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Diminished Response (diminished + response)
Selected AbstractsImmunogenicity of synthetic saccharide fragments of Vibrio cholerae O1 (Ogawa and Inaba) bound to Exotoxin AFEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 2 2006Terri K. Wade Abstract Recombinant exotoxin A (rEPA) from Pseudomonas aeruginosa conjugated to Vibrio cholerae O1 serotype-specific polysaccharides (mono-, di- and hexasaccharide) were immunogenic in mice. Monosaccharide conjugates boosted the humoral responses to the hexasaccharide conjugates. Prior exposure to purified Ogawa lipopolysaccharide (LPS) enabled contra -serotype hexasaccharide conjugates to boost the vibriocidal response, but Inaba LPS did not prime for an enhanced vibriocidal response by a contra -serotype conjugate. Prior exposure to the carrier, and priming B cells with the LPS of either serotype, resulted in enhanced vibriocidal titers if the Ogawa hexasaccharides were used, but a diminished response to the Inaba LPS. These studies demonstrate that the ,functional' B cell epitopes on the LPS differ from those of the neoglycoconjugates and that the order of immunization and the serotype of the boosting conjugate can influence the epitope specificity and function of the antisera. [source] Caregiving behavior and interactions of prenatally depressed mothers (antidepressant-treated and non-antidepressant-treated) during newborn acute pain,INFANT MENTAL HEALTH JOURNAL, Issue 4 2009Fay F. Warnock This exploratory study aimed to examine time-based measures of the behaviors and interactions of prenatally depressed serotonin reuptake inhibitors (SRI)-medicated mothers to their infant's pain (n = 10) by comparing them with similar measures obtained from prenatally depressed nonmedicated mothers and their infants (n = 10), and nondepressed mothers and their infants (n = 10). During the second trimester of their pregnancy, the 30 study mothers were assessed for depression and anxiety, with no further measures of maternal mood taken. Maternal and infant interactions were continuously videorecorded while the infant underwent a scheduled heel lance for routine blood screening that occurred when study infants were between the ages of 24 and 60 hr. Maternal behavior and infant cry, for all 30 cases, were coded second-by-second for the full duration of each infant's heel lance using a reliable coding system and analyzed using odds ratio and regression analyses. Infants exposed to prenatal SRIs and depressed maternal mood were more likely to have lower Apgar scores and to exhibit weak and absent cry. Even when duration of the heel lance was controlled for, women with depression during the second trimester were more likely to exhibit depressed behavior at 2 days' postpartum despite sustained SRI antidepressant treatment. Both groups of prenatally depressed mothers were more likely to exhibit diminished response to their infants' pain cue although nonmedicated mothers' expressions of depressed behavior were more similar to healthy controls. Comprehensive understanding is essential to optimize the clinical care of mothers and their infants in this complex setting. This study contributes preliminary new findings that warrant prospective and longitudinal studies to clarify further the impacts of prenatal SRI and maternal mental mood (e.g., chronic depression and anxiety) effects on the mother,infant interaction and infant pain and stress reactivity. [source] Effects of Alcohol Consumption on Iron Metabolism in Mice with Hemochromatosis MutationsALCOHOLISM, Issue 1 2007Jonathan M. Flanagan Background: Alcoholic liver disease is associated with increased hepatic iron accumulation. The liver-derived peptide hepcidin is the central regulator of iron homeostasis and recent animal studies have demonstrated that exposure to alcohol reduces hepcidin expression. This down-regulation of hepcidin in vivo implies that disturbed iron sensing may contribute to the hepatosiderosis seen in alcoholic liver disease. Alcohol intake is also a major factor in expression of the hemochromatosis phenotype in patients homozygous for the C282Y mutation of the HFE gene. Methods: To assess the effect of alcohol in mice with iron overload, alcohol was administered to mice with disrupted Hfe and IL-6 genes and Tfr2 mutant mice and their respective 129x1/SvJ, C57BL/6J, and AKR/J wild-type congenic strains. Iron absorption, serum iron levels, and hepcidin expression levels were then measured in these mice compared with water-treated control mice. Results: Alcohol was shown to have a strain-specific effect in 129x1/SvJ mice, with treated 129x1/SvJ mice showing a significant increase in iron absorption, serum iron levels, and a corresponding decrease in hepcidin expression. C57BL/6J and AKR/J strain mice showed no effect from alcohol treatment. 129x1/SvJ mice heterozygous or homozygous for the Hfe knockout had a diminished response to alcohol. All 3 strains were shown to have high blood alcohol levels. Conclusions: The effect of alcohol on iron homeostasis is dependent on the genetic background in mice. In an alcohol-susceptible strain, mutation of the Hfe gene diminished the response of the measured iron indices to alcohol treatment. This indicates that either maximal suppression of hepcidin levels had already occurred as a result of the Hfe mutation or that Hfe was a component of the pathway utilized by EtOH in suppressing hepcidin production and increasing iron absorption. [source] Regulatory T Cells in children with intestinal parasite infectionPARASITE IMMUNOLOGY, Issue 10 2009M. H. GARCÍA-HERNÁNDEZ Summary Chronic intestinal parasite infection can induce both persistent immune activation and defective responsiveness of T cells. This study aimed to assess the number and function of T regulatory (Treg) cells in children with intestinal parasite infection. We have studied the peripheral blood from 93 children, 53 of them parasitized with protozoa, helminths, or both; the remainder were non parasitized, healthy controls. The number and function of CD4+ CD25high and CD4+ Foxp3+ cells were similar in parasitized and control children. In contrast, there was a significant increase in the levels of CD3+ CD69+, CD4+ CTLA-4+, and CD8+ CD28, T cells in helminth infected children. Moreover, some of these patients showed a diminished response to CD3/CD28 stimulation in comparison with the control children. Our data strongly suggest that whilst Treg cells are not affected by intestinal parasite infection, CD3+ CD69+, CD4+ CTLA-4+ and CD8+ CD28, lymphocytes may play an important, but as yet undetermined role in the diminished immune competence observed in parasitized children. [source] Ellis,van Creveld syndrome and Weyers acrodental dysostosis are caused by cilia-mediated diminished response to hedgehog ligands,AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 4 2009Victor L. Ruiz-Perez Abstract Ellis,van Creveld syndrome (EvC; OMIM 225500) is a recessive disorder comprising chondrodysplasia, polydactyly, nail dysplasia, orofacial abnormalities and, in a proportion of patients, cardiovascular malformations. Weyers acrodental dysostosis (Weyers; OMIM 193530) is an allelic dominant disorder comprising polydactyly, nail dysplasia, and orofacial abnormalities. EvC results from loss-of-function mutations in EVC or EVC2, the phenotype associated with the mutations in these two genes being indistinguishable. Three convincing causative mutations have been identified in patients with Weyers acrodental dysostosis, which are clustered in the last coding exon of EVC2 and lead to production of a truncated protein lacking the final 43 amino acids. Localization and function of EVC and EVC2 are inferred from studying the murine orthologs. Both Evc and Evc2 proteins localize to the basal bodies of primary cilia and analysis of an Ellis,van Creveld mouse model, which includes the limb shortening and tooth abnormalities of EvC patients, has demonstrated Hedgehog signaling defects in the absence of Evc. The loss of Evc2 has not been studied directly, but Hedgehog signaling is impaired when a mutant murine Evc2 Weyer variant is expressed in vitro. We conclude that the phenotypic abnormalities in EvC and Weyers syndrome result from tissue specific disruption of the response to Hh ligands. © 2009 Wiley-Liss, Inc. [source] Cigarette smoke suppresses in vitro allergic activation of mouse mast cellsCLINICAL & EXPERIMENTAL ALLERGY, Issue 5 2009E. Mortaz Summary Background Mast cells are important effector cells in innate or acquired immunity that contribute to host defence. Excessive activation of mast cells can result in the development of allergic diseases, including atopic asthma. Mast cell activation by IgE and specific antigen induces the cells to release spasmogenic, vasoactive and pro-inflammatory mediators, which enhance airway smooth muscle contraction, vascular permeability and inflammatory cell recruitment. Recently, we have demonstrated that exposure of mast cells to cigarette smoke medium (CSM) triggered mast cells to produce chemokines. On the other hand, smoking may decrease the risk of allergic sensitization, which could be explained by a reduced IgE production or a diminished response of mast cells to activation of the IgE receptor. Objective In this study, we investigated the effect of CSM on the allergic activation of mast cells through IgE and antigen. Methods Primary cultured murine mast cells were exposed to CSM and activated with IgE and antigen or lipopolysaccharide (LPS). The release of granules, production of leukotrienes, chemokines and cytokines was determined in the supernatants by ELISA. The effect of CSM exposure on intracellular signalling, especially the nuclear factor (NF)-,B and extracellular signal-regulated kinase (Erk)1/2 pathways, was analysed by Western blotting. Results CSM suppressed IgE-mediated degranulation and cytokine release, but no effect was observed on leukotriene release. CSM induced phosphorylation of Erk1/2 in mast cells. In CSM-exposed mast cells, activating transcription factor (ATF)-1 was phosphorylated after stimulation with IgE/Ag. LPS-activated mast cells were not influenced by CSM. Conclusion Our study suggests that exposure to cigarette smoke may lead to a reduced allergic activation of mast cells without affecting their response to activation via e.g. bacterial-derived LPS. [source] s -CARBOXYMETHYLCYSTEINE INHIBITS CARBACHOL-INDUCED CONSTRICTION OF EPITHELIUM-DENUDED RAT AND HUMAN AIRWAY PREPARATIONSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2008Dragan Pavlovic SUMMARY 1The effects of s-carboxymethyl-l-cysteine (S-CMC), either administered orally to rats or incubated with tissue preparations from rats and humans, on isometric contractions of tracheal smooth muscle were investigated in the present study using an improved in vitro model of tracheal tube or ring preparations. The involvement of the tracheal epithelium in the observed effects was also investigated. 2The experimental model permitted selective perfusion of the airway tube, luminal-IN or serosal,OUT, and measurement of airway smooth muscle contraction or relaxation in preparations with (+) or without (,) epithelium (Ep), excluding direct effects of airway mucus. 3We found that oral pretreatment of rats with S-CMC (mixed with water; 200 mg/kg per day for 2 weeks), but not short pre-incubation of preparations in vitro (10,3 mol/L S-CMC for 1 h), diminished the sensitivity of ,Ep preparations to carbachol compared with controls (EC50 (,log10 mol/L) values: 5.5 ± 0.1 vs 5.8 ± 0.1, respectively, for IN perfusion (P < 0.005); 5.6 ± 0.1 vs 5.9 ± 0.1, respectively, for OUT perfusion (P < 0.005)), whereas the sensitivity of preparations to aminophylline was not affected. Normal sensitivity to carbachol stimulation was re-established if preparations were pre-incubated with capsaicin. 4It was also found that longer pre-incubation (4 h) of ring-preparations of human bronchus with S-CMC (10,5 mol/L) in vitro resulted in a diminished response to carbachol stimulation. 5In conclusion, S-CMC had small inhibitory effects on the sensitivity of rat and human airway smooth muscle to carbachol, particularly in endothelium-denuded preparations. Whether the epithelium was responding to S-CMC by producing some contracting factor(s) requires further investigation. [source] | ||||||||||