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PubMed2005

Up-regulation and profibrotic role of osteopontin in human idiopathic pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disorder characterized by fibroproliferation and excessive accumulation of extracellular matrix in the lung. METHODS AND FINDINGS: Using oligonucleotide arrays, we identified osteopontin as one of the genes that significantly distinguishes IPF from normal lungs. Osteopontin was localized to alveolar epithelial cells in IPF lungs and was also significantly elevated in bronchoalveolar lavage from IPF patients. To study the fibrosis-relevant effects of osteopontin we stimulated primary human lung fibroblasts and alveolar epithelial cells (A549) with recombinant osteopontin. Osteopontin induced a significant increase of migration and proliferation in both fibroblasts and epithelial cells. Epithelial growth was inhibited by the pentapeptide Gly-Arg-Gly-Asp-Ser (GRGDS) and antibody to CD44, while fibroproliferation was inhibited by GRGDS and antibody to alphavbeta3 integrin. Fibroblast and epithelial cell migration were inhibited by GRGDS, anti-CD44, and anti-alphavbeta3. In fibroblasts, osteopontin up-regulated tissue inhibitor of metalloprotease-1 and type I collagen, and down-regulated matrix metalloprotease-1 (MMP-1) expression, while in A549 cells it caused up-regulation of MMP-7. In human IPF lungs, osteopontin colocalized with MMP-7 in alveolar epithelial cells, and application of weakest link statistical models to microarray data suggested a significant interaction between osteopontin and MMP-7. CONCLUSIONS: Our results provide a potential mechanism by which osteopontin secreted from the alveolar epithelium may exert a profibrotic effect in IPF lungs and highlight osteopontin as a potential target for therapeutic intervention in this incurable disease.

Bronchoalveolar Lavage Fluid↗
PubMed2002

[A case of Paragonimus miyazakii with migrating infiltrates: use of ELISA in diagnosis and treatment].

A 47-year-old man was referred to our clinic with abnormal chest radiographs. He was free of symptoms, but his chest CT demonstrated transient migrating infiltrates. Peripheral blood revealed eosinophilia and eosinophilic pneumonia was suspected. However, the bronchoalveolar lavage fluid showed no increase in eosinophils. Later, the patient's pleural effusion did contain eosinophils. His total IgE level was continuously elevated despite the absence of allergic disease, and so parasitic infection was suspected. Ouchterlony's double diffusion test after absorption of Paragonimus westermanii antigen was positive for Paragonimus miyazakii antigen. The ELISA values of both serum sample and pleural effusion were increased. As the ELISA value of the pleural effusion was higher than the serum one, we realised that pleural effusion was caused by Paragonimus miyazakii. Treatment with praziquantel for 3 days resulted in disappearance of the abnormal chest radiographic findings, and a reduced blood eosinophil level, IgE level and ELISA titre for Paragonimus miyazakii. We concluded that ELISA was useful in the diagnosis and assessment for treatment in Paragonimus miyazakii infections although there was no clearly relevant history.

Animals↗
PubMed1976

Cellular immune reactions against common antigen, small intestine, and colon antigen in patients with Crohn's disease, ulcerative colitis, and cirrhosis of the liver.

Patients with ulcerative colitis showed in 71-93%, patients with cirrhosis of the liver in 64-91%, cellular immunity against Common Antigen (CA) and human fetal intestinal antigens as measured by the leucocyte migration test (LMIT). Patients with Crohn's disease exhibited cellular immune reactions to a lesser degree - from these only patients without immunosuppressive therapy differed significantly from normal controls (p less than 0.05). Approximately 30% of patients with Crohn's disease and ulcerative colitis had elevated antibody titers against intestinal antigens and CA. A high percentage of patients in both diseases showed a reciprocal relationship between cellular and humoral immunity. It was concluded that Crohn's disease and ulcerative colitis can be separated in most cases using intestinal antigens and CA in the LMIT. The occurrence of cellular immunity against these antigens cannot be interpreted as being the only pathogenetic principle in these two diseases. It is also concluded that there appears to be only a weak immune tolerance against intestinal antigens. The high percentage of cellular immune reactions in patients with cirrhosis of the liver demonstrates that this group may have an impairment of the physiological elimination of antigens by the liver.

Antibodies↗
PubMed1992

Effects of Azadirachta indica A Juss on some biochemical, immunological and visceral parameters in normal and stressed rats.

Effects of A. indica (AI) were evaluated on some biochemical, immunological and visceral parameters in normal and stress rats. AI (100 mg/kg) lowered blood glucose, triglyceride and SGOT levels in normal rats, and attenuated stress-induced elevations of cholesterol and urea levels. In rats immunized with SRBC, AI enhanced the humoral antibody response to the antigen. Further, AI facilitated the footpad thickness response to SRBC in sensitized mice and also enhanced leucocyte migration in immunized rats. In stressed rats, AI significantly attenuated the stress-induced (a) suppression of humoral immune response and (b) gastric ulcerogenesis. These results are discussed in light of the possible mechanisms involved in the effects of AI in normal and stressful situations.

Alanine Transaminase↗
PubMed1991

Cytokine-activated human endothelial monolayers support enhanced neutrophil transmigration via a mechanism involving both endothelial-leukocyte adhesion molecule-1 and intercellular adhesion molecule-1.

rIL-1 beta treatment of cultured human endothelial cells (HEC) promotes polymorphonuclear leukocyte (PMN) adhesion and transmigration. Using in vitro quantitative monolayer adhesion and videomicroscopic transmigration assays, we have examined the contributions of endothelial-leukocyte adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and the leukocyte adhesion complex, CD11/CD18, to these processes. Maximal enhancement of PMN adhesion and transmigration were observed after 4 h of rIL-1 beta treatment, when surface expression of ELAM-1 had peaked and ICAM-1 was modestly increased. Blocking mAb directed to either ELAM-1 or ICAM-1 inhibited greater than 90% of the up-regulated PMN transmigration. Blocking mAb directed to either CD11a/CD18 (LFA-1, a ICAM-1 counter-receptor), CD11b/CD18 (Mo-1), or CD18 (common beta 2-integrin) also blocked greater than 90% of PMN transmigration. At later time points (24 or 48 h), ELAM-1 surface expression was markedly decreased, whereas ICAM-1 expression was increased over the 4-h level; PMN adhesion remained elevated (approximately 50 to 60% of 4 h level), but transmigration returned to levels seen with unactivated HEC. These data indicate that PMN interaction with at least two distinct HEC adhesion molecules is necessary for transendothelial migration and suggests that PMN adhesion and transmigration, although interrelated, are mechanistically distinct processes.

Antigens, CD↗
PubMed1986

Acute pancreatitis: a complication of Foley catheter gastrostomy.

Acute pancreatitis can be caused by inadvertent migration into the duodenum of the inflated balloon of a Foley gastrostomy catheter. The clinical picture is that of an acute abdomen. The diagnosis is made with a high index of suspicion and confirmed by marked elevation of serum and urine amylase levels. The treatment consists of repositioning of the gastrostomy tube and supportive therapy. Careful external fixation of the tube to the abdominal wall can prevent this complication.

Acute Disease↗
PubMed1985

Glycosphingolipids in murine lymphocytes from thymus and spontaneous and X-ray induced thymomas.

Lymphocytes from spontaneous thymoma in AKR mice and from X-ray induced thymoma in C57B1/6 mice showed elevated levels (by 50% and 100%, respectively) of lipid-bound sialic acid as compared with lymphocytes from normal thymuses used as controls. Some ganglioside fractions in thymomas were elevated 4-6-fold over those in normal thymuses while other fractions decreased or disappeared. Neutral glycosphingolipid (NGSL) content in lymphocytes from thymomas was also changed. Thin-layer chromatography of NGSLs showed that the fractions migrating as ceramide monohexoside (CMH), dihexoside (CDH) and below globoside standards were increased, respectively, 2-3-fold, 3-6-fold and 2-fold in both types of thymomas. Methylation and gas-liquid chromatography analysis confirmed the presence of CMH, CDH and globoside in NGSLs isolated from X-ray induced thymoma.

Animals↗
PubMed1995

Cholinergic regulation of [Ca2+]i during cell division and differentiation in the mammalian retina.

Transmitter-like molecules are thought to influence many aspects of neuronal development, often by regulating the levels of intracellular calcium. Using the Ca2+ sensitive dye, fura-2, this study demonstrates that in the rabbit retina, ACh analogs stimulate a rise in cytosolic free Ca2+ concentration ([Ca2+]i) in many cell types, and in cells at various stages of differentiation during embryonic and neonatal development. The elevation in [Ca2+]i in cells within the ventricular zone (VZ) resulted primarily from the activation of muscarinic receptors. By contrast, the cholinergic regulation of [Ca2+]i of ganglion cells and amacrine cells, cell types which migrate to their final destinations early in fetal life, was largely mediated by nicotinic receptors. The muscarinic response of the VZ cells was mediated by the M1, rather than the M2-type of muscarinic receptor. This response was abolished in the absence of extracellular Ca2+ and in the presence of NiCl2, but it was not affected by verapamil or omega-conotoxin, thus suggesting that while Ca2+ influx occurred, it did not involve L- and N-type voltage-gated Ca2+ channels. The muscarinic response in the VZ disappeared at the end of the period of cell division in the retina, just prior to eye opening. By contrast, nicotinic-induced changes in [Ca2+]i in ganglion cells and amacrine cells persisted throughout development. Since previous studies have implicated that the precursors of ganglion cells and amacrine cells also possess muscarinic receptors (Yamashita and Fukuda, 1993), the concomitant emergence of different functional cholinergic receptor (AChR) subtypes with differentiation in vivo suggests that ACh may play diverse and temporally regulated roles in the developing retina.

Aging↗
PubMed1993

[Immune reactivity in pneumoconiosis and coniotuberculosis in machine builders].

Immune status was examined in 231 patients facing pneumoconiosis and coniotuberculosis so as to observe a dependence on pneumoconiosis type (silicosis, electric welder's pneumoconiosis), severity of the process, activity of tuberculosis. Markedly changed T and B immunity, having already appeared at initial stage of the disease, were revealed. Those changes due to the tuberculosis activity were characterized by lymphocytosis, marked functional immaturity of T lymphocytes, depressed B lymphocytes count, elevated serum Ig level.

Adult↗
PubMed1996

Serum amyloid A binds specific extracellular matrix glycoproteins and induces the adhesion of resting CD4+ T cells.

Serum amyloid A (SAA), a prototypic acute phase protein reactant, exists naturally in the serum of healthy individuals. However, the levels of SAA in serum and its presence in sites of inflammation increase during certain chronic diseases associated with a local elevation of cytokine concentrations. Although the chemical structure of SAA is defined, its putative immunologic role(s) is still obscure. Nevertheless, it has been shown that 1) SAA acts as a chemoattractant and regulator of the migration of monocytes, polymorphonuclear cells, and T lymphocytes through endothelial cell monolayers; and 2) SAA and its proteolytically degraded N-terminal amyloid A fragment contain an extracellular matrix (ECM)-related cell adhesion epitopes. Herein, we examined whether SAA can associate with specific ECM moieties, and whether immobilized SAA-ECM complexes affect T lymphocyte adhesion. Radiolabeled human rSAA ([125I]rSAA) interacted avidly (Kd = 10(-9) M) and transiently with intact ECM, laminin, and vitronectin, but not with fibronectin or collagen type II. The binding of [125I]rSAA to ECM and laminin was inhibited by unlabeled rSAA and by the AA fragment, but not by the C-terminal portion of SAA (amino acid residues 2-82 and 77-104, respectively). Upon interactions with SAA or amyloid A, immobilized ECM, laminin, and vitronectin induced the adhesion of resting human CD4+ T cells in an apparently beta 1-integrin-mediated manner. Thus, the ECM appears to serve as a temporary anchorage site for SAA and amyloid A, and these ECM-complexed molecules seem to be involved in regulating the recruitment and accumulation of immunocytes in extravascular inflammatory compartments.

Amino Acid Sequence↗
PubMed1990

Human C-reactive protein inhibits neutrophil chemotaxis in vitro: possible implications for the adult respiratory distress syndrome.

C-reactive protein (CRP) is an acute-phase protein whose serum concentration can rise dramatically after onset of inflammation. Although the precise physiologic role of elevated CRP is not known, in vitro studies have shown that CRP potentially has both pro- and anti-inflammatory properties. We hypothesized that an elevation in serum CRP may be a mechanism to control acute inflammation by down-regulating some neutrophil functions. Therefore, elevated serum CRP levels in an inflammatory state in the lung, such as the adult respiratory distress syndrome (ARDS), may have a protective effect. We observed that highly purified CRP, at levels greater than 25 micrograms/ml, inhibited both random neutrophil movement and C5a-induced chemotaxis. Neutrophils incubated with CRP showed a dose-dependent diminution of migration toward chemotactic stimuli, with complete inhibition occurring at 100 micrograms/ml. This inhibitory effect of CRP on neutrophil movement was only partially reversed by washing the CRP-treated cells before assaying their chemotactic movement to 1 nmol/L C5a. Next we examined the neutrophil chemotactic activity of serum collected from normal nonsmokers, from patients at high risk for developing ARDS, and patients with ARDS. Both high-risk and ARDS serums has significantly less (p less than 0.001) neutrophil chemotactic activity than serums from normal subjects. In addition, serums from high-risk and ARDS patients had significantly elevated (p less than 0.001) levels of CRP compared with normal subjects. Anti-CRP treatment of ARDS and high-risk serum samples resulted in a significant increase (p less than 0.05) in the neutrophil chemotactic activity. Finally, addition of highly purified CRP to normal serum significantly reduces its neutrophil chemotactic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2004

Macrophage migration inhibitory factor: an intracellular inhibitor of angiotensin II-induced increases in neuronal activity.

Angiotensin II (Ang II) elicits Ang II type 1 receptor (AT1-R)-mediated increases in neuronal firing within the hypothalamus and brainstem that are ultimately responsible for physiological actions such as increased blood pressure and fluid intake. Although there is a growing literature on the intracellular mechanisms that mediate the actions of Ang II via AT1-R in neurons, little is known about the mechanisms that diminish or "switch-off" the neuronal chronotropic action of Ang II. In the present study, we identified macrophage migration inhibitory factor (MIF) as an intracellular inhibitor of the actions of Ang II in neurons. The evidence is as follows. First, Ang II, acting via AT1-R, increases the intracellular levels of MIF in neurons cultured from rat hypothalamus and brainstem. Second, elevation of intracellular MIF by Ang II prevents further chronotropic actions of this peptide. Third, intracellular application of exogenous recombinant MIF abolishes the Ang II-induced chronotropic action in neurons. Finally, intracellular application of the MIF peptide fragment MIF-(50-65), which harbors the thiol oxidoreductase property of the MIF molecule, mimics the inhibitory actions of MIF on Ang II-stimulated neuronal firing. Thus, this study is the first to demonstrate the existence of an intracellular negative regulator of Ang II-induced actions in neurons and indicates that MIF may act as a physiological brake for the chronotropic effects of Ang II in rat neurons.

Action Potentials↗
PubMed2005

Ca2+ regulation in the absence of the iplA gene product in Dictyostelium discoideum.

BACKGROUND: Stimulation of Dictyostelium discoideum with cAMP evokes an elevation of the cytosolic free Ca2+ concentration ([Ca2+]i). The [Ca2+]i-change is composed of liberation of stored Ca2+ and extracellular Ca2+-entry. The significance of the [Ca2+]i-transient for chemotaxis is under debate. Abolition of chemotactic orientation and migration by Ca2+-buffers in the cytosol indicates that a [Ca2+]i-increase is required for chemotaxis. Yet, the iplA- mutant disrupted in a gene bearing similarity to IP3-receptors of higher eukaryotes aggregates despite the absence of a cAMP-induced [Ca2+]i-transient which favours the view that [Ca2+]i-changes are insignificant for chemotaxis. RESULTS: We investigated Ca2+-fluxes and the effect of their disturbance on chemotaxis and development of iplA- cells. Differentiation was altered as compared to wild type amoebae and sensitive towards manipulation of the level of stored Ca2+. Chemotaxis was impaired when [Ca2+]i-transients were suppressed by the presence of a Ca2+-chelator in the cytosol of the cells. Analysis of ion fluxes revealed that capacitative Ca2+-entry was fully operative in the mutant. In suspensions of intact and permeabilized cells cAMP elicited extracellular Ca2+-influx and liberation of stored Ca2+, respectively, yet to a lesser extent than in wild type. In suspensions of partially purified storage vesicles ATP-induced Ca2+-uptake and Ca2+-release activated by fatty acids or Ca2+-ATPase inhibitors were similar to wild type. Mn2+-quenching of fura2 fluorescence allows to study Ca2+-influx indirectly and revealed that the responsiveness of mutant cells was shifted to higher concentrations: roughly 100 times more Mn2+ was necessary to observe agonist-induced Mn2+-influx. cAMP evoked a [Ca2+]i-elevation when stores were strongly loaded with Ca2+, again with a similar shift in sensitivity in the mutant. In addition, basal [Ca2+]i was significantly lower in iplA- than in wild type amoebae. CONCLUSION: These results support the view that [Ca2+]i-transients are essential for chemotaxis and differentiation. Moreover, capacitative and agonist-activated ion fluxes are regulated by separate pathways that are mediated either by two types of channels in the plasma membrane or by distinct mechanisms coupling Ca2+-release from stores to Ca2+-entry in Dictyostelium. The iplA- strain retains the capacitative Ca2+-entry pathway and an impaired agonist-activated pathway that operates with reduced efficiency or at higher ionic pressure.

Animals↗
PubMed1991

Spurious elevation of serum high-density lipoprotein cholesterol in patients with cholestatic liver diseases.

Strikingly discrepant values were obtained by two commercial precipitating reagents for serum HDL cholesterol determination in three patients with cholestatic liver diseases (two patients with primary biliary cirrhosis and one patient with chronic hepatitis). An abnormal alpha 2-migrating lipoprotein (slow alpha-lipoprotein) was observed in agarose gel electrophoresis for each serum. The slow alpha-lipoprotein was partly recovered in the supernatant by precipitation with polyethylene glycol, and was completely precipitated with a polyanion-containing reagent, which well explains the discrepancy. The slow alpha-lipoprotein isolated from one of the cases is notable for (1) having an intermediate particle size between normal LDL and normal HDL, (2) containing apo E as the major apolipoprotein, and (3) being enriched with cholesterol (esterified and free) and phospholipid. Cholesterol accumulation was also found in another HDL subclass, alpha 1-migrating HDL. A severe impediment in the clearance of cholesterol-loaded HDL particles from plasma was implied. Electrophoresis of serum lipoproteins and/or the measurement of serum apo E concentrations are necessary to avoid an erroneous estimation of HDL cholesterol in patients with hepatobiliary diseases.

Adult↗
PubMed1988

Stage migration and the increasing proportion of complete responders in patients with advanced germ cell tumors.

The proportion of patients with metastatic germ cell tumors achieving complete remission increased, and the total survival improved between 1975 and 1982. Several analyses were undertaken to evaluate the influence of stage migration on treatment outcome in patients with germ cell tumors. (a) A logistic regression analysis showed that a formulation of time was an independent statistically significant variable (P = 0.025) in addition to the total number of sites of metastasis (P less than 0.001) and pretreatment values of human chorionic gonadotropin (P less than 0.001) and lactate dehydrogenase (P = 0.002). (b) The proportion of patients with lung metastases and elevated levels of human chorionic gonadotropin and alpha-fetoprotein decreased, and the number of patients with retroperitoneal metastases and without prior radiation therapy increased significantly. (c) The number of patients with a high likelihood of complete response increased significantly over time (P less than 0.001). Computerized tomography of the abdomen permits detection of large but asymptomatic retroperitoneal disease, and such patients are now being treated with chemotherapy rather than surgery and are included in advanced disease treatment results. Stage migration has played a role in the increasing proportion of complete responders in clinical trials of patients with germ cell tumors.

Humans↗
PubMedDate not supplied

A role for the endocrine and pro-inflammatory mediator MIF in the control of insulin secretion during stress.

The systemic response to injury or infection is often accompanied by significant alterations in host metabolism and glucose homeostasis. Within the liver, these changes include a decrease in glycogenesis and an increase in gluconeogenesis, and in peripheral tissues, the development of insulin resistance and the increased utilization of glucose by non-insulin-dependent pathways. Depending on the severity and the duration of the response, both hyper- and hypoglycemia can ensue and each can become a clinically important manifestation of the systemic inflammatory response. The protein known as macrophage migration inhibitory factor (MIF) has been identified recently to play a central role in host immunity and to regulate glucocorticoid effects on the immune and inflammatory systems. MIF is released in vivo from activated immune cells as well as by the anterior pituitary gland upon stimulation of the hypothalamic-pituitary-adrenal axis. MIF also has been found to be secreted together with insulin from the pancreatic beta-cells and to act as an autocrine factor to stimulate insulin release. Since circulating MIF levels are elevated during stress or systemic inflammatory processes, this protein may play a central role in the control of insulin secretion during various disease states.

Humans↗
PubMed2005

Neuronal migration is transiently delayed by prenatal exposure to intermittent hypoxia.

BACKGROUND: Neonatal neurodevelopment is influenced by a variety of external factors, although the mechanisms responsible are poorly understood. Prenatal hypoxia, from physiological or chemical sources, can have no discernible effect, or can result in a broad spectrum of abnormalities. METHODS: To mimic some of the maternal effects of smoking, we developed a model that investigates the effects of intermittent hypoxia (IH), with or without concurrent nicotine in timed pregnant Sprague-Dawley rats. RESULTS: We found no significant differences between litter sizes or birthweight of pups from any treatment group, but animals exposed to IH (with or without nicotine) showed long term diminished body weights. Animals subjected to IH consistently showed a transient delay in neuronal migration early in the postpartum period, which was amplified by concurrent nicotine administration. We observed increased c-Abl protein levels in animals from the IH treatment groups. Multiple proteins involved in the intricate control of neuronal migration were also altered in response to this treatment, primarily the downstream targets of c-Abl: Cdk5, p25, and the cytoskeletal elements neurofilament H and F-actin and catalase. Catalase activity and protein levels, already elevated in response to IH, were further amplified by simultaneous nicotine exposure. CONCLUSIONS: This new model provides a novel system for investigating the effects of low grade IH in the developing brain and suggests that concurrent nicotine further aggravates many of the deleterious effects of IH.

Actins↗
PubMed1993

Bergmann glia require continuous association with Purkinje cells for normal phenotype expression.

Bergmann glia (Bg) respond to the early postnatal Purkinje cell (Pc) death in Lurcher (Lc) mutant mouse cerebellum by down-regulating expression of the enzyme glycerol-3-phosphate dehydrogenase (GPDH). To determine whether glial GPDH expression requires the continued presence of Pcs in adults, we used single intracerebellar injections of kainic acid to kill Pcs in wild-type mice from 7 weeks to 11 months old. Bg at all ages tested responded to Pc loss by down-regulating GPDH expression. To learn whether a high level of GPDH could be reinduced following down-regulation in Lc Bg, we grafted wild-type fetal Pcs into Lc cerebella. The influence of grafted Pcs on GPDH expression is host-age and implant-position dependent. Only Pcs implanted into hosts less than 6 weeks old were later found to be associated with GPDH-positive Bg. Grafted Pcs that migrated into the anterior folia of young hosts were more likely to be associated with GPDH-positive Bg than Pcs migrating to other positions. EM analysis showed that Bg ensheathment of grafted Pcs is thinner and more discontinuous, but qualitatively similar to normal. The results suggest that the interaction between host Bg and grafted Pcs can sustain elevated GPDH expression in Bg that have not yet down-regulated, but is not adequate to reinduce expression in those cells that have.

Age Factors↗