c mice following vaccination with irradiated larvae. Both protocols have a common factor, the high production of IL-5 and eosinophilia. However, protection occurs later in primary infected transgenic mice because specific antibodies are not yet present at the time of challenge.
Peptidoglycan and Lipoteichoic Acid fromStaphylococcus aureusInduce Tumor Necrosis Factor Alpha, Interleukin 6 (IL-6), and IL-10 Production in Both T Cells and Monocytes in a Human Whole Blood Model
Authors: Wang J. E. , Jørgensen P. F. , Almlöf M. , Thiemermann C. , Foster S. J. , Aasen A. O. , Solberg R. 
Published: July 2002

ABSTRACTWe have examined the ability of peptidoglycan (PepG) and lipoteichoic acid (LTA) isolated fromStaphylococcus aureusto induce the release of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), and IL-10 in whole human blood and identified the cellular origins of these cytokines. Both PepG and LTA induced transient increases in TNF-α and IL-10 in plasma, with peak values at 6 and 12 h, respectively. IL-6 values increased throughout the experimental period (24 h). The TNF-α, IL-6, and IL-10 release induced by PepG and LTA was dose dependent. Only PepG was a potent inducer of TNF-α secretion. After stimulation of whole blood with PepG or LTA, very pure populations of monocytes (CD14 positive), T cells (CD2 positive), B cells (CD19 positive), and granulocytes (CD15 positive) were isolated by immunomagnetic separation and analyzed by reverse transcription-PCR for mRNA transcripts encoding TNF-α, IL-6, and IL-10. The TNF-α mRNA results were inconclusive. In contrast, PepG induced IL-6 and IL-10 mRNA accumulation in both T cells and monocytes. LTA, as well as lipopolysaccharide, induced IL-6 and IL-10 mRNA production in monocytes and possibly in T cells. Whether granulocytes and B cells produce cytokines in response to bacterial stimuli remains obscure. Blockade of the CD14 receptors with monoclonal antibodies (18D11) had no influence on the PepG-induced release of TNF-α but attenuated the LTA-induced release of the same cytokine. In conclusion, our data indicate that circulating T cells and monocytes contribute to cytokine production in sepsis caused by gram-positive bacteria.
Prophylactic and Therapeutic Efficacy of Antibodies to a Capsular Polysaccharide Shared among Vancomycin-Sensitive and -Resistant Enterococci
Authors: Huebner Johannes , Quaas Alexander , Krueger Wolfgang A. , Goldmann Donald A. , Pier Gerald B. 
Published: July 2002

ABSTRACT

Enterococci are important nosocomial pathogens that are increasingly difficult to treat due to intrinsic and acquired resistance to antibiotics, including vancomycin. A recently described capsular polysaccharide (CP) isolated from
Enterococcus faecalis
12030 was used to evaluate the potential efficacy of active or passive immunotherapy regimens as adjunctive treatments. Evaluation of protective efficacy was carried out in immunocompetent mice challenged intravenously (i.v.) with live enterococci. In nonimmune mice, i.v. inoculations resulted in high levels of bacteria in kidneys, spleens, and livers 5 days after challenge. Mice immunized with four 10-μg doses of CP antigen/mouse were protected against challenge with the homologous
E. faecalis
strain. High-titer opsonic immunoglobulin G was also induced by immunizing rabbits with the purified CP, and passive transfer of this antiserum to mice produced significantly lower bacterial counts in organs than did normal rabbit serum or sterile saline. Antibodies to the polysaccharide isolated from
E. faecalis
12030 were protective against
Enterococcus faecalis
OG1RF and against two serologically related, vancomycin-resistant
Enterococcus faecium
clinical isolates. Antibodies to this CP antigen were also effective as a therapeutic reagent in mice when passive therapy was initiated 48 h after live bacterial challenge. These data indicate that CP antigens from enterococci are potential targets of protective antibodies and that these antibodies may be useful for prophylaxis and treatment of enterococcal infections.
Structural Analysis of Phage-Borne
stx
Genes and Their Flanking Sequences in Shiga Toxin-Producing
Escherichia coli
and
Shigella dysenteriae
Type 1 Strains
Authors: Unkmeir Alexandra , Schmidt Herbert 
Published: July 2002

ABSTRACT

The
stx
-flanking regions of 49 Shiga toxin-producing
Escherichia coli
strains and nine
Shigella dysenteriae
serotype 1 strains containing either
stx
,
stx
1
,
stx
2
, or
stx
2
variant genes, were examined. We analyzed these regions by PCR using a set of primers with one primer specific for the respective
stx
gene and a second primer complementary to sequences of Stx phages H-19B and 933W. We further characterized the amplification products by restriction endonuclease digestion and nucleotide sequencing. PCR products of
stx
1
-containing
E. coli
strains of serogroups O157, O26, and 0103 showed the same lengths and similar restriction patterns. However, we failed to amplify the 3′
stx
-flanking region in
stx
1
-harboring
E. coli
O111:H
−
strains. Stx2-producing
E. coli
strains revealed amplification products of different lengths and restriction patterns, suggesting greater heterogeneity than in
stx
1
-positive strains. We also obtained specific PCR products for two Stx2c-producing and seven Stx2f-producing
E. coli
strains when they were subjected to PCR analysis. In nine
S. dysenteriae
type 1 strains, H-19B- and 933W-specific primers amplified only the 3′
stx
-flanking region. The results of our study demonstrate that the
stx
genes of all strains investigated are continuous with phage sequences. Whereas almost all strains except
E. coli
O111:H
−
strains were associated with a S-like gene, association with Q could not be demonstrated in nine
S. dysenteriae
type 1 strains and three
E. coli
strains. Furthermore, we showed that the organization of the
stx
-flanking regions is similar in all strains investigated, whereas fine-structure analysis showed subtle differences among the sequences examined. Our results support the hypothesis that
stx
genes in
E. coli
and
S. dysenteriae
are generally phage-borne.
Invasion Genes Are Not Required forSalmonella entericaSerovar Typhimurium To Breach the Intestinal Epithelium: Evidence ThatSalmonellaPathogenicity Island 1 Has Alternative Functions during Infection
Authors: Murray Rose Ann , Lee Catherine A. 
Published: July 2002

ABSTRACTSalmonella entericaserovar Typhimurium invasion genes are necessary for bacterial invasion of intestinal epithelial cells and are thought to allow salmonellae to enter and cross the intestinal epithelium during infection. Many invasion genes are encoded onSalmonellapathogenicity island 1 (SPI1), and their expression is activated by HilA, a transcription factor also encoded on SPI1. We have studied the role ofSalmonellainvasion genes during infection of mice following intragastric inoculation. We have found that strains containing a mutation inhilAorinvGwere recovered from the intestinal contents, intestinal tissues, and systemic tissues at a lower frequency than their parental wild-type strain. In contrast, a strain in which SPI1 is deleted was recovered from infected mice at a frequency similar to that of its parental wild-type strain. The ΔSPI1 phenotype indicates thatS. entericadoes not require invasion genes to cross the intestinal epithelium and infect systemic tissues. This result has forced us to reconsider the long-held belief that invasion genes directly mediate bacterial infection of the intestinal mucosa and traversion of the intestinal barrier during infection. Instead, our results suggest thathilAis required for bacterial colonization of the host intestine. The seemingly contradictory phenotype of the ΔSPI1 mutant suggests that deletion of another gene(s) encoded on SPI1 suppresses thehilAmutant defect. We propose a model forS. entericapathogenesis in whichhilAand invasion genes are required for salmonellae to overcome a host clearance response elicited by another SPI1 gene product(s).
Lipooligosaccharide P
k
(Galα1-4Galβ1-4Glc) Epitope of
Moraxella catarrhalis
Is a Factor in Resistance to Bactericidal Activity Mediated by Normal Human Serum
Authors: Zaleski Anthony , Scheffler N. Karoline , Densen Peter , Lee Frank K. N. , Campagnari Anthony A. , Gibson Bradford W. , Apicella Michael A. 
Published: July 2002

ABSTRACT

Moraxella catarrhalis
is a respiratory pathogen responsible for acute bacterial otitis media in children and exacerbation of chronic bronchitis in adults.
M. catarrhalis
strains are frequently resistant to the bactericidal activity of normal human serum. In order to determine if the lipooligosaccharide (LOS) of
M. catarrhalis
has a role in serum resistance, the UDP-glucose-4-epimerase (
galE
) gene was identified, cloned, and sequenced and a deletion/insertion mutation was introduced into
M. catarrhalis
strain 2951. GalE enzymatic activity, measured in whole-cell lysates, was ablated in
M. catarrhalis
2951
galE
. Mass spectrometric analysis of LOS isolated with hot phenol-water confirmed that strain 2951 produced a type A LOS. These studies showed that the LOS from 2951
galE
had lost two hexose residues due to the
galE
mutation and that the resultant LOS structure lacked the (Galα1-4Galβ1-4Glc) P
k
epitope found on
M. catarrhalis
2951. Wild-type
M. catarrhalis
2951 is resistant to complement-mediated serum bactericidal activity. In contrast, a greater than 2-log
10
-unit reduction in CFU occurred after incubation of 2951
galE
in either 50 or 25% pooled human serum (PNHS), and CFU in 10% PNHS decreased by about 1 log
10
unit. These studies suggest that the P
k
epitope of the LOS may be an important factor in the resistance of
M. catarrhalis
to the complement-mediated bactericidal effect of normal human serum.
Decreased Infectivity in
Borrelia burgdorferi
Strain B31 Is Associated with Loss of Linear Plasmid 25 or 28-1
Authors: Labandeira-Rey Maria , Skare Jonathan T. 
Published: July 2002

ABSTRACT

Previous reports indicated a correlation between loss of plasmids and decreased infectivity of
Borrelia burgdorferi
strain B31, suggesting that plasmids may encode proteins that are required for pathogenesis. In this study, we expand on this correlation. Using the
B. burgdorferi
genomic sequence, we designed primers specific for each plasmid, and by using PCR we catalogued 11 linear and 2 circular plasmids from 49 clonal isolates of a mid-passage
B. burgdorferi
strain B31, initially derived from infected mouse skin, and 20 clones obtained from mouse skin infected with a low-passage isolate of
B. burgdorferi
strain B31. Among the 69 clones analyzed, nine distinct genotypes were identified relative to wild-type
B. burgdorferi
strain B31. Among the nine clonal genotypes obtained, only the 9-kb circular plasmid (cp9), the 25-kb linear plasmid (lp25), and either the 28-kb linear plasmid 1 or 4 (lp28-1 and lp28-4, respectively) were missing, in different combinations. We compared the infectivity of the wild-type strain, containing all known
B. burgdorferi
plasmids, with those of single mutants lacking either lp28-1, lp28-4, or lp25 and a double mutant missing both cp9 and lp28-1. The infectivity data indicated that
B. burgdorferi
strain B31 cells lacking lp28-4 were modestly attenuated in all tissues analyzed, whereas samples missing lp25 were completely attenuated in all tissues, even at the highest inoculum tested. Isolates without lp28-1 infected the joint tissue yet were not able to infect other tissues as effectively. In addition, we have observed a selection in vivo in the skin, bladder, and joint for cells containing lp25 and in the skin and bladder for cells containing lp28-1, indicating that lp25 and lp28-1 encode proteins required for colonization and short-term maintenance in these mammalian tissues. In contrast, there was no selection in the joint for cells containing lp28-1, suggesting that genes on lp28-1 are not required for colonization of
B. burgdorferi
within the joint. These observations imply that the dynamic nature of the
B. burgdorferi
genome may provide the genetic heterogeneity necessary for survival in the diverse milieus that this pathogen occupies in nature and may contribute to tropism in certain mammalian host tissues.
Effect of Influenza A Virus Infection on Nasopharyngeal Colonization and Otitis Media Induced by Transparent or Opaque Phenotype Variants of
Streptococcus pneumoniae
in the Chinchilla Model
Authors: Tong H. H. , Weiser J. N. , James M. A. , DeMaria T. F. 
Published: July 2002

ABSTRACT

Phase variation in the colonial opacity of
Streptococcus pneumoniae
has been implicated as a factor in bacterial adherence, colonization, and invasion in the pathogenesis of pneumococcal disease. Additionally, the synergistic effects of influenza A virus and
S. pneumoniae
in the development of otitis media (OM) have been reported. This study examined the ability of opaque or transparent
S. pneumoniae
from the same strain in combination with an antecedent influenza A virus infection to colonize the nasopharynx and invade the middle ear in the chinchilla model. Our data indicated that there was no significant difference in the level of nasopharyngeal colonization and induction of OM between the opaque and transparent variants unless there was a prior challenge with influenza A virus. Subsequent to influenza A virus infection, there was a significant difference between the variants in the ability to colonize and persist in the nasopharynx and middle ear. The concentrations of the opaque variant in nasopharyngeal-lavage samples and middle-ear fluid remained consistently higher than those of the transparent variant for 10 days postinoculation. Data from this study indicate that the effects of influenza A virus on the pathogenesis of experimental
S. pneumoniae
-induced OM differ depending on the opacity phenotype involved.