Biomedical subjects

L Aloe

Publications and source records attributed to L Aloe.

At least 127 records · Page 7Linked to original sources

PubMed1997

Presence of nerve growth factor in the thymus of prenatal, postnatal and pregnant rats.

The presence of Nerve Growth Factor (NGF) and the expression of low- and high-affinity NGF receptor were investigated in prenatal, postnatal and pregnant rats. Using ELISA and immunohistochemistry it was found that both NGF and its receptors are present in the medulla of the thymus and are more strongly expressed in pre- and early postnatal life and nearly absent in adult and ageing rats. It was also found that during pregnancy, which is characterised by an involution of the cortex and hypertrophy of the medulla, the level of NGF in the thymus increases. The present study showed not only that NGF is produced in a specific compartment of the thymus, the medulla, but that its synthesis declines with age, following thymus involution. These results suggest that NGF may be critically involved in the proliferation and differentiation of thymic cells.

Animals↗

PubMed1996

Circulating nerve growth factor levels are increased in humans with allergic diseases and asthma.

Nerve growth factor (NGF) serum levels were measured in 49 patients with asthma and/or rhinoconjunctivitis and/or urticaria-angioedema. Clinical and biochemical parameters, such as bronchial reactivity, total and specific serum IgE levels, and circulating eosinophil cationic protein levels, were evaluated in relation to NGF values in asthma patients. NGF was significantly increased in the 42 allergic (skin-test- or radioallergosorbent-test-positive) subjects (49.7 +/- 28.8 pg/ml) versus the 18 matched controls (3.8 +/- 1.7 pg/ml; P < 0.001). NGF levels in allergic patients with asthma, rhinoconjunctivitis, and urticaria-angioedema were 132.1 +/- 90.8, 17.6 +/- 6.1, and 7.6 +/- 1.8 pg/ml (P < 0.001, P < 0.002, and P < 0.05 versus controls), respectively. Patients with more than one allergic disease had higher NGF serum values than those with a single disease. When asthma patients were considered as a group, NGF serum values (87.6 +/- 59.8 pg/ml) were still significantly higher than those of control groups (P < 0.001), but allergic asthma patients had elevated NGF serum levels compared with nonallergic asthma patients (132.1 +/- 90.8 versus 4.9 +/- 2.9 pg/ml; P < 0.001). NGF serum levels correlate to total IgE serum values (rho = 0.43; P < 0.02). The highest NGF values were found in patients with severe allergic asthma, a high degree of bronchial hyperreactivity, and high total IgE and eosinophil cationic protein serum levels. This study represents the first observation (that we know of) that NGF is increased in human allergic inflammatory diseases and asthma.

Adolescent↗

PubMed1996

Nerve growth factor is an autocrine survival factor for memory B lymphocytes.

Production of nerve growth factor (NGF) was assessed in cultures of human T and B lymphocytes and macrophages. NGF was constitutively produced by B cells only, which also expressed surface p140trk-A and p75NGFR molecules and hence efficiently bound and internalized the cytokine. Neutralization of endogenous NGF caused disappearance of Bcl-2 protein and apoptotic death of resting lymphocytes bearing surface IgG or IgA, a population comprising memory cells, while surface IgM/IgD "virgin" B lymphocytes were not affected. In vivo administration of neutralizing anti-NGF antibodies caused strong reduction in the titer of specific IgG in mice immunized with tetanus toxoid, nitrophenol, or arsonate and reduced numbers of surface IgG or IgA B lymphocytes. Thus, NGF is an autocrine survival factor for memory B lymphocytes.

Animals↗

PubMed1996

Modification of lymphoid and brain nerve growth factor levels in systemic lupus erythematosus mice.

In the present work we investigated the production of nerve growth factor (NGF) in the brain and peripheral tissues of female NZB/W F1 mice, a well characterized model of murine lupus. Our results indicate that while no significant difference in the NGF content was observed in the sera and tissues of NZB/W mice and its parental strains during the first months of life, the levels of circulating NGF and the NGF content in the kidneys significantly increase in the autoimmune mice during the development of the disease. The NGF-producing brain regions showed a decrease in NGF concentration in 8 month-old NZB/W mice. Moreover, we found a modification of the NGF concentration in the spleens of autoimmune mice at 5 and 8 months. Our data support the hypothesis of a correlation between NGF and the inflammatory state of systemic lupus erythematosus (SLE) and indicate that NGF could have a role in the pathogenesis of this disease.

Aging↗

PubMed1996

Nerve growth factor stimulates production of neuropeptide Y in human lymphocytes.

The production of neuropeptide Y (NPY) in lymphocytes obtained from human tonsils was investigated using radioimmunoassay. While unstimulated lymphocytes did not produce detectable amounts of NPY, NPY synthesis was induced after cell activation. Our results show that the addition of nerve growth factor (NGF) to unstimulated lymphocytes has an effect similar to that of mitogens, both leading to production of NPY. The study of purified B and T cells confirmed that only activated cells are able to synthesize NPY. The stimulatory effect of NGF on NPY production is not a common characteristic of all lymphocytes: only unstimulated T cells respond to NGF by synthesizing NPY. No such effects is seen in purified B cells.

B-Lymphocytes↗

PubMed1996

Intracerebral injection of human immunodeficiency virus type 1 coat protein gp120 differentially affects the expression of nerve growth factor and nitric oxide synthase in the hippocampus of rat.

We have studied the neuropathological characteristics of the brain of rats receiving daily intracerebroventricular administration of freshly dissolved human immunodeficiency virus type 1 recombinant protein gp120 (100 ng per rat per day) given for up to 14 days. Histological examination of serial brain sections revealed no apparent gross damage to the cortex or hippocampus, nor did cell counting yield significant neuronal cell loss. However, the viral protein caused after 7 and 14 days of treatment DNA fragmentation in 10% of brain cortical neurons. Interestingly, reduced neuronal nitric oxide synthase (NOS) expression along with significant increases in nerve growth factor (NGF) were observed in the hippocampus, where gp120 did not cause neuronal damage. No changes in NGF and NOS expression were seen in the cortex, where cell death is likely to be of the apoptotic type. The present data demonstrate that gp120-induced cortical cell death is associated with the lack of increase of NGF in the cerebral cortex and suggest that the latter may be important for the expression of neuropathology in the rat brain. By contrast, enhanced levels of NGF may prevent or delay neuronal death in the hippocampus, where reduced NOS expression may be a reflection of a subcellular insult inflicted by the viral protein.

Animals↗

PubMed1996

Neurobehavioral alterations in developing transgenic mice expressing TNF-alpha in the brain.

During development, neuronal circuitry and memory formation are associated with the synthesis and release of several biological mediators, including cytokines. Among the numerous cytokines, the role of tumor necrosis factor-alpha (TNF-alpha) in neurobehavioral development is largely unknown. Thus, the recently generated transgenic mice expressing murine TNF-alpha in the brain represent a valid animal model for investigating the role of TNF-alpha in neurobehavioral processes. Using these mice, we showed that an overexpression of murine TNF-alpha increases grooming in the novel object investigation test, decreases rearing as a reaction to novel olfactory cues, and produces a retardation of passive avoidance acquisition while enhancing the thermal response in the hot-plate test, a task regulated by both peripheral and central mechanisms. The possibility that these effects are associated with endogenous changes in concentration of the NGF, known to be modulated by TNF-alpha, is discussed.

Animals↗

PubMed1996

Schistosoma mansoni: influence of infection on mouse behavior.

Schistosoma mansoni infection in humans and animals induces abnormal neurobehavioral responses following granuloma formation. In mice, granulomas in the liver are observed 8 weeks after infection, while after 15-20 weeks, the presence of eggs and granulomas in the brain has been reported. In this study, outbred CD-1 female mice were infected with S. mansoni and examined in several behavioral tests (open field, novel object investigation, black/white box, and hot plate) 8 and 15 weeks after infection. The detected effects of schistosome infection were a reduction of body weight in 8-week infected mice, marked changes in exploration/activity, rearing, and wall-rearing in 8- and 15-week infected mice, an enhancement of sniffing and grooming in 8-week infected mice, and finally an increase in the threshold of pain response to the hot plate in 15-week infected mice. The results of the present study indicate that S. mansoni infection markedly alters exploratory behavior of mice, affecting particularly the vertical movements of the animals, and suggests that the differences in behavioral abnormalities between 8- and 15-week infected mice might be associated with modifications in the levels of nerve growth factor and cytokines induced by granulomas.

Analysis of Variance↗

PubMed1996

Nerve growth factor delays retinal degeneration in C3H mice.

BACKGROUND: The aim of the present study was to investigate the biological role of nerve growth factor (NGF) on retinal degeneration in the C3H mouse strain. This strain is characterized by a single gene mutation (rd) which leads to photoreceptor degeneration resembling human retinitis pigmentosa. METHODS: Neural retinas from 1- to 25 day-old C3H mice were dissected from outer ocular tissues, dissociated in cell suspension, stained with a vital dye and counted in a hemocytometer. For in vivo study, NGF was injected into the intraocular or retro-ocular area, and at the end of the treatment the mice were killed. The eyes were enucleated, fixed and cut by cryostat into 14-microns serial sections. The serial sections were stained with hematoxylin-eosin and the outer nuclear layer (ONL) was measured using a computerized image analysis system. RESULTS: An intraocular injection of NGF, or repeated retro-ocular injections, induced a significant increase in ONL thickness compared to controls. CONCLUSION: Our data show that NGF inhibits retinal degeneration in C3H mice. The mechanism(s) underlying the protective action of NGF against retinal cell death remains to be established.

Animals↗

PubMed1996

Histopathological evaluation of retinal damage during intraocular hypertension in rabbit: involvement of ganglion cells and nerve fiber layer.

BACKGROUND: Current clinical tests do not detect glaucomatous signs until the onset of substantial retinal damage. Therefore animal models are required to investigate the very early histopathological alterations in glaucoma disease. We used an experimental model of intraocular hypertension to compare early changes in retinal ganglion cell (RGC) density with the thickness of the nerve fiber layer (NFL). METHODS: Methylcellulose 2% was injected into the anterior chamber of 18 eyes of 18 New Zealand albino rabbits. Intraocular pressure was measured 6 h after the injection and thenceforth once a day using a Shiötz tonometer. Histopathological analysis was performed on days 4, 10, and 15 following the induction of hypertension (six eyes for each group). Sections from the upper temporal retina were stained with hematoxylin-eosin and immunohistochemically using a polyclonal antibody PGP 9.5 to identify RGC. An image analysis system was used to evaluate the RGC and the thickness of the NFL. RESULTS: We observed a significant increase in intraocular pressure until the end of the experiment. Histological analysis showed, after 10 days of ocular hypertension, a significant decrease in RGC density (P < 0.05) and a significant increase (P < 0.05) in glial cell density. We found a significant correlation between RGC loss and cell area at 4 days (P < 0.01; Cc = 0.86) and at 10 days (P < 0.002; Cc = 0.91) of intraocular hypertension. We did not observe a significant decrease in the NFL thickness until 10 days of intraocular hypertension. CONCLUSIONS: Our study confirms the size-dependent RGC loss during intraocular hypertension and shows no early decrease in NFL thickness.

Animals↗

PubMed1996

Chronic parasite infection in mice induces brain granulomas and differentially alters brain nerve growth factor levels and thermal responses in paws.

Schistosoma mansoni infection, both in humans and in animal models, is known to induce granulomas in the liver and intestine. It has also been reported that in humans the eggs of this parasite can reach the brain, causing psychiatric and neuropathological disorders. Whether this also occurs in rodents is unknown. To answer this question, mice were infected with this parasite and the central nervous system (CNS) examined at various time intervals. The results show that schistosomiasis induced granulomas in several regions of the CNS and increased nerve growth factor (NGF) levels in the cortex, hypothalamus and brain stem, but not in the hippocampus. The infection also caused paw hyperalgesia, as determined by the hot-plate test, and a local increase in NGF, but not in substance P. These findings indicate that the murine model of infection can be used for studying mechanisms leading to human neuroschistosomiasis and suggest that the neuropathological disorders and the sensory deficits observed in human schistosomiasis are associated with impaired levels of NGF in the peripheral and central nervous system.

Animals↗

PubMed1996

Evidence of a role for nerve growth factor in the effect of sialoadenectomy on body temperature of parasite-infected mice.

Mice infected with Schistosoma mansoni were used to investigate the role of the submaxillary salivary gland and nerve growth factor (NGF) in temperature response. The results showed that the infection increased (36.5 +/- 0.3 vs 35.7 +/- 0.2), while sialoadenectomy decreased (34.4 +/- 0.2 vs 35.1 +/- 0.2) body temperature. These temperature changes were associated with high or low circulating NGF levels, respectively. It was also found that infection altered the distribution of oxytocin-positive neurones in the hypothalamus and that administration of 20 mu g of purified NGF in normal mice raised (36.1 +/- 0.2 vs 35.1 +/- 0.2) and of NGF antibodies decreased (34.0 +/- 0.2 vs 35.1 +/- 0.2) body temperature. Taken together, these observations suggest that salivary NGF influences the temperature set-point in adult rodents, but the mechanism regulating these events remains to be elucidated.

Animals↗

PubMed1996

Serum NGF levels increase during lactation and following maternal aggression in mice.

In the present study, serum levels of nerve growth factor (NGF) were assessed in virgin and in lactating female CD-1 mice. In the case of the lactating females, NGF levels were assessed both under basal conditions and 60 and 180 min following a 10 min encounter with a male or a nonlactating female mouse. Basal serum NGF levels of lactating females were higher than those of virgin females but did not increase significantly above base after an aggressive encounter with a male or a female conspecific. Female intruders were attacked in a ritualized manner. In contrast, males received numerous bites to vulnerable regions of their body. A positive correlation was found between serum NGF levels and pattern of aggression in females confronting male conspecifics. Thus, in lactating mice, serum NGF levels following an aggressive encounter relate to the specific pattern of behavior the female uses to defend the offspring.

Aggression↗

PubMed1996

NGF regulatory role in stress and coping of rodents and humans.

Nerve growth factor (NGF) is a polypeptide growth factor which exerts trophic and differentiative effects on specific peripheral and central populations of neurons. Recent data showing that various cellular types of the endocrine and immune systems are able to synthesize and release NGF have suggested that this neurotrophic factor may also play an important role in vertebrate physiologic homeostasis. Previous studies using a mouse model of aggressive behavior have shown that NGF levels increase in both plasma and the CNS following intermale agonistic encounters. More recently, we have extended this research area to include other species: in particular, humans. The data now available indicate that labour and lactation, or the occurrence of a stressful event such as the very first jump with a parachute causes in NGF plasma levels as well as changes in the distribution of NGF receptors on lymphocytes. This review aimed to outline the current understanding of NGF role in vertebrates in stress-related events.

Adaptation, Psychological↗

PubMed1996

Haloperidol treatment decreases nerve growth factor levels in the hypothalamus of adult mice.

1. In a first study different doses of haloperidol (0.6, 1.2, 2.5, 5, 10, or 20 mg/kg; intraperitoneally) were administered to adult male mice (CD-1 strain) and tested for their ability to induce catalepsy. 2. The minimal haloperidol dose inducing complete catalepsy was found to be the 10 mg/kg dose and selected for the second experiment. 3. Using an immunoenzymatic assay (ELISA) hypothalamic nerve growth factor (NGF) level was measured 20 or 180 min following haloperidol injection (10 mg/kg). 4. Haloperidol treatment decreased NGF levels in mouse hypothalamus and this effect did not differ at the two time points tested. 5. The role of hypothalamic NGF in stress-related events is discussed.

Animals↗

PubMed1996

mRNA for NGF and p75 in the central nervous system of rats affected by experimental allergic encephalomyelitis.

In this study we measured the concentration of nerve growth factor (NGF) and the expression of NGF and the low affinity NGF-receptor (NGF-r) mRNA in the central nervous system (CNS) of rats affected by experimental allergic encephalomyelitis (EAE) during the acute phase of the disease. Significant levels of NGF protein were found in thalamus and cortex on day 13 post-immunization. Molecular analysis of the NGF gene expression and of its NGF-r revealed that they were enhanced in several regions of the CNS of EAE rats when compared with untreated animals. These results suggest a functional link between local NGF synthesis and this autoimmune inflammatory disease.

Animals↗

PubMed1996

Changes in human plasma nerve growth factor level after chronic alcohol consumption and withdrawal.

Numerous studies reported in recent years have shown that withdrawal from chronic consumption of drugs induces high levels of anxiety, both in humans and in animal models. In the present study, we demonstrated that withdrawal from chronic consumption of either ethanol or heroin causes a significant increase in plasma nerve growth factor, suggesting that the resulting anxiety condition triggers the release of this molecule. Although the functional significance of this phenomenon needs to be better defined, it is hypothesized that the increased levels of circulating nerve growth factor might be involved in homeostatic adaptive and/or reparative mechanisms.

Adult↗

PubMed1996

Increased circulating nerve growth factor is directly correlated with disease activity in juvenile chronic arthritis.

OBJECTIVE: To determine the circulating serum concentrations of nerve growth factor (NGF) and compare them with indices of disease activity in juvenile chronic arthritis. METHODS: NGF concentrations were evaluated with a two site immunoenzymatic assay (ELISA), in 17 children with systemic, 39 with polyarticular, and 24 with pauciarticular onset juvenile chronic arthritis. Each subset was divided according to different variables, appropriate to each subset, reflecting active and inactive disease. RESULTS: NGF concentrations were significantly higher in children with systemic [254 (SD 256.1) pg ml-1; P < 0.001], polyarticular [165.2 (300.8) pg ml-1; P < 0.05], and pauciarticular [106.8 (111.8) pg ml-1; P < 0.005] onset juvenile chronic arthritis than in controls. In all subsets, NGF concentrations were higher in the active than in the inactive phase of the disease. A significant direct correlation between NGF concentrations and erythrocyte sedimentation rate was found both in the systemic and in the polyarticular onset juvenile chronic arthritis. CONCLUSIONS: The increase in NGF concentrations in all juvenile chronic arthritis subsets and the correlation with disease activity suggest that NGF may take an active part in joint inflammation.

Anti-Inflammatory Agents, Non-Steroidal↗