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Effects of antipsychotic drugs on cytokine networks.

It has been known since the 1950s that phenothiazines have immunomodulatory effects. This review summarizes recent evidence suggesting that antipsychotic drugs, in particular chlorpromazine and the atypical compound clozapine, influence the production of cytokines. Cytokines, organized in networks of related peptides with pleiotropic functions, are pivotal humoral mediators of infection and inflammation, and they play an important role in hematopoiesis and autoimmunity. Therefore, the effects of antipsychotic drugs on cytokine networks are important for the understanding of immune-mediated side effects of these drugs, e.g. agranulocytosis. In addition, modulation of cytokine production by antipsychotic agents suggests that these drugs might be useful for the treatment of diseases which primarily involve the immune system. Moreover, because cytokines are known to have numerous effects on the CNS, they may mediate effects of antipsychotic drugs on brain functions. Finally, the influence of antipsychotic drugs on cytokine networks is an important confounding factor in studies investigating disease-related immunopathology in psychiatric disorders. This review provides a synopsis of the data published on these topics and outlines future research perspectives.

Antipsychotic Agents↗
PubMed1999

State and trait anxiety in women affected by allergic and vasomotor rhinitis.

It is still debatable whether anxiety and depression in patients affected by rhinitis could play a role in the genesis of the disease, whether they are a consequence of the symptoms. The aim of this study was to evaluate anxiety levels in both state and trait forms, and depression, in patients affected by allergic (AR) and vasomotor rhinitis (VMR). A total of 45 women, 24 AR and 21 VMR were compared with 64 healthy nonallergic women matched for age and sociodemographic characteristics. All subjects were administered the State and Trait Anxiety Inventory (STAI) and the Zung self-rating depression scale. The percentage of subjects with high levels of state anxiety was significantly higher in AR (p<0.005) and VMR (p<0.01) with respect to controls. The percentage of subjects with high levels of trait anxiety was significantly higher in AR (p<0.001) and VMR (p<0.05) than controls. There was no significant difference in depression between AR and VMR and controls. No significant difference was found in state anxiety, trait anxiety, or depression between AR and VMR. In conclusion, anxiety in patients with rhinitis is present both as a state and as a trait, at least when measured with the STAI.

Adolescent↗
PubMed2003

Endocrine and lymphoproliferative response changes produced by social stress in mice.

Daily dyadic resident-intruder encounters and uninterrupted cohabitation in pairs were used to assess the impact of different durations (5 and 15 days) of dominance and subordination experiences on splenic lymphoproliferative responses in male OF1 strain mice. HPA axis activity was assessed by measuring serum corticosterone levels, whereas splenic norepinephrine (NE) content provided a sympathetic activity index. Corticosterone levels in subordinate subjects were generally higher than in their control or dominant counterparts in both treatment paradigms. Corticosterone levels in dominant subjects were lower than in their control counterparts in both. Increasing the duration of treatments generally decreased such titers, especially so in subordinate subjects. No differences were detected in splenic NE content. Animals subjected to social interaction generally showed greater proliferation than their control counterparts. This effect was more pronounced in subordinates than dominants and after longer- rather than short-duration treatments. There was no inverse relation between proliferative responses and the subject's corticosterone levels. While corticosterone may have a general immunomodulating effect, other mediators apparently account for the effects produced by these social stress paradigms on splenic proliferative response.

Agonistic Behavior↗
PubMed2002

Modulation of neuroendocrine--immune signaling by L-deprenyl and L-desmethyldeprenyl in aging and mammary cancer.

The aging process is characterized by a decline in cellular functions of diverse systems of the body, including the neuroendocrine-immune network. One neuroendocrinological theory of aging is based on findings that the loss of hypothalamic neurotransmitter functions and an imbalance in hormonal secretion contribute to the cessation of reproductive cycles and the development of mammary and pituitary tumors. One potential cause of immunosenescence is an age-related decline in the regulatory functions of sympathetic noradrenergic nerve fibers whose neurotransmitters signal lymphoid cells in the bone marrow, thymus, spleen, and lymph nodes. In addition to impairment caused by the generation of free radicals during numerous biochemical processes, there is a shift in the pro-oxidant/anti-oxidant balance resulting in cellular oxidative stress and hastening the aging process. Altered interactions between the neuroendocrine system and the immune system are associated with increased incidence, development, and growth of breast cancer and other neoplastic diseases. We have demonstrated that the disruption in the neuroendocrine-immune interactions in old rats, and in female rats with mammary tumors, can be reversed by deprenyl, a monoamine oxidase inhibitor. Deprenyl treatment leads to enhanced central and peripheral catecholaminergic activity and a readjustment of immunological responses. In this brief review, the nature and changes in the bi-directional communication between the neuroendocrine system and immune system and the possible mechanism(s) of actions of deprenyl in restoring these interactions during aging and mammary cancer are discussed.

Aging↗
PubMed2003

Interrelationships among brain, endocrine and immune response in ageing and successful ageing: role of metallothionein III isoform.

Metallothionein-III (MT-III) a brain-specific member of metallothionein family contributes to zinc neuronal homeostasis, and zinc is an important regulator of many brain functions, including the activity of hormone realising factors by hippocampus. Among them, somatostatin is pivotal because affecting thyroid hormones turnover and consequently thymic and peripheral immune efficiency (Natural Killer, NK) cell activity. Somatostatin is in turn affected by somatomedin-C, which is also zinc-dependent. Therefore, somatomedin-C may be a marker of somatostatin status in the hippocampus. MTs sequester and release zinc in transient stress, as it may occur in young age, to protect cells by reactive oxygen species. In order to accomplish this task, MTs are induced by IL-6 for a prompt immune and anti-inflammatory response. During ageing, MTs are high with a role of sequester of zinc, but with very limited role in zinc release because stress-like condition and inflammation is persistent. Therefore, high MTs may become to protective in young age to harmful during ageing leading to low zinc ion bioavailability for many body homeostatic mechanisms, including brain function. As a consequence, an altered physiological cascade from the brain (upstream) to endocrine and immune system (downstream) may occur. The aim of this work is to study the role of MT-III in the interrelationships among brain-endocrine-immune response in ageing and successful ageing. The main results are: (1) MT-III and IL-6 gene expressions increase in the hippocampus from old mice, in comparison with young and very old mice. (2) Somatomedin-C plasma levels decrease in old mice in comparison with young and very old mice. (3) Low zinc ion bioavailability (tested by the ratio total thymulin/active thymulin) is coupled with altered thyroid hormone turnover and depressed IL-2 in old mice in comparison with young and very old mice. (4) 'In vitro' experiments display more increments on NK cells activity by adding zinc-bound active thymulin than T3 alone. In conclusion, low MT-III in the hippocampus from young and very old mice leads to good zinc ion bioavailability that it is upstream coupled with normal hippocampal function affecting downstream normal thyroid hormones turnover and satisfactory NK cell activity, via complete saturation of zinc-bound active thymulin molecules. Therefore, a correct MTs homeostasis is pivotal for brain-endocrine-immune response in order to reach successful ageing.

Aging↗
PubMed2003

Prions and the immune system: a journey through gut, spleen, and nerves.

For more than two decades it has been contended that prion infection does not elicit immune responses: transmissible spongiform encephalopathies do not go along with conspicuous inflammatory infiltrates, and antibodies to the prion protein are typically undetectable. Why is it, then, that prions accumulate in lymphoid organs, and that various states of immune deficiency prevent peripheral prion infection? This review revisits the current evidence of the involvement of the immune system in prion diseases, while attempting to trace the elaborate mechanisms by which peripherally administered prions invade the brain and ultimately cause damage. The investigation of these questions leads to unexpected detours, including the neurophysiology of lymphoid organs, and even the function of a prion protein homolog in male fertility.

Animals↗
PubMed2003

Roles of the semaphorin family in immune regulation.

The immune system and the nervous system have distinct roles in maintaining physiological homeostasis. These independent systems, however, influence each other while sharing common resources, including the cytokines and members of the immunoglobulin superfamily. Semaphorins are one of these shared molecular families that are biologically active in both systems. Although semaphorins were originally identified as axon guidance factors functioning in the nervous system, recent studies have uncovered additional immunological functions. For example, ligand-receptor systems distinct from those characterized in the nervous system govern class IV semaphorin, CD100/Sema4D and Sema4A activity in immune responses. This review provides an overview of the currently emerging immunoregulatory functions of "Immuno-semaphorins."

Animals↗
PubMed1990

Neuroimmunology.

Explore the source record for details and available documents.

Animals↗
PubMed2004

S100B in schizophrenic psychosis.

Recent findings have strengthened the hypothesis that a dysfunction of neuronal synapses and dendrites is relevant for the pathogenesis of schizophrenia. It might be present during neurodevelopment as well as in degenerative and regenerative processes of the mature brain. S1OOB, a small, Ca2+-binding, astrocytic protein, plays an important role in modulating the proliferation and differentiation of neurons and glia cells. It is involved in the regulation of cellular energy metabolism and interacts with many immunological functions of the brain. This review addresses findings from cell cultural and animal experiments potentially pertinent for the pathogenesis of schizophrenic psychoses. Morphological and functional data are analyzed and clinical studies reporting alterations of S1OOB concentrations in schizophrenic patients are reviewed. Evidence and limitations of the available studies are pointed out and promising future research strategies are outlined.

Animals↗
PubMed2004

Expression of nerve growth factor in the airways and its possible role in asthma.

Nerve growth factor (NGF), in addition to its essential role in neuronal growth and survival, may also act as an inflammatory mediator. As several animal studies have shown, NGF appears to play a part in the development of airway hyperresponsiveness and in the increased sympathetic and sensory innervation of the lung. It also has a profound effect on airway inflammation and asthma-related symptoms. Sources of NGF in the airways are numerous: inflammatory cells infiltrated into the bronchial mucosa, and structural cells including lung fibroblasts, airway epithelial and smooth muscle cells. These cells, by releasing more NGF in inflammatory conditions, may contribute to the increased NGF levels observed in bronchoalveolar lavage fluid and serum from patients with asthma. Taken together, these results suggest that NGF is an important mediator in both inflammation and asthma.

Animals↗
PubMed2004

Neurotrophins and neurotrophin receptors in allergic asthma.

The neurotrophins nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 (NT-3) and NT-4 play a pivotal role in the development of the nervous system. Despite their well-known effects on neurons, elevated neurotrophin concentrations have been observed under pathological conditions in sera of patients with inflammatory disorders. Patients with asthma feature both airway inflammation and an abnormal airway reactivity to many unspecific stimuli, referred to as airway hyperresponsiveness, which is, at least partly, neuronally controlled. Interestingly, these patients show increased levels of neurotrophins in the blood as well as locally in the lung. It has been demonstrated that neurotrophin release from immune cells is triggered by allergen contact. The presence of neurotrophins and the neurotrophin receptors p75 (p75NTR), tyrosine kinase A (TrkA), TrkB and TrkC have been described in several immune cells. There is strong evidence for an involvement of neurotrophins in regulation of hematopoiesis and, in addition, in modulation of immune cell function in mature cells circulating in blood or resting in lymphatic organs and peripheral tissues. The aim of this review is to demonstrate possible roles of neurotrophins during an allergic reaction in consideration of the temporospatial compartimentalization.

Airway Obstruction↗
PubMed2004

Role of nerve growth factor and other trophic factors in brain inflammation.

Inflammation in the brain is a double-edged process that may be beneficial in promoting homeostasis and repair, but can also result in tissue injury through the damaging potential of inflammatory mediators. Thus, control mechanisms that minimize the extent of the inflammatory reaction are necessary in order to help preserve brain architecture and restore function. The expression of neurotrophic factors such as nerve growth factor (NGF) is increased after brain injury, in part mediated by effects on astrocytes of pro-inflammatory mediators and cytokines produced by immune cells. Conversely, cells of the immune system express NGF receptors, and NGF signaling modulates immune function. Multiple sclerosis (MS) and the disease model experimental autoimmune encephalomyelitis are neurodegenerative disorders whereby chronic destruction of the brain parenchyma results from an autoaggressive, immune-mediated inflammatory process and insufficient tissue regeneration. Here, we review evidence indicating that the increased production of NGF and other trophic factors in central nervous system (CNS) during these diseases can suppress inflammation by switching the immune response to an anti-inflammatory, suppressive mode in a brain-specific environment. Thus, trophic factors networks in the adult CNS not only protects axons and myelin but appear to also actively contribute to the maintenance of the brain immune privilege. These agents may represent good targets for therapeutic intervention in MS and other chronic CNS inflammatory diseases.

Animals↗
PubMed2004

Remyelination in multiple sclerosis: a new role for neurotrophins?

Multiple sclerosis (MS) is a common neurological disease, which affects young adults. Its course is unpredictable and runs over decades. It is considered as an autoimmune disease, and is neuropathologically characterized by demyelination, variable loss of oligodendroglial cells, and axonal degeneration. Demyelination provides a permitting condition for axonal degeneration, which seems to be causative of permanent neurological deficits. Hence, the current treatment, which works preferentially immunmodulatory, should be complemented by therapeutics, which improves remyelination not only for restoring conduction velocity but also for preventing an irreversible axonal damage. One strategy to achieve this aim would be to promote remyelination by stimulating oligodendroglial cells remaining in MS lesions. While central nervous system neurons were already known to respond to neurotrophins (NT), interactions with glial cells became apparent more recently. In vitro and in vivo studies have shown that NT influence proliferation, differentiation, survival, and regeneration of mature oligodendrocytes and oligodendroglial precursors in favor of a myelin repair. Two in vivo models provided direct evidence that NT can improve remyelination. In addition, their neuroprotective and anti-inflammatory role would support a repair. Hence, a wealth of data point to NT as promising therapeutical candidates.

Animals↗
PubMed2004

Role of NGF and neurogenic inflammation in the pathogenesis of psoriasis.

A contributing role of neurogenic inflammation has provided a new dimension in understanding the pathogenesis of various cutaneous and systemic inflammatory diseases such as atopic dermatitis, urticaria, rheumatoid arthritis, ulcerative colitis and bronchial asthma. Several critical observations, such as (i) psoriasis resolves at sites of anaesthesia, (ii) neuropeptides are upregulated, and (iii) there is a marked proliferation of terminal cutaneous nerves in psoriatic plaques, encouraged us to search for a mechanism of neural influence in inflammation and inflammatory diseases. In immunohistochemical studies, we found that keratinocytes in lesional and nonlesional psoriatic tissue express high levels of nerve growth factor (NGF) and that there is a marked upregulation of NGF receptors, p75 neurotrophin receptor (p75NTR) and tyrosine kinase A (TrkA), in the terminal cutaneous nerves of psoriatic lesions. As keratinocytes of psoriatic plaques express increased levels of NGF, it is likely that murine nerves will promptly proliferate into the transplanted plaques on a severe combined immunodeficient mouse. Indeed, we have noted marked proliferation of nerve fibers in transplanted psoriatic plaques compared with the few nerves in transplanted normal human skin. By double label immunofluorescence staining, we have further demonstrated that in these terminal cutaneous nerves there is a marked upregulation of neuropeptides, such as substance P and calcitonin gene-related protein. These observations, as well as recent findings about NGF-induced chemokine expression in keratinocytes, further substantiate a role of the NGF-p75NTR-TrkA system in the inflammatory process of psoriasis. Currently, we are evaluating antagonists to selected neuropeptides and NGF/receptors, with the expectation of identifying pharmacological agents to counter neurogenic inflammation in psoriasis.

Animals↗