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Proliferation Response (proliferation + response)

Distribution by Scientific Domains

Medical Sciences	38%
Life Sciences	38%

Selected Abstracts

Effects of Monochromatic Light on Proliferation Response of Splencyte in Broilers

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 5 2008
D. Xie
Summary To investigate the effects of various monochromatic lights on splenocyte proliferation responses, a total of 260 Arbor Acre male broilers on P1 (post-hatching day 1) were exposed to blue light (BL), green light (GL), red light (RL) and white light treatments by light emitting diode system for 7 weeks, respectively. All light sources were equalized on the intensity of 15 lx and light period of 23 h daily. Morphological change of spleen and response of splenocyte proliferation were assessed by using histochemistry staining and colorimetric test in cultures of purified splenic cells. The results were as follows: (1) At P21, GL increased significantly the spleen weight by 163.6% and spleen index by 118.8% compared with RL (P < 0.05). Until P49, BL enhanced significantly the spleen weights by 42.2% compared with RL (P < 0.05), but no significant difference was found in the spleen index among four light-treated groups (P > 0.05). (2) Compared with RL, GL increased significantly the diameter of splenic nodule and area of periarterial lymphatic sheath at P21 by 87.2 and 58.1%, respectively (P < 0.05); BL increased significantly the diameter of splenic nodule and area of periarterial lymphatic sheath at P49 by 64.4 and 50.5%, respectively (P < 0.05). (3) At P21, GL enhanced spleen lymphocytes proliferation in response to concanavalin A compared with RL by 50.0% (P < 0.05). Until P49, the mitogenic response in BL was significantly higher (29.4%) than that of RL (P < 0.05). (4) The interleukin-2 (IL-2) bioactivity was significantly increased to 34.3% in GL than in RL at P21 (P < 0.05). Until P49, the IL-2 bioactivity in BL was significantly higher (62.2%) than that of RL (P < 0.05). (5) There was no significant difference in the nitric oxide (NO) concentration of splenocyte among RL, GL and BL groups at P21 (P > 0.05), but the concentration in RL group at P49 was significantly increased, 59.0 and 63.7% compared to that of GL and BL groups, respectively (P < 0.05). These results suggested that the monochromatic light affected splenocyte proliferation mainly because of alterations in IL-2 bioactivity and NO production in splenocyte of broiler. In early stage of broiler growth, the action of GL was obvious, while the response of BL was stronger in later stage. [source]

Allergenicity testing of supermethrin, phenoxyacetic acid and DNCB using in vivo and in vitro modifications of the local lymph node assays, maximization and epicutaneous testing

JOURNAL OF APPLIED TOXICOLOGY, Issue 4 2001
M. Kuricova
Abstract The purpose of this study was to compare two methods of testing for allergenicity: in vivo and in vitro modifications of local lymph node assays (LLNA) in mice and the maximization and epicutaneous skin tests in guinea pigs as per the Organization for Economic Cooperation and Development (1981). Two pesticides,the synthetic pyrethroid insecticide supermethrin (SM) and the herbicide phenoxyacetic acid (PAA),were evaluated using this testing battery. 1-Chloro-2,4-dinitrobenzene (DNCB) was selected as a reference allergen for the local lymph node assay. In vitro modification of LLNA proliferative response per standard cell count in lymphocyte cultures derived from treated Balb/c mice did not differ from control mice. Results of the in vivo modification showed that treatment with 50% PAA and 50% SM resulted in a lower proliferation response of lymphocytes in lymph nodes compared with control animals. The vigour of the proliferative response varied more in in vivo modification of LLNA. Stimulation indices were <3, so PAA and SM did not indicate classification as allergens. Lymphocyte proliferation in 1% DNCB-activated lymph nodes was approximately fivefold higher than in those derived from control mice. Proliferation response in vitro calculated as stimulation index was higher in DNCB-treated mice than those observed in vivo, but differences were not dramatic. Auricular lymph node weight and cellularity in mice treated with PAA and SM were similar to controls. The DNCB stimulation index for lymph node cellularity was 5.5. Lymph node weight was three times higher in comparison with controls. In the maximization test in guinea pigs SM and PAA acid resulted in 40% and 50% of animals demonstrating sensitization, respectively. Epicutaneous administration resulted in weaker reaction. Both SM and PAA are mildly strong sensitizers by this battery. Copyright © 2001 John Wiley & Sons, Ltd. [source]

Novel B and T cell epitopes of chicken ovomucoid (Gal d 1) induce T cell secretion of IL-6, IL-13, and IFN-,

CLINICAL & EXPERIMENTAL ALLERGY, Issue 6 2001
E. Holen
Background Chicken ovomucoid (OM, Gal d 1) has an important role in the pathogenesis of IgE-mediated allergic reactions to hen's egg white. Objectives The purpose of this study was to clarify the mechanisms of T cell recognition of ovomucoid using intact OM and chemically modified, characterized and homogeneous solid phase synthetic peptides covering the whole molecule. Methods Eighteen overlapping peptides were prepared by solid phase F-moc polyamide peptide synthesis (SPPS), characterized and high-pressure liquid chromatography (HPLC) purified. The peptides, together with intact, denatured and oxidized OM, were used to stimulate patient-derived cell cultures for mapping T cell epitopes. Proliferation responses, T cell phenotype and cytokine secretion using peripheral blood mononuclear cells (PBMC) from eight individuals and T cell lines (TCL) derived from six hen's egg-allergic patients, were examined. In addition, intact, denatured, oxidized and deglycosylated OM, as well as the peptides solely or with their keyhole limpet haemocyanin (KLH) complexes, were tested. For locating IgE and IgG B cell epitopes, seven egg-allergic patient sera and three OM-polyclonal sera were used. Healthy non-allergic individuals were included as controls. Results Seven peptides were recognized by specific IgE, while OM-specific TCL recognized 10 peptides. Six of the OM peptides were commonly recognized both by patient S-IgE and blood-derived TCL. Among those, one novel epitope, peptide OM 61,74, had the ability to bind IgE. Another peptide, OM 101,114, was recognized by IgE and IgG sera, but not by any of the TCLs. In contrast, the peptides OM 41,56, OM 71,84, OM 131,144 and OM 171,186 were exclusively T cell epitopes with no affinity to specific antibodies. Abundant TCL secretion of IFN-,, IL-6, IL-4, IL-13, IL-10 and TNF-, in response to OM stimulation indicates the contribution of Th2 as well as Th1/Th0 CD4+ cell subsets. For allergic patients moderate amounts of IFN-,, IL-13, and high amounts of IL-6, were secreted in response to TCL stimulation by OM peptides. High amounts of IL-6 were secreted in response to all molecular forms of OM (intact-, modified-OM and the peptides 71,84 and 51,64) when TCLs from two non-allergic donors were used. Conclusions One novel B cell epitope (OM 61,74) and 10 T cell epitopes have been identified. The most reactive epitopes of the OM molecule comprise the motifs 1,14 to 71,84, the overlapping peptide-pairs OM 121,134 and OM 131,144 and peptides OM 161,174 and 171,186. Peptides OM 1,14 and 171,186 are the only ones capable of inducing IL-4 secretion. Only one peptide (OM 11,24) induces IL-10 secretion. Those peptides recognized as both T and B cell epitopes or only T cell epitopes, have the potential to induce T cell secretion of moderate to high amounts of IL-13, IFN-, and particularly IL-6. [source]

Oestrogenic activity of isobutylparaben in vitro and in vivo

JOURNAL OF APPLIED TOXICOLOGY, Issue 4 2002
P. D. Darbre
Abstract The alkyl esters of p -hydroxybenzoic acid (parabens) are used widely as preservatives in foods, pharmaceuticals and cosmetics to which the human population is exposed. Recent studies have reported that methylparaben, ethylparaben, n -propylparaben and n -butylparaben all possess oestrogenic activity in several in vitro assays and in animal models in vivo. This study reports on the oestrogenic activity of isobutylparaben in a panel of assays in vitro and in vivo. Isobutylparaben was able to displace [3H]oestradiol from cytosolic oestrogen receptor , of MCF7 human breast cancer cells by 81% at 100 000-fold molar excess. Using a clonal line of MCF7 cells containing a stably transfected oestrogen-responsive ERE-CAT reporter gene, CAT gene expression could be increased by isobutylparaben such that the magnitude of the response was the same at 10,5 M isobutylparaben as with 10,8 M 17,-oestradiol. Isobutylparaben could also increase expression of the endogenous oestrogen-responsive pS2 gene in MCF7 cells and maximal expression at 10,5 M isobutylparaben could be inhibited with the anti-oestrogen ICI 182 780. The proliferation of two oestrogen-dependent human breast cancer cell lines MCF7 and ZR-75-1 could be increased with isobutylparaben such that at concentrations of 10,5 M the proliferation response was of the same magnitude as with 10,8 M 17,-oestradiol. Evidence for oestrogen receptor mediation of proliferation effects was provided by the inability of isobutylparaben to influence the growth of oestrogen-unresponsive MDA-MB-231 human breast cancer cells and by the ability of the anti-oestrogen ICI 182 780 to inhibit the isobutylparaben effects on MCF7 cell growth. The proliferation response to 10,10 M 17,-oestradiol was not antagonized with isobutylparaben at any concentration from 10,9 M to 10,4 M in either MCF7 or ZR-75-1 cells. Finally, subcutaneous administration of isobutylparaben was able to increase the uterine weight in the immature mouse after three daily doses of 1.2 or 12.0 mg per mouse. Previous work using linear-alkyl-chain parabens has shown that oestrogenic activity increases with alkyl chain length from methylparaben to n -butylparaben. The results here show that branching of the alkyl chain to isobutylparaben increases oestrogenic activity beyond that of the equivalent length linear alkyl chain in n -butylparaben. Copyright © 2002 John Wiley & Sons, Ltd. [source]

Allergenicity testing of supermethrin, phenoxyacetic acid and DNCB using in vivo and in vitro modifications of the local lymph node assays, maximization and epicutaneous testing

Cloning and expression profile of FLT3 gene during progenitor cell-dependent liver regeneration

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2007
Iraz T Aydin
Abstract Background and Aim:, The liver has a unique capacity to regenerate upon exposure to viral infections, toxic reactions and cancer formation. Liver regeneration is a complex phenomenon in which several factors participate during its onset. Cellular proliferation is an important component of this process and the factors that regulate this proliferation have a vital role. FLT3, a well-known hematopoietic stem cell and hepatic lineage surface marker, is involved in proliferative events of hematopoietic stem cells. However, its contribution to liver regeneration is not known. Therefore, the aim of this study was to clone and examine the role of FLT3 during liver regeneration in rats. Methods:, Partial cDNA of rat homolog of FLT3 gene was cloned from thymus and the tissue specific expression of this gene at mRNA and protein levels was examined by RT-PCR and Western blot. After treating with 2-AAF and performing hepatectomy in rats to induce progenitor-dependent liver regeneration, the mRNA and protein expression profile of FLT3 was investigated by real-time PCR and Western blot during liver regeneration. In addition, cellular localization of FLT3 protein was determined by immunohistochemistry. Results:, The results indicated that rat FLT3 cDNA has high homology with mouse and human FLT3 cDNA. It was also found that FLT3 is expressed in most of the rat tissues and during liver regeneration. In addition, its intracellular localization is altered during the late stages of liver regeneration. Conclusion:, The FLT3 receptor is activated at the late stages of liver regeneration and participates in the proliferation response that is observed during progenitor-dependent liver regeneration. [source]

Differential in vitro CD4+/CD8+ T-cell response to live vs. killed Leishmania major

PARASITE IMMUNOLOGY, Issue 2 2010
M. NATEGHI ROSTAMI
Summary Clinical trials of killed Leishmania vaccines showed a limited efficacy compared with leishmanization (LZ). The reason for this difference in protection against cutaneous leishmaniasis (CL) is not known and in vivo studies on T-cell function may provide valuable information. Nevertheless, there are limited studies on the nature of the stimulatory effects of live vs. killed parasites on human T cells in vitro. A total of nine Leishmanin Skin Test+ volunteers with a history of self-healing CL (HCL) and seven healthy volunteers were included in this study. 5,6-carboxyfluroescein diacetate succinimidyl ester-labelled CD4+/CD8+ lymphocytes were cultured with killed Leishmania Lysate (Killed LL) or live Leishmania major (Live LM) and analysed for proliferation using flow cytometry. Culture supernatants were used for cytokine titration. In HCL volunteers, upon stimulation with killed LL, the number of proliferated CD4+/CD8+ cells was significantly more than that of unstimulated (P < 0·001) or live LM stimulated (P < 0·05) cells, or cells from controls (CD4+/CD8+: P < 0·05/P < 0·001). Stimulation of CD4+ cells with Live LM (P < 0·001) or Killed LL (P < 0·05) induced a significantly higher IFN-, production compared with that of controls, but Live LM induced significantly (P < 0·05) more IFN-, than Killed LL. A significantly (P < 0·05) higher IFN-, production was observed when CD8+ cells were stimulated with Live LM. Cells from HCL volunteers showed significantly more IL-10 production to Live LM stimulation compared with that of controls (CD4+: P < 0·05 /CD8+: P < 0·001) or cells stimulated with Killed LL (CD4+/CD8+: P < 0·001/P < 0·0005). Whereas Killed LL induced more proliferation response in purified T cells, Live LM induced cytokine production without significant induction of proliferation. The results from healed CL volunteers in this study could be implicated in further studies on T-cell response in vaccinated individuals. [source]

Signal transduction responses to lysophosphatidic acid and sphingosine 1-phosphate in human prostate cancer cells

THE PROSTATE, Issue 14 2009
Terra C. Gibbs
Abstract BACKGROUND Lysophosphatidic acid (LPA) and sphingosine-1-phosphate (S1P) are lipid mediators that bind to G-protein-coupled receptors. In this study, signaling responses to 18:1 LPA and S1P were examined in parallel in three human prostate cancer cell lines: PC-3, Du145, and LNCaP. METHODS Receptor expression was assessed by RT-PCR, Northern blotting, and immunoblotting. Cellular responses to mediators were studied by proliferation assays, phosphoprotein immunoblotting, and phospholipid metabolism assays. RESULTS All cell lines express mRNA for both LPA and S1P receptors. PC-3 and Du145, but not LNCaP, proliferate in response to LPA and S1P. Epidermal growth factor (EGF), phorbol 12-myristate 13-acetate (PMA), LPA, and S1P induce activation of Erks in PC-3 and Du145; only EGF and PMA activate Erks in LNCaP. In Du145 and PC-3, Akt is activated by EGF, LPA, and S1P. Akt is constitutively active in LNCaP; EGF but not LPA or S1P stimulates further phosphorylation. FAK is phosphorylated in response to both LPA and S1P in PC-3 and Du145, but not in LNCaP. LPA and S1P stimulate phospholipase D (PLD) activity to varying extents in the different cell lines. Notably, both lipid mediators activate PLD in LNCaP. In Du145, LPA, but not S1P, activates PLD and enhances cellular production of LPA. CONCLUSIONS Although both LPA and S1P induce signal transduction in all prostate cancer cell lines studied, a proliferation response is observed only when the Erk, Akt, and FAK pathways are activated. Other responses to the lipid mediators, such as PLD activation, likely contribute to other cellular outcomes. Prostate 69: 1493,1506, 2009. © 2009 Wiley-Liss, Inc. [source]

Laminin-2 stimulates the proliferation of epithelial cells in a conjunctival epithelial cell line

CELL PROLIFERATION, Issue 2 2004
J. Dowgiert
To test the hypothesis that LN-2 can additionally modulate epithelial cell biology, an analysis of the role of LN-2 in cell adhesion, activation of signalling intermediates and proliferation was undertaken. A virally transformed human conjunctival epithelial cell line (HC0597) was utilized in this study. Adhesion assays using function-inhibiting antibodies demonstrated that ,3,1 integrin is essential for the rapid attachment of conjunctival epithelial cells to LN-2. Bromodeoxyuridine (BrdU) incorporation analyses revealed that, compared with LN-1 or LN-10, LN-2 significantly promotes epithelial proliferation. Phosphorylation of the signalling intermediates Erk1/2 and Akt-1 was observed within 15 min of cell adhesion to LN-2. Inhibiting ,3,1 integrin function decreased total cellular phosphotyrosine levels, specifically inhibited phosphorylation of Erk1/2 and Akt-1, and dampened the proliferation response of epithelial cells adherent to LN-2. Inhibition of Erk or Akt activation inhibited cell proliferation in a dose-dependent manner. However, the inhibition of Erk resulted in a stronger suppression of proliferation compared with Akt inhibition. From these results, it is concluded that human conjunctival epithelial cells adhere to immobilized LN-2 using ,3,1 integrin. ,3,1 integrin/LN-2 signalling, transduced primarily through an Erk pathway, enhances epithelial cell proliferation. These results demonstrate that LN-2 can impact on epithelial cell biology in addition to nerve and muscle, and provide information regarding the role of this isoform in ocular surface epithelial cells. [source]

Infection with Toxoplasma gondii results in dysregulation of the host cell cycle

CELLULAR MICROBIOLOGY, Issue 5 2008
Robert E. Molestina
Summary Mammalian cells infected with Toxoplasma gondii are characterized by a profound reprogramming of gene expression. We examined whether such transcriptional responses were linked to changes in the cell cycle of the host. Human foreskin fibroblasts (HFFs) in the G0/G1 phase of the cell cycle were infected with T. gondii and FACS analysis of DNA content was performed. Cell cycle profiles revealed a promotion into the S phase followed by an arrest towards the G2/M boundary with infection. This response was markedly different from that of growth factor stimulation which caused cell cycle entry and completion. Transcriptional profiles of T. gondii -infected HFF showed sustained increases in transcripts associated with a G1/S transition and DNA synthesis coupled to an abrogation of cell cycle regulators critical in G2/M transition relative to growth factor stimulation. These divergent responses correlated with a distinct temporal modulation of the critical cell cycle regulator kinase ERK by infection. While the kinetics of ERK phosphorylation by EGF showed rapid and sustained activation, infected cells displayed an oscillatory pattern of activation. Our results suggest that T. gondii infection induces and maintains a ,proliferation response' in the infected cell which may fulfill critical growth requirements of the parasite during intracellular residence. [source]

Proliferative responses to growth factors decline rapidly during postnatal maturation of mammalian hair cell epithelia

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2007
Rende Gu
Abstract Millions of lives are affected by hearing and balance deficits that arise as a consequence of sensory hair cell loss. Those deficits affect mammals permanently, but hearing and balance recover in nonmammals after epithelial supporting cells divide and produce replacement hair cells. Hair cells are not effectively replaced in mammals, but balance epithelia cultured from the ears of rodents and adult humans can respond to hair cell loss with low levels of supporting cell proliferation. We have sought to stimulate vestibular proliferation; and we report here that treatment with glial growth factor 2 (rhGGF2) yields a 20-fold increase in cell proliferation within sheets of pure utricular hair cell epithelium explanted from adult rats into long-term culture. In epithelia from neonates, substantially greater proliferation responses are evoked by rhGGF2 alone, insulin alone and to a lesser degree by serum even during short-term cultures, but all these responses progressively decline during the first 2 weeks of postnatal maturation. Thus, sheets of utricular epithelium from newborn rats average >,40% labelling when cultured for 72 h with bromo-deoxyuridine (BrdU) and either rhGGF2 or insulin. Those from 5- and 6-day-olds average 8,15%, 12-day-olds average <,1% and after 72 h there is little or no labelling in epithelia from 27- and 35-day-olds. These cells are the mammalian counterparts of the progenitors that produce replacement hair cells in nonmammals, so the postnatal quiescence described here is likely to be responsible for at least part of the mammalian ear's unique vulnerability to permanent sensory deficits. [source]

Differential Effects of Stress on Adult Hippocampal Cell Proliferation in Low and High Aggressive Mice

JOURNAL OF NEUROENDOCRINOLOGY, Issue 7 2007
A. H. Veenema
Male wild house mice selected for a long (LAL) or a short (SAL) latency to attack a male intruder generally show opposing behavioural coping responses to environmental challenges. LAL mice, unlike SAL mice, adapt to novel challenges with a highly reactive hypothalamic-pituitary-adrenal axis and show an enhanced expression of markers for hippocampal plasticity. The present study aimed to test the hypothesis that these features of the more reactive LAL mice are reflected in parameters of hippocampal cell proliferation. The data show that basal cell proliferation in the subgranular zone (SGZ) of the dentate gyrus, assessed by the endogenous proliferation marker Ki-67, is lower in LAL than in SAL mice. Furthermore, application of bromodeoxyuridine (BrdU) over 3 days showed an almost two-fold lower cell proliferation rate in the SGZ in LAL versus SAL mice. Exposure to forced swimming resulted, 24 h later, in a significant reduction in BrdU + cell numbers in LAL mice, whereas cell proliferation was unaffected by this stressor in SAL mice. Plasma corticosterone and dentate gyrus glucocorticoid receptor levels were higher in LAL than in SAL mice. However, no differences between the SAL and LAL lines were found for hippocampal NMDA receptor binding. In conclusion, the data suggest a relationship between coping responses and hippocampal cell proliferation, in which corticosterone may be one of the determinants of line differences in cell proliferation responses to environmental challenges. [source]