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PubMed2006

Coordinated regulation of two independent cell-cell signaling systems and swarmer differentiation in Salmonella enterica serovar Typhimurium.

Almost all members of the genus Salmonella differentiate and migrate on semisolid surfaces in a coordinated population behavior known as swarming. Important virulence determinants are coupled to swarmer differentiation in several other pathogenic organisms, collectively suggesting that conditions that trigger swarming in the laboratory may fortuitously promote the cells to enter a robust physiological state relevant to the host environment. Here, we present evidence that expression of two independent cell-cell signaling systems are also coupled to swarmer differentiation in S. enterica serovar Typhimurium. Expression of both pfs and sdiA genes was up-regulated in the actively migrating swarmers compared to their vegetative counterparts propagated in broth or spread plated on the surface of swim, swarm, and solid media. Accordingly, swarmers produced elevated levels of a universally recognized signaling molecule, autoinducer-2, and exhibited increased sensitivity to N-acyl homoserine lactones (AHLs), signaling molecules that Salmonella does not produce. Expression of the rck operon was concomitantly up-regulated in the swarmers in an SdiA-dependent manner only in the presence of exogenous AHLs. In addition to the previously reported adaptive antibiotic resistance phenotype and global shift in metabolism, this work presents another component of the physiological changes that are specifically associated with swarmer differentiation in serovar Typhimurium and not simply due to growth on a surface.

4-Butyrolactone↗
PubMed2004

Sequential roles of receptor binding and low pH in forming prehairpin and hairpin conformations of a retroviral envelope glycoprotein.

A general model has been proposed for the fusion mechanisms of class I viral fusion proteins. According to this model a metastable trimer, anchored in the viral membrane through its transmembrane domain, transits to a trimeric prehairpin intermediate, anchored at its opposite end in the target membrane through its fusion peptide. A subsequent refolding event creates a trimer of hairpins (often termed a six-helix bundle) in which the previously well-separated transmembrane domain and fusion peptide (and their attached membranes) are brought together, thereby driving membrane fusion. While there is ample biochemical and structural information on the trimer-of-hairpins conformation of class I viral fusion proteins, less is known about intermediate states between native metastable trimers and the final trimer of hairpins. In this study we analyzed conformational states of the transmembrane subunit (TM), the fusion subunit, of the Env glycoprotein of the subtype A avian sarcoma and leukosis virus (ASLV-A). By analyzing forms of EnvA TM on mildly denaturing sodium dodecyl sulfate gels we identified five conformational states of EnvA TM. Following interaction of virions with a soluble form of the ASLV-A receptor at 37 degrees C, the metastable form of EnvA TM (which migrates at 37 kDa) transits to a 70-kDa and then to a 150-kDa species. Following subsequent exposure to a low pH (or an elevated temperature or the fusion promoting agent chlorpromazine), an additional set of bands at >150 kDa, and then a final band at 100 kDa, forms. Both an EnvA C-helix peptide (which inhibits virus fusion and infectivity) and the fusion-inhibitory agent lysophosphatidylcholine inhibit the formation of the >150- and 100-kDa bands. Our data are consistent with the 70- and 150-kDa bands representing precursor and fully formed prehairpin conformations of EnvA TM. Our data are also consistent with the >150-kDa bands representing higher-order oligomers of EnvA TM and with the 100-kDa band representing the fully formed six-helix bundle. In addition to resolving fusion-relevant conformational intermediates of EnvA TM, our data are compatible with a model in which the EnvA protein is activated by its receptor (at neutral pH and a temperature greater than or equal to room temperature) to form prehairpin conformations of EnvA TM, and in which subsequent exposure to a low pH is required to stabilize the final six-helix bundle, which drives a later stage of fusion.

Gene Products, env↗
PubMed1986

Microbes, warfare, religion, and human institutions.

A significant number of practicing microbiologists are not aware of the historical impact of infectious agents on the development of human institutions. Microbes have played a profound role in warfare, religion, migration of populations, art, and in diplomacy. Boundaries of nations have changed as a result of microbial diseases. Infectious agents have terminated some kingdoms and elevated others. There is a need for microbiologists to have a historical perspective of some of the major ways in which a pathogen may influence civilized populations. Conditions may exist in contemporary society for a repeat of some of the kinds of plagues suffered by previous societies. The purpose of this paper is to review examples of situations where pathogenic microbes have forced societal modifications on centers of human population.

Animals↗
PubMed1992

Regulation of expression of fibronectin and its receptor, alpha 5 beta 1, during development and regeneration of peripheral nerve.

The extracellular matrix glycoprotein, fibronectin, is a potent promoter of peripheral neurite outgrowth. Interactions of peripheral neurons with fibronectin have been shown to be primarily mediated by the beta 1 class of integrin heterodimers. In the present study, we have examined the expression and regulation of fibronectin and its integrin receptor, alpha 5 beta 1, in developing and regenerating chick peripheral nerve. We show that fibronectin and alpha 5 beta 1 are expressed at comparatively high levels in developing nerve with alpha 5 beta 1 expression on axons and non-neuronal cells. With nerve maturation, both proteins are less prominently expressed and the cellular pattern of alpha 5 beta 1 expression becomes more restricted. Following lesion of mature nerve, both fibronectin and alpha 5 beta 1 are strongly induced with prominent expression of alpha 5 beta 1 on regenerating neurites and Schwann cells. The elevation in fibronectin levels in the regenerating nerve is highest in the vicinity of the lesion, an area undergoing extensive cellular remodeling including Schwann cell migration and growth cone extension. Our results suggest that fibronectin and its receptor, alpha 5 beta 1, may mediate functionally important interactions in the development and regeneration of peripheral nerve.

Animals↗
PubMed1993

Transient preservation of photoreceptors on the flanks of argon laser lesions in the RCS rat.

In the RCS rat there is a progressive degeneration of the photoreceptors which starts at two to three weeks after birth. We have demonstrated that there is prolonged survival of photoreceptors on the flanks of argon laser lesions made at post-natal day 23, just as degeneration begins. The cells in the outer nuclear layer retained a relatively normal appearance on the flanks of the lesions for the first two weeks and there was a very low percentage of pyknotic cells. By one month some cell loss occurred but much less than in non-irradiated regions where very few cells remained. At two months after lesion there were still elevated numbers on the flanks but only 2-3 rows of cells remained. The prolonged survival correlated with disruption to the pigment epithelial layer, increased migration of phagocytic cells into the outer segment/debris layer and a reduction in thickness of the debris layer at late stages. The mechanisms of this effect are unknown however laser lesions provide a well controlled and reproducible situation in which to study these mechanisms.

Animals↗
PubMed1997

A new method of culturing and transferring iris pigment epithelium.

PURPOSE: To optimize a culture technique and transfer iris pigment epithelial (IPE) cells for cellular studies in vitro. METHODS: Porcine iris tissues were obtained, and IPE cells were isolated and cultured at high densities by plating them in the form of drops. Spherically shaped structures containing a high concentration of cells were formed after 7 to 10 days of culture. Cells were subcultured by transferring spheres to new culture dishes without employing enzymatic dissociation. The purity of IPE cells was determined by pigmentation and cytokeratin labeling. Proliferation was assessed by incorporation of 5-bromo-2'-deoxyuridine. Cellular structure was analyzed under the light and electron microscopes and function was assayed by rod outer segment phagocytosis. RESULTS: Iris pigment epithelial cells, when cultured at high densities, tended to form elevated spherical structures containing viable cells. The cultured cells were pigmented and showed positive labeling with a monoclonal cytokeratin antibody. The IPE cells proliferated and migrated from the spheres to form monolayers. Cells originating from the transferred spheres also continued to proliferate and to migrate in a similar manner to the originally cultivated cells to form monolayers after 7 to 10 days. These cells were able to phagocytose rod outer segments. CONCLUSIONS: This new method provides a simple method of culturing a large quantity of IPE cells. The high yield of pure IPE cells and the ease of transfer provide an ideal means to study them at the cellular level.

Animals↗
PubMed2001

Elevated expression of transforming growth factor betas and the tumor necrosis factor family in lung adenocarcinomas induced by N-nitrosobis(2-hydroxypropyl)amine in rats.

Expression of transforming growth factor betas (TGF betas), tumor necrosis factor (TNF) family members, interferons (IFNs), macrophage migration inhibitory factor (MIF) and granulocyte macrophage colony stimulating factor (GM-CSF) in lung adenocarcinomas induced by N-nitrosobis(2-hydroxypropyl)amine (BHP) in rats was investigated using a multiprobe RNase protection assay (RPA) followed by densitometric quantification. Male Wistar rats, 6 weeks of age, were given 2,000 ppm BHP in their drinking water for 12 weeks and maintained without further treatment until killed at week 25. Total RNAs were extracted from 15 adenocarcinomas. Four samples of normal lung tissue from untreated rats served as controls. The expression of TGFbeta1, TGFbeta2, TGFbeta3, TNFalpha, TNFbeta and lymphotoxin beta (Ltbeta) was significantly higher in adenocarcinomas than in normal lung tissues. In contrast, MIF was expressed at the same level in neoplasms and normal tissue and no expression of IFNbeta, IFNgamma and GM-CSF was apparent in either adenocarcinomas or normal lung tissues. These results suggest that elevated expression of TGFbetas and TNF family members may contribute to the development and progression of lung adenocarcinomas induced by BHP in rats.

Adenocarcinoma↗
PubMed2026

Multimodal Analysis Reveals Aberrant Expression of SUMO2 and Its Significant Association With Key Mechanisms of Metabolic Pathways in Hepatocellular Carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. However, the role of small ubiquitin-like modifier 2 (SUMO2), a core member of the small ubiquitin-like modifier (SUMO) family, regarding its expression patterns and metabolism-related functions in HCC remains inadequately understood. METHODS: A multidimensional analytical framework was applied, integrating immunohistochemistry (153 HCC vs. 21 non-HCC samples), proteomics (159 paired samples), bulk transcriptomics (3240 HCC vs. 2267 non-HCC samples), single-cell RNA sequencing (RNA-seq) (10 HCC vs. 8 non-HCC samples), spatial transcriptomics, and external CRISPR/Cas9 functional genomics data. Systematic analyses included standardized mean difference (SMD), pathway enrichment, pseudotime trajectory inference, in silico knockout, cell-cell communication, metabolic flux scoring, immune infiltration, clinical correlation, drug sensitivity prediction, and molecular docking. RESULTS: At the protein level, immunohistochemistry (nuclear positivity) and external proteomic data collectively demonstrated consistent SUMO2 overexpression in HCC. Consistent upregulation was also observed at the mRNA level across large-scale cohorts. Single-cell RNA-seq and spatial transcriptomics localized SUMO2 enrichment to malignant hepatocytes and tumor-dominant regions. CRISPR-mediated SUMO2 knockout suppressed proliferation in multiple HCC cell lines. Mechanistically, high SUMO2 expression was significantly associated with metabolic reprogramming involving glycolysis/gluconeogenesis, pyruvate metabolism, and the tricarboxylic acid cycle. SUMO2-high malignant hepatocyte subpopulations exhibited enhanced activity of the macrophage migration inhibitory factor signaling axis and enhanced iron-sensor interactions. Further, the immune infiltration analysis revealed a negative correlation between SUMO2 expression and M1 macrophages and a positive correlation between follicular helper T cells and regulatory T cells. Clinically, elevated SUMO2 levels were found to be associated with adverse prognostic features. Furthermore, high SUMO2 expression was associated with increased sensitivity to dasatinib, and molecular docking simulations predicted potential binding between SUMO2 and dasatinib, with a Vina score of -8.5 kcal/mol. CONCLUSIONS: SUMO2 is aberrantly expressed at the protein, mRNA, single-cell, and spatial transcriptomic levels in HCC and is significantly associated with metabolic reprogramming and altered migration inhibitory factor (MIF)-mediated intercellular communication, suggesting its potential as a novel biomarker for diagnosis and treatment.

Humans↗
PubMed1982

Immune responses to chlamydial antigens in humans.

Antibody titer, lymphocyte stimulation and leukocyte migration inhibition with chlamydial antigens were determined repeatedly over many months on human subjects. The volunteers were retrospectively placed into four groups on the basis of clinical, laboratory and epidemiologic criteria. Group A consisted of persons with proven or probable chlamydial infection, including an illness confirmed by chlamydial isolation or seroconversion, or a clinically compatible illness with positive serologic results. Group B were sexual partners or close contacts of group A individuals. Group C were laboratory workers with prolonged exposure to viable chlamydiae or their antigens. Group D included persons of comparable age as those in groups A and B, but lacking a history of symptomatic chlamydial infection or of contact with chlamydiae. Individual cases illustrated the rise of antibody and some cell mediated immunity reactions (CMI) with active chlamydial infection. By contrast, laboratory exposure resulted in elevation of CMI but not of antibody. Statistical analysis of the results in 46 volunteers tested repeatedly indicated a strong association of specific antibody with lymphocyte stimulation, but not with leukocyte migration inhibition. Regression analysis suggested that the type of exposure markedly influenced the relationship between antibody and lymphocyte stimulation. Measurement of immunotype-specific antibody titer by microimmunofluorescence (or an equally sensitive method) remains the best laboratory indicator of past chlamydial infection. Neither antibody nor CMI can, as yet, be definitely related to resistance to re-infection in humans.

Acute Disease↗
PubMed2026

Targeting SUV4-20H2-mediated H4K20 methylation restrains growth and migration in pediatric high-grade astrocytomas.

Pediatric astrocytomas are characterized by increased molecular and clinical heterogeneity with epigenetic alterations contributing to aggressiveness and therapy resistance. The repressive histone mark H4K20 trimethylation (H4K20me3) and the methyltransferase SUV4-20H2 (KMT5C) are critical regulators of chromatin integrity and genome stability, with limited investigation in pediatric astrocytomas. KMT5C mRNA levels were evaluated in a publicly available pediatric gliomas database using bioinformatic analysis. Investigation of SUV4-20H2 and H4K20me3 expression was performed in a cohort of 43 pediatric astrocytoma tissues by immunohistochemistry. Their functional role and mechanism of action was investigated in pediatric glioma cell lines by using the substrate-competitive inhibitor of SUV4-20, A-196. Cell viability, apoptosis and migration were assessed using XTT, cleaved PARP, and wound healing assays, respectively. Effects of treatment on H4K20 methylation, DNA damage, mitotic stress [Polo-like kinase (PLK1) expression], and invasion markers (N-cadherin, β-catenin expression) were examined by western immunoblotting. KMT5C mRNA was significantly enriched in pediatric high-grade astrocytomas compared to low-grade tumors. A significant elevation of SUV4-20H2 and H4K20me3 expression was detected in astrocytoma tissues indicating epigenetic dysregulation contributing to malignancy. Treatment with A-196 reduced cell proliferation of pediatric glioma cell lines and induced apoptosis in a dose-dependent manner. It further impaired cell migration, accompanied by reduced N-cadherin and β-catenin expression. Mechanistically, inhibition of SUV4-20 depleted H4K20me3, inducing chromatin destabilization, replication-associated DNA damage and was associated with increased PLK1 expression, consistent with activation of a mitotic stress response. Our findings indicate that SUV4-20H2-mediated H4K20 activity in pediatric high-grade astrocytomas maintains their growth and migratory potential by regulating chromatin integrity and may serve as potential therapeutic target.

H4K20me2/3↗
PubMed2001

Migratory costs and the evolution of egg size and number in introduced and indigenous salmon populations.

The trade-off between reproductive investment and migration should be an important factor shaping the evolution of life-history traits among populations following their radiation into habitats with different migratory costs and benefits. An experimentally induced difference in migratory rigor for families of chinook salmon (Oncorhynchus tshawytscha), of approximately 86 km and 413 m elevation, exacted a cost to somatic energy reserves (approximately 17% reduction in metabolizable mass) and ovarian investment (13.7% reduction in ovarian mass). This cost was associated with a reduction in egg size and paralleled the phenotypic pattern of divergence between two introduced New Zealand populations of common origin, presently breeding at sites with different migration distances. The genetic pattern of divergence of these same populations, detected under common rearing, was consistent with compensation for migratory costs (the population that migrates farther invested more in ovarian mass), but egg number more than egg size was associated with this evolution. These evolutionary patterns are consistent with what is known of the inheritance of these traits and with trade-offs and constraints favoring initial evolution in offspring number over offspring size. Analysis of egg number-size patterns of other Pacific salmon populations in their native range supported the hypothesis that migration strongly influences patterns of reproductive allocation, favoring a higher ratio of egg number to egg size with greater migration distance.

Animal Migration↗
PubMed2003

ERK and RhoA differentially regulate pseudopodia growth and retraction during chemotaxis.

Nonmotile cells extend and retract pseudopodia-like structures in a random manner, whereas motile cells establish a single dominant pseudopodium in the direction of movement. This is a critical step necessary for cell migration and occurs prior to cell body translocation, yet little is known about how this process is regulated. Here we show that myosin II light chain (MLC) phosphorylation at its regulatory serine 19 is elevated in growing and retracting pseudopodia. MLC phosphorylation in the extending pseudopodium was associated with strong and persistent amplification of extracellular-regulated signal kinase (ERK) and MLC kinase activity, which specifically localized to the leading pseudopodium. Interestingly, inhibition of ERK or MLC kinase activity prevented MLC phosphorylation and pseudopodia extension but not retraction. In contrast, inhibition of RhoA activity specifically decreased pseudopodia retraction but not extension. Importantly, inhibition of RhoA activity specifically blocked MLC phosphorylation associated with retracting pseudopodia. Inhibition of either ERK or RhoA signals prevents chemotaxis, indicating that both pathways contribute to the establishment of cell polarity and migration. Together, these findings demonstrate that ERK and RhoA are distinct pathways that control pseudopodia extension and retraction, respectively, through differential modulation of MLC phosphorylation and contractile processes.

3T3 Cells↗
PubMed1993

Migrated fetal astrocytes modulate nerve growth factor expression in host nucleus gracilis of the medulla after grafting in third cervical hindlimb dorsal columns of the spinal cord.

Nerve growth factor (NGF) immunoreactivity in the nucleus gracilis of the medulla was quantitated for 90 days after aspiration of the C3 spinal hindlimb dorsal columns of 36 adult rats. Half the lesioned animals were a lesion-only group. The remaining lesioned animals received an immediate graft of two 1.0-mm pieces of 14 day gestation fetal rat cervical spinal cord (prelabeled with Phaseolus vulgaris leucoagglutinin) into the aspiration pocket (graft group). There were 3 normal controls. Groups of animals were analyzed at 7, 14, 21, 30, 60, and 90 days. At 90 days, NGF immunoreactivity was significantly elevated in the nucleus gracilis of lesion-only animals. This increase in NGF immunoreactivity was augmented in glial end-feet surrounding neurons and was also observed in the cytoplasm of astrocytes and some neurons. Previous experiments have shown that the cluster neurons of the nucleus gracilis undergo atrophy at this time with a concomitant decrease in hindlimb placement. NGF immunoreactivity (90 days) in grafted animals, however, was significantly less than in lesion-only animals (P < 0.05) but remained significantly elevated above control animals (P < 0.05). Unlike in lesion-only animals, there were no NGF positive neurons in the nucleus gracilis of grafted animals. Previous experiments have shown that astrocytes from fetal spinal cord grafts migrate to the nucleus gracilis, maintain cluster neuron cell size, and improve hindlimb placement at 90 days. The present data indicate that modulation of detrimental increases in NGF appeared to be a mechanism by which migrated fetal astrocytes can be used as a system for cell therapy.

Animals↗
PubMed2005

Inhibition of in vitro neutrophil migration through a bilayer of endothelial and epithelial cells using beta2-agonists: concomitant effects on IL-8 and elastase secretion and impact of glucocorticosteroids.

BACKGROUND: Beta2-agonists and glucocorticosteroids are two common treatments for COPD and they are often used in combination. Glucocorticosteroids mediate the anti-inflammatory response through the glucocorticosteroid receptors (GRs). Beta2-agonists are potent bronchodilators but they can have some anti-inflammatory properties by elevating the level of intracellular cAMP. In this study we aimed to investigate the anti-inflammatory effect of combination therapy in vitro. METHODS: Neutrophils or the bilayer of endothelial and epithelial cells were preincubated with salbutamol, budesonide or budesonide followed by salbutamol. FMLP-induced IL-8, elastase release and neutrophil migration through the bilayer was measured. RESULTS: Salbutamol at concentrations of 10(-4), 10(-5) and 10(-9) M inhibited IL-8, elastase release and migration of neutrophils in an inverse bell-shaped concentration-response manner. When given after budesonide (10(-9) and 10(-8)M), the inhibitory effect on migration was additive. This additive effect was not observed for elastase and IL-8 release. CONCLUSIONS: Salbutamol inhibits neutrophil migration and IL-8 and elastase release in a concentration-dependent manner. Preincubation with low concentration of budesonide enhanced the inhibition of migration achieved by low concentrations of salbutamol.

Adrenergic beta-Agonists↗
PubMed1999

Increased production of macrophage migration inhibitory factor by PBMCs of atopic dermatitis.

BACKGROUND: Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disorder. The underlying cause of AD is multifactorial, and several cytokines are considered to be involved in this severe inflammatory skin disease. Macrophage migration inhibitory factor (MIF) is an immunoregulatory cytokine essential for T-cell activation and delayed-type hypersensitivity. Recently we demonstrated that serum MIF content was significantly elevated in patients with AD. Consistent with this, expression of MIF messenger RNA in keratinocytes of the eczematous skin lesion was up-regulated. OBJECTIVE AND METHOD: Although keratinocytes are considered to be a potential source of increased serum MIF content in AD, precise evaluation has not been carried out in other tissues. MIF is ubiquitously expressed in various cells, including T cells and macrophages. In this study we examined MIF production and its messenger RNA level of PBMCs from patients with AD to investigate the contribution of these cells to elevated serum MIF content and to its pathologic characteristics. RESULTS: Consistent with our previous findings, the serum MIF content of patients with AD was significantly elevated compared with nonatopic healthy control subjects and patients with chronic urticaria without eczema. As for the MIF productivity of unstimulated PBMCs, the MIF content in the culture medium of PBMCs obtained from patients with AD (40.4 +/- 8.4 ng/mL) (mean +/- SEM) was significantly increased compared with that from healthy control subjects (6.6 +/- 1.1 ng/mL) and patients with chronic urticaria (8.5 +/- 1.4 ng/ml) (P <.0001). When PBMCs were stimulated by concanavalin A, MIF production by PBMCs of patients with AD was more enhanced than in control subjects or patients with chronic urticaria. The increased ratio of MIF production by PBMCs in response to concanavalin A was significantly correlated with the severity of clinical features of AD. Supporting these results, the level of MIF mRNA in PMBCs of patients with AD was significantly higher than in nonatopic healthy control subjects. CONCLUSIONS: The current results showed that PBMCs should be an important source of increased serum MIF in AD. Because MIF has the potential to induce local and systemic inflammatory and immune responses, it is conceivable that MIF produced by PBMCs may affect local and systemic pathologic features in AD.

Adolescent↗
PubMed1985

Heterogeneity of high-mobility-group protein 2. Enrichment of a rapidly migrating form in testis.

A determination of the absolute amounts of high-mobility-group proteins 1 and 2 (HMG1 and HMG2) in rat tissues demonstrated that amounts of HMG2 were low in non-proliferating tissues, somewhat higher in proliferating and lymphoid tissues, but were extremely elevated in the testis. This increase was due to a germ-cell-specific form of HMG2 with increased mobility relative to somatic HMG2 on acid/urea/polyacrylamide-gel electrophoresis. To determine if the findings in the rat were a general feature of spermatogenesis, testis (germinal), spleen (lymphoid), and liver (non-proliferating) tissues from various vertebrate species were examined for their relative amounts of HMG1 and HMG2, and for HMG2 heterogeneity. Bull, chimpanzee, cynomologus monkey, dog, gopher, guinea pig, hamster, mouse, opossum, rabbit, rat, rhesus monkey, squirrel and toad (Xenopus) tissues were analysed. Nearly all species showed relatively high contents of HMG2 in testis tissue, whereas HMG1 contents were similar in all species and tissues. Ten of thirteen species showed a rapidly migrating HMG2 subtype in testis tissue, separable by acid/urea/polyacrylamide-gel electrophoresis. Xenopus, which lacks HMG2 in somatic tissues, showed an HMG2-like protein in testis tissue. Although the rapidly migrating HMG2 subtype in species other than rat was not testis-specific, it was always enriched in the testis. This study indicates that increased amounts of HMG2 and the enrichment of a rapidly migrating HMG2 subtype are general features of spermatogenic cells.

Animals↗
PubMed2001

Restraint stress-induced elevation of endogenous glucocorticoids decreases Peyer's patch cell numbers via mechanisms that are either dependent or independent on apoptotic cell death.

In this study, we investigated whether restraint stress induces either apoptotic cell death or lymphocyte migration in Peyer's patches. Exposure to stress induced a striking decrease in the number of CD3+CD4+, CD3+CD8+ and B220+ cells. Such decreases were accompanied by the enhanced induction of apoptosis in Peyer's patches. The apoptosis of Peyer's patch cells was completely reversed by pretreatment with either high or low doses of RU-486, a glucocorticoid receptor antagonist. In contrast, the stress-induced lymphopenia was little affected by administration of low doses of RU-486, although such lymphopenia was perfectly inhibited by treatment with high doses of RU-486. Taken together, these results suggest that the stress-induced lymphopenia in Peyer's patches is partly due to apoptotic cell death, although other systems such as lymphocyte migration, may contribute to such a reduction in the number of Peyer's patch cells.

Animals↗
PubMed1999

Elevated serum intercellular adhesion molecule-1 and vascular adhesion molecule-1 among patients with stable angina pectoris who suffer cardiovascular death or non-fatal myocardial infarction.

AIMS: Inflammatory mechanisms have been implicated in the pathogenesis of atherosclerosis. Cell adhesion molecules, expressed on endothelial cells and leukocytes, mediate transendothelial migration of leukocytes into the vessel wall, but also circulate in soluble forms. In the present study we related soluble cell adhesion molecules to the risk of suffering a cardiovascular death or a non-fatal myocardial infarction (cardiovascular death/myocardial infarction) in a substudy to the Angina Prognosis Study in Stockholm (APSIS). METHODS AND RESULTS: Soluble intercellular adhesion molecule-1, vascular adhesion molecule-1 and E-selectin were measured in serum collected on inclusion in the APSIS study. During follow-up, seven patients suffered non-fatal myocardial infarction or cardiovascular death, whereas 86 patients were event-free. Cardiovascular death/myocardial infarction was associated with elevated intercellular adhesion molecule-1 (354+/-142 vs 282+/-62ng x ml-1;P<0.01) and vascular adhesion molecule-1 (538+/-138 vs 433+/-135ng x ml-1;P =0.05), and E-selectin levels tended to be higher (72+/-54 vs 49+/-20ng x ml-1). Clinical risk factors (history of hypertension, previous myocardial infarction, diabetes and smoking) were more abundant in the event group. Subgroup analyses showed that hypertension, smoking or male sex were associated with elevated intercellular adhesion molecule-1, whereas previous myocardial infarction or male sex were associated with elevated vascular adhesion molecule-1. CONCLUSION: Patients with stable angina pectoris who developed cardiovascular death/myocardial infarction had elevated serum levels of soluble cell adhesion molecules, indicating increased inflammatory activity. The value of soluble cell adhesion molecules as prognostic markers in patients with stable ischaemic heart disease merits further study.

Aged↗