bluuebunny/crossref_metadata_2025_split huggingface dataset:
Histamine induces Toll‐like receptor 2 and 4 expression in endothelial cells and enhances sensitivity to Gram‐positive and Gram‐negative bacterial cell wall components
Authors: Talreja Jaya , Kabir Mohammad H. , B. Filla Michael , Stechschulte Daniel J. , Dileepan Kottarappat N. 
Published: September 2004

SummaryHistamine is a major inflammatory molecule released from the mast cell, and is known to activate endothelial cells. However, its ability to modulate endothelial responses to bacterial products has not been evaluated. In this study we determined the ability of histamine to modulate inflammatory responses of endothelial cells to Gram‐negative and Gram‐positive bacterial cell wall components and assessed the role of Toll‐like receptors (TLR) 2 and 4 in the co‐operation between histamine and bacterial pathogens. Human umbilical vein endothelial cells (HUVEC) were incubated with lipopolysaccharide (LPS), lipoteichoic acid (LTA), or peptidoglycan (PGN) in the presence or absence of histamine, and the expression and release of interleukin‐6 (IL‐6), and NF‐κB translocation were determined. The effect of histamine on the expression of mRNA and proteins for TLR2 and TLR4 was also evaluated. Incubation of HUVEC with LPS, LTA and PGN resulted in marked enhancement of IL‐6 mRNA expression and IL‐6 secretion. Histamine alone markedly enhanced IL‐6 mRNA expression in HUVEC, but it did not stimulate proportional IL‐6 release. When HUVEC were incubated with LPS, LTA, or PGN in the presence of histamine marked amplification of both IL‐6 production and mRNA expression was noted. HUVEC constitutively expressed TLR2 and TLR4 mRNA and proteins, and these were further enhanced by histamine. The expression of mRNAs encoding MD‐2 and MyD88, the accessory molecules associated with TLR signalling, were unchanged by histamine treatment. These results demonstrate that histamine up‐regulates the expression of TLR2 and TLR4 and amplifies endothelial cell inflammatory responses to Gram‐negative and Gram‐positive bacterial components.
Resistance to re‐challenge in the Brown Norway rat model of vasculitis is not always complete and may reveal separate effector and regulatory populations
Authors: Vinen C. S. , Turner D. R. , Oliveira D. B. G. 
Published: September 2004

SummaryAdministration of mercuric chloride to Brown Norway rats results in T helper type 2 (Th2)‐ dominated autoimmunity characterized by high immunoglobulin E (IgE) concentrations, the production of multiple IgG autoantibodies, including those to glomerular basement membrane (GBM), arthritis and caecal vasculitis. After 14 days animals immunoregulate and auto‐immunity resolves even if mercuric chloride injections are continued. In a third phase, if animals are re‐challenged with mercuric chloride 6 weeks later, they show only attenuated autoimmunity with lower anti‐GBM antibody concentrations and arthritis scores. Resistance to the induction of anti‐GBM antibodies can also be achieved following an initial challenge with low‐dose (one‐tenth standard dose) mercuric chloride. We have now studied this resistant phase in more detail. We have shown, first, that following an initial full‐dose mercuric chloride challenge, resistance also affects susceptibility to caecal vasculitis. Second, following an initial full‐dose mercuric chloride challenge, the IgE response upon re‐challenge is initially accelerated but subsequently enters a resistant phase and third, following an initial challenge with low‐dose mercuric chloride, resistance is also seen to the induction of caecal vasculitis but is not seen in IgE serology (where results suggest competing effector and regulatory cell populations). Studying such regulatory phases in animal models of autoimmunity may be of benefit in the future in designing new therapies for human vasculitis.
CD4+ CCR5+ and CD4+ CCR3+ lymphocyte subset and monocyte apoptosis in patients with acute visceral leishmaniasis
Authors: Potestio Marcella , D'Agostino Pietro , Romano Giuseppina Colonna , Milano Salvatore , Ferlazzo Viviana , Aquino Alessandra , Di Bella Gloria , Caruso Rosalba , Gambino Giuseppe , Vitale Giustina , Mansueto Serafino , Cillari Enrico 
Published: September 2004

SummaryThe potential involvement of apoptosis in the pathogenesis of visceral leishmaniasis (VL) was examined by studying spontaneous and Leishmania antigen (LAg)‐induced apoptosis using cryopreserved peripheral blood mononuclear cells (PBMC) of Sicilian patients with VL. Results indicate that monocytes and T lymphocytes from acute VL patients show a significantly higher level of apoptosis compared with that observed in healed subjects. The percentage of apoptotic cells was higher in monocytes than in T lymphocytes. T cells involved in programmed cell death (PCD) were mainly of the CD4+ phenotype. In particular, the T helper 1‐type (Th1) subset, as evaluated by chemokine receptor‐5 (CCR5) expression, is involved in this process. Cell death in Th1‐type uses a CD95‐mediated mechanism. Furthermore, Th1‐type CCR5+ cells are prone to cell suicide in an autocrine or paracrine way, as attested by enhanced expression of CD95L in acute VL patients. The reduction in Th1‐type cells by apoptosis was confirmed by the decrease in interferon‐γ secretion. In conclusion, apoptosis of monocytes, CD4+ and CD4+ CCR5+ T cells could be involved in the failure of cell mediated immunity that is responsible for severe immune‐depression in VL.
Loss of CD154 impairs the Th2 extrafollicular plasma cell response but not early T cell proliferation and interleukin‐4 induction
Authors: Cunningham Adam F. , Serre Karine , Mohr Elodie , Khan Mahmood , Toellner Kai‐Michael 
Published: September 2004

SummaryLigation of CD40 by CD4 T cells through CD154 is key both to germinal centre induction and follicular T‐dependent Ig class switching, but its requirement for aspects of T cell priming and extrafollicular antibody responses is less clear. Here comparison of the T helper (Th) type 2 response in lymph nodes from wild‐type mice and CD154‐deficient mice after immunization with alum‐precipitated antigen reveals selective effects of this immunodeficiency. The timing and magnitude of the early interleukin (IL)‐4 induction and proliferation in T cells of the T zone were unaltered by CD154 deficiency. As expected, germinal centres were not induced. Additionally the T‐dependent extrafollicular antibody response, which initially requires T cell help but expands without further T cell involvement, was severely curtailed. The median number of extrafollicular antigen‐specific plasma cells was 370‐fold lower in CD154‐deficient mice. Of these plasma cells the median proportion that had switched to IgG1 was <5%, while in wild‐type mice the proportion was 89%. Surprisingly, some CD154‐deficient lymph nodes showed substantial switching to IgG1. Commensurately, increases in γ1 germline transcripts and Blimp‐1 mRNA were observed, albeit significantly lower than in controls, but activation‐induced cytidine deaminase mRNA was undetectable in CD154‐deficient mice. These experiments demonstrate that the acquisition of some T cell priming characteristics can be CD154‐independent; in contrast, T‐dependent extrafollicular responses require CD154. Thus functional CD154 ligation during the first encounter of T cells and B cells in the T zone is critical for follicular and extrafollicular antibody responses.
Haemophilus influenzae type b conjugate vaccines
Authors: Kelly Dominic F. , Moxon E. Richard , Pollard Andrew J. 
Published: September 2004

Summary Haemophilus influenzae type b (Hib) is one of the leading causes of invasive bacterial infection in young children worldwide. During childhood, acquisition of antibody directed against the polysaccharide capsule of the organism, presumably as a result of asymptomatic carriage, confers protection and disease is much less common after the age of 4 years. Like other polysaccharides, the polyribosyl ribitol phosphate (PRP) of the Hib capsule is a T‐independent antigen and not immunogenic when administered as a vaccine in infancy. Because the highest rates of disease occur in the first 2 years of life, efficacious Hib vaccines have been designed by covalently linking the PRP capsule to a carrier protein that recruits T‐cell help for the polysaccharide immune response and induces anti‐PRP antibody production even in the first 6 months of life. Introduction of Hib protein–polysaccharide conjugate vaccines into many industrialized countries over the past 15 years has resulted in the virtual elimination of invasive Hib disease. However, despite the success of the vaccine programme several factors may interfere with the effectiveness of the vaccine in the routine programme, as observed in the UK recently. Such factors may include interference with other concomitant vaccines, waning immunity in the absence of booster doses of vaccine, and reduced natural boosting as a result of decreased transmission of the organism. However, the burden of disease remains highest in resource‐poor countries and urgent efforts are needed to provide the benefits of this vaccine for children living in regions where it cannot be used for economic and logistical reasons.
Di‐(2‐ethylhexyl) phthalate induces severe aspermatogenesis in mice, however, subsequent antioxidant vitamins supplementation accelerates regeneration of the seminiferous epithelium
Authors: Ablake Maira , Itoh Masahiro , Terayama Hayato , Hayashi Shogo , Shoji Sunao , Naito Munekazu , Takahashi Kodo , Suna Shigeru , Jitsunari Fumihiko 
Published: September 2004

SummaryDi‐(2‐ethylhexyl) phthalate (DEHP), now regarded as an endocrine disruptor, can experimentally induce spermatogenic disturbance in laboratory animals. Our previous study demonstrated that antioxidant vitamins (vitamins C and E) supplementation during DEHP‐treatment significantly protected the rat seminiferous epithelium from DEHP‐gonadotoxicity. In the present study, we gave these antioxidant vitamins to mice already having fully developed aspermatogenesis because of DEHP to determine whether or not the vitamins can cure the injured seminiferous epithelium. CD‐1 male mice were fed on a DEHP‐containing diet for 15 days and then fed on the DEHP‐free normal diet with or without supplementation of vitamins C and E in drinking water for another 50 days. The results showed that severe aspermatogenesis was induced by the DEHP‐treatment but that the damaged seminiferous epithelium spontaneously recovered whether the vitamins were provided or not. This indicates that the DEHP‐induced aspermatogenesis was reversible. However, the supplementation of antioxidant vitamins significantly accelerated regeneration of the injured seminiferous epithelium, suggesting that the vitamins have a therapeutic effect on DEHP‐induced aspermatogenesis.
Ontogenesis and cell specific localization of Fas ligand expression in the rat testis
Authors: D'Abrizio Piera , Baldini Enke , Russo Paola F. , Biordi Leda , Graziano Filomena M. , Rucci Nadia , Properzi Giuliana , Francavilla Sandro , Ulisse Salvatore 
Published: September 2004

SummaryOver the past few years, a number of experimental evidences suggested the involvement of Fas Ligand (FasL) expressing Sertoli cells to induce apoptosis of Fas bearing germ cells. However, the FasL expression during testicular development and its cell specific localization within the testis is still a matter of debate. In the present study, we have monitored FasL expression during rat testis development by semiquantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR) and evaluated cell specific localization of FasL expression, by in situ RT‐PCR and immunohistochemistry, on adult rat testis. RT‐PCR analysis, performed on total RNA from rat testes obtained from 1 day up to 1‐year‐old animals, demonstrated the presence of FasL transcripts at all developmental stages examined. In situ RT‐PCR analysis clearly indicated the presence of FasL mRNA in Sertoli cells of adult testis, while we could never detect FasL transcripts in germ cells. Immunohistochemistry experiments showed a strong immunostaining for FasL in Sertoli cells of adult testis and again, no immunopositivity was observed in germ cells. In conclusion, our data suggest that FasL expression in rat testis is present from the early postnatal days up to the adult, and the Sertoli cells is the main FasL expressing cell within the seminiferous tubule.
Effects of cigarette smoking on sperm plasma membrane integrity and DNA fragmentation
Authors: Belcheva Antoaneta , Ivanova‐Kicheva Maria , Tzvetkova Petia , Marinov Mihail 
Published: September 2004

SummaryCigarette smoking is a serious health problem of our society. It is known that cigarette smoke is a cell mutagen and carcinogen, and that it may affect adversely male fertility. The possible detrimental effects on sperm cells are of great interest but the data available to support this statement are somewhat elusive. To approach this problem we examined conventional semen parameters, plasma membrane translocation of phosphatidylserine (PS) (annexin V/6‐CFDA cell staining) and sperm DNA integrity (comet assay) in a group of healthy man smoking cigarettes on a regular basis. The results of the study were compared with the results of the same tests in healthy non‐smoking donors. Significant difference in standard sperm parameters between the two groups was not found. Intensive expression of PS on the sperm plasma membrane surface (assayed by annexin V positive staining) was detected in the smokers group. There is a significant increase of population of apoptotic spermatozoa in ejaculates of smokers. Albeit DNA damages (high frequencies of double‐ and single‐ stranded DNA breaks) in spermatozoa of smokers are increased compared with non‐smokers, but this difference is not statistically significant. Sperm DNA integrity of healthy smokers remains in the normal range, but a clear negative trend is observed, especially in respect of disturbance of plasma membrane phospholipid asymmetry.
Concentrations of polychlorinated biphenyls in blood and the risk for testicular cancer
Authors: Hardell Lennart , Van Bavel Bert , Lindström Gunilla , Carlberg Michael , Eriksson Mikael , Dreifaldt Ann Charlotte , Wijkström Hans , Starkhammar Hans , Hallquist Arne , Kolmert Torgny 
Published: September 2004

SummaryAn increasing incidence of testicular cancer has been reported from several western countries during the last decades. According to current hypothesis testicular cancer is initiated during the foetal period and exposure to endocrine disruptors such as some persistent organic pollutants has been of concern. We have previously reported the results for concentrations of polychlorinated biphenyls (PCBs), p,p′‐dichlorodiphenyl‐dichloroethylene (pp′‐DDE), hexachlorobenzene (HCB) and chlordanes in 58 cases with testicular cancer, 61 age‐matched controls and 44 case mothers and 45 control mothers. In that report, significant increase of odds ratio (OR) was found for sum of PCBs, HCB, trans‐ and cis‐nonachlordane in case mothers. These data have now been further analysed for 37 congeners of PCBs. No significant differences were found among cases and controls. However, case mothers had significantly increased concentrations of a number of PCB congeners. A priori decided grouping of PCBs yielded for oestrogenic PCBs OR = 2.4, 95% confidence interval (CI) = 0.95–6.0, enzyme‐inducing PCBsOR = 2.6, 95% CI = 1.03–6.5 and toxic equivalents (TEQ) yielded OR = 3.3, 95% CI = 1.3–8.4. These data further elucidate the role of foetal exposure to different PCB congeners in the aetiology of testicular cancer.
Neuroprotective actions of eicosapentaenoic acid on lipopolysaccharide‐induced dysfunction in rat hippocampus
Authors: Lonergan Peter E. , Martin Darren S. D. , Horrobin David F. , Lynch Marina A. 
Published: September 2004

AbstractEicosapentaenoic acid (EPA) protects hippocampus from age‐related and irradiation‐induced changes that lead to impairment in synaptic function; the evidence suggests that this is due to its anti‐inflammatory effects, specifically preventing changes induced by the proinflammatory cytokine, interleukin‐1β (IL‐1β). In this study, we have investigated the possibility that EPA may prevent the effects of lipopolysaccharide (LPS) administration, which have been shown to lead to deterioration of synaptic function in rat hippocampus. The data indicate that treatment of hippocampal neurones with EPA abrogated the LPS‐induced increases in phosphorylation of the mitogen‐activated protein kinase, c‐Jun N‐terminal kinase (JNK), the transcription factor, c‐Jun and the mitochondrial protein, Bcl‐2. In parallel, we report that intraperitoneal administration of LPS to adult rats increases phosphorylation of JNK, c‐Jun and Bcl‐2 in hippocampal tissue and that these changes are coupled with increased IL‐1β concentration. Treatment of rats with EPA abrogates these effects and also blocks the LPS‐induced impairment in long‐term potentiation in perforant path‐granule cell synapses that accompanies these changes. We propose that the neuroprotective effect of EPA may be dependent on its ability to inhibit the downstream consequences of JNK activation.
P2Y2 receptors activate neuroprotective mechanisms in astrocytic cells
Authors: Chorna Nataliya E. , Santiago‐Pérez Laura I. , Erb Laurie , Seye Cheikh I. , Neary Joseph T. , Sun Grace Y. , Weisman Gary A. , González Fernando A. 
Published: September 2004

AbstractMechanical or ischemic trauma to the CNS causes the release of nucleotides and other neurotransmitters into the extracellular space. Nucleotides can activate nucleotide receptors that modulate the expression of genes implicated in cellular adaptive responses. In this investigation, we used human 1321N1 astrocytoma cells expressing a recombinant P2Y2 receptor to assess the role of this receptor in the regulation of anti‐apoptotic (bcl‐2 and bcl‐xl) and pro‐apoptotic (bax) gene expression. Acute treatment with the P2Y2 receptor agonist UTP up‐regulated bcl‐2 and bcl‐xl, and down‐regulated bax, gene expression. Activation of P2Y2 receptors was also coupled to the phosphorylation of cyclic AMP responsive element binding protein that positively regulates bcl‐2 and bcl‐xl gene expression. Cyclic AMP responsive element decoy oligonucleotides markedly attenuated the UTP‐induced increase in bcl‐2 and bcl‐xl mRNA levels. Activation of P2Y2 receptors induced the phosphorylation of the pro‐apoptotic factor Bad and caused a reduction in bax/bcl‐2 mRNA expression ratio. All these signaling pathways are known to be involved in cell survival mechanisms. Using cDNA microarray analysis and RT–PCR, P2Y2 receptors were found to up‐regulate the expression of genes for neurotrophins, neuropeptides and growth factors including nerve growth factor 2; neurotrophin 3; glia‐derived neurite‐promoting factor, as well as extracellular matrix proteins CD44 and fibronectin precursor – genes known to regulate neuroprotection. Consistent with this observation, conditioned media from UTP‐treated 1321N1 cells expressing P2Y2 receptors stimulated the outgrowth of neurites in PC‐12 cells. Taken together, our results suggest an important novel role for the P2Y2 receptor in survival and neuroprotective mechanisms under pathological conditions.
PchC Thioesterase Optimizes Nonribosomal Biosynthesis of the Peptide Siderophore Pyochelin in
Pseudomonas aeruginosa
Authors: Reimmann Cornelia , Patel Hiten M. , Walsh Christopher T. , Haas Dieter 
Published: September 2004

ABSTRACT

In
Pseudomonas aeruginosa
, the antibiotic dihydroaeruginoate (Dha) and the siderophore pyochelin are produced from salicylate and cysteine by a thiotemplate mechanism involving the peptide synthetases PchE and PchF. A thioesterase encoded by the
pchC
gene was found to be necessary for maximal production of both Dha and pyochelin, but it was not required for Dha release from PchE and could not replace the thioesterase function specified by the C-terminal domain of PchF. In vitro, 2-aminobutyrate, a cysteine analog, was adenylated by purified PchE and PchF proteins. In vivo, this analog strongly interfered with Dha and pyochelin formation in a
pchC
deletion mutant but affected production of these metabolites only slightly in the wild type. Exogenously supplied cysteine overcame the negative effect of a
pchC
mutation to a large extent, whereas addition of salicylate did not. These data are in agreement with a role for PchC as an editing enzyme that removes wrongly charged molecules from the peptidyl carrier protein domains of PchE and PchF.
A Multifunction ABC Transporter (Opt) Contributes to Diversity of Peptide Uptake Specificity within the Genus
Lactococcus
Authors: Lamarque Mauld , Charbonnel Pascale , Aubel Dominique , Piard Jean-Christophe , Atlan Danièle , Juillard Vincent 
Published: September 2004

ABSTRACT

Growth of
Lactococcus lactis
in milk depends on the utilization of extracellular peptides. Up to now, oligopeptide uptake was thought to be due only to the ABC transporter Opp. Nevertheless, analysis of several Opp-deficient
L. lactis
strains revealed the implication of a second oligopeptide ABC transporter, the so-called Opt system. Both transporters are expressed in wild-type strains such as
L. lactis
SK11 and Wg2, whereas the plasmid-free strains MG1363 and IL-1403 synthesize only Opp and Opt, respectively. The Opt system displays significant differences from the lactococcal Opp system, which made Opt much more closely related to the oligopeptide transporters of streptococci than to the lactococcal Opp system: (i) genetic organization, (ii) peptide uptake specificity, and (iii) presence of two oligopeptide-binding proteins, OptS and OptA. The fact that only OptA is required for nutrition calls into question the function of the second oligopeptide binding protein (Opts). Sequence analysis of oligopeptide-binding proteins from different bacteria prompted us to propose a classification of these proteins in three distinct groups, differentiated by the presence (or not) of precisely located extensions.
Relationships of the
Escherichia coli
O157, O111, and O55 O-Antigen Gene Clusters with Those of
Salmonella enterica
and
Citrobacter freundii
, Which Express Identical O Antigens
Authors: Samuel Gabrielle , Hogbin John-Paul , Wang Lei , Reeves Peter R. 
Published: September 2004

ABSTRACT

Escherichia coli
O157,
Salmonella enterica
O30, and
Citrobacter freundii
F90 have identical O-antigen structures, as do
E. coli
O55 and
S. enterica
O50. The O-antigen gene cluster sequences for
E. coli
O157 and
E. coli
O55 have been published, and the genes necessary for O-antigen biosynthesis have been identified, although transferase genes for glycosidic linkages are only generic and have not been allocated to specific linkages. We determined sequences for
S. enterica
O30 and
C. freundii
F90 O-antigen gene clusters and compared them to the sequence of the previously described
E. coli
O157 cluster. We also determined the sequence of the
S. enterica
O50 O-antigen gene cluster and compared it to the sequence of the previously described
E. coli
O55 cluster. For both the
S. enterica
O30-
C. freundii
F90-
E. coli
O157 group and the
S. enterica
O50-
E. coli
O55 group of O antigens, the gene clusters have identical or nearly identical organizations. The two sets of gene clusters had comparable overall levels of similarity in their genes, which were lower than the levels determined for housekeeping genes for these species, which were 55 to 65% for the genes encoding glycosyltransferases and O-antigen processing proteins and 75 to 93% for the nucleotide-sugar pathway genes. Nonetheless, the similarity of the levels of divergence in the five gene clusters required us to consider the possibility that the parent gene cluster for each structure was in the common ancestor of the species and that divergence is faster than expected for the common ancestor hypothesis. We propose that the identical O-antigen gene clusters originated from a common ancestor, and we discuss some possible explanations for the increased rate of divergence that is seen in these genes.