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Results for “Neuroimmune regulation”

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At least 19 recordsLinked to original sources
PubMed1991

Neuroimmune regulation of colonic secretion in guinea pigs.

The role of submucosal neurons in anaphylactic-like responses in colonic epithelium from immunized guinea pigs was examined 6-8 wk after inoculation with 2 x 10(3) infective Trichinella spiralis larvae. Serosal addition of T. spiralis antigen (20 micrograms/ml) to muscle-stripped segments of colon set up in flux chambers evoked a maximum increase in short-circuit current within 5 min in immune, but not nonimmune, guinea pigs. Quercetin, a membrane-stabilizing drug, and pyrilamine, a histamine H1 receptor antagonist, attenuated epithelial responses evoked by T. spiralis antigen. Antigen-induced epithelial responses were reduced by neural blockade with tetrodotoxin and by the muscarinic receptor antagonist atropine but not by blockade of nicotinic receptors with mecamylamine. Antigenic challenge of colonic mucosa from immune guinea pigs enhanced the secretory responses to endogenously released neurotransmitters evoked by electrical field stimulation and substance P. In the presence of antigen, the tetrodotoxin-insensitive component of the carbachol response was enhanced and was reversed by quercetin but not pyrilamine. The results suggest that submucosal cholinergic nerves play a role in mediating the rapid epithelial responses evoked by worm antigen in the colonic mucosa of T. spiralis-immune guinea pigs. Interaction of immunological mediators with neurotransmitters in the submucosal plexus augments the secretory mucosal response triggered by T. spiralis in immunized hosts.

Animals↗
PubMed2002

Neuroimmunal regulation of electroacupuncture (EA) on the traumatic rats.

EA has a wide range of function, many of them is mediated by the release of the endogenous opioid peptides. Using surgical traumatic stress model, it was observed that EA could improve the depression of cell mediated immune response. Based on the above results, we focused our work on the elucidation of the mechanism of EA in the central nervous system. The results showed that trauma amplified the activity of peritoneal macrophage, but inhibited Orphanin FQ and its receptor NP4 transcripts in the central nervous system, in the mean time, IL-1beta transcripts in the central nervous system was also augmented. EA stimulation of"Zusanli" (St. 36) and "Lanwei" (Extra. 37) points could inhibit all the above responses, but it had no influence on the normal rat. The results suggested that EA could modulate immune response via the interaction between Orphanin FQ and IL-1beta.

Animals↗
PubMed2003

A neuroimmune regulation at peripheral level on the steroidogenesis of polycystic ovary in rats.

It is known that noradrenergic sympathetic nerve fibers connect the ovary and the spleen from the celiac ganglion. The modulation of the ovarian steroidogenesis in rats with polycystic ovary (PCO) by secretions of culture splenocytes from control (non PCO), PCO and PCO rats with superior ovarian nerve transection (PCO+SON-t) is investigated. Splenocytes from PCO rats increased progesterone (P) and decreasing estradiol (E) and androstenedione (A) release, a steroidogenic response different from that obtained with splenocytes of control rats. PCO also decreased the number of splenocyte beta-adrenergic receptors (betaR). SON transection reverted the effect of PCO on splenocytes betaR numbers and secretions of these splenocytes also reverted the stimulatory effect of PCO on P release, while norepinephrine (NE) treatment to PCO+SON-t splenocytes decreased their betaR number and their secretions restored the stimulation on progesterone release. Inversely, PCO+SON-t splenocyte secretions intensified the inhibition in estradiol with no effect on A. Treatment of PCO+SON-t splenocytes with NE or neuropeptide Y partially reverted the effects of PCO and SON-t The P and E-A response of PCO ovary might be differentially regulated by the splenocyte secretions through the neural connection involving ovary, SON, celiac ganglion and spleen and the neurotransmitter NE.

Animals↗
PubMed1994

The effects of kainic acid-induced lesions in the lateral septal area on cell-mediated immune function.

The lateral septal area (LSA) is a primary control region for psychoneuroendocrine functions, and we have previously reported that kainic acid (KA) lesions in the LSA and the hippocampus have inhibitory and facilitatory effects, respectively, on the humoral immune response of female rats. Thus, these limbic structures may selectively participate in directing neuroimmune regulation. In order to assess the fundamental role of the LSA in neuroimmune regulation, we have evaluated the effects of neurotoxic septal lesions on various cell-mediated immune measures. Animals received stereotaxically guided bilateral infusions of KA (2.0 micrograms/microliter) or physiological saline (SHAM) into the LSA. Following a 2-week recovery period, animals were sacrificed and the spleen cells analyzed for natural killer (NK) cell activity and T-cell responsiveness to mitogen (ConA) or to anti T-cell receptor mAb (R73). A separate group of LSA-lesioned animals were immunized with sheep red blood cells 4 days prior to harvesting the spleen for plaque forming cell (PFC) number determination and measurement of TNF-alpha secretion from splenic macrophages. The results indicate that rats with KA lesions in the LSA have significantly higher NK cell activity, significantly lower numbers of splenic PFCs, and significantly reduced TNF-alpha secretion from splenic macrophages, relative to controls. There was a statistical tendency (p < .1) for reduced T-cell lymphoproliferative responses to ConA stimulation in LSA-lesioned animals, relative to SHAMs. However, the T-cell lymphoproliferative response to specific activation via the T-cell receptor was not significantly different between lesioned and control groups. These results further demonstrate the importance of KA-sensitive LSA neurons in neuroimmunoregulation. Moreover, selective alterations of different components of the immune system are observed in LSA-lesioned animals, suggesting that the LSA is involved in the complex and differential regulation of immunity.

Animals↗
PubMed2000

5-HT-moduline controls serotonergic activity: implication in neuroimmune reciprocal regulation mechanisms.

The serotonergic neurotransmission is known as a neuromodulatory system exerting its activity in the central nervous system (CNS) as well as at the periphery. The anatomical and morphological organization of the system based on a marked centralization of the cellular bodies and the large, almost ubiquitary, presence of axonal projections of the neurons is in good agreement with this modulatory role. Furthermore, a very high number of varicosities located along the axonal branches are capable of releasing serotonin (5-HT). The amine stimulates a number of different specific receptor types which allows 5-HT to exert different activities on its various cellular targets. Among these receptors, the 5-HT1B subtypes play a particular role as they are autoreceptors located on 5-HT neurons terminals and heteroreceptors located on non-serotonergic terminals where they control the release of the neurotransmitter. 5-HT-moduline, an endogenous tetrapeptide, regulates the efficacy of these 5-HT1B receptors, hence, is able to control the serotonergic activity in a synchronous manner for the various varicosities from a single neuron and thus may favour the differential effect of that neuron on distinct cerebral functions. Accordingly, the peptide allows the 'fine tuning' of the cerebral activity by the serotonergic system to elaborate the response given by the brain to a particular stimulus, that is, stress situations. At the periphery, the serotonergic system also appears to possess a regulatory activity via 5-HT1B receptors. In particular, the receptors located on immunocompetent cells control their activity and are themselves regulated by 5-HT-moduline likely originating from adrenal medulla and released after acute stress. The serotonergic system appears to play a major role in the reciprocal signalling existing between the neuronal and the immune system. The participation of 5-HT-moduline is likely in physiological functions as well as in pathological disorders affecting central and peripheral activities.

Animals↗
PubMed1996

Integrative neuroimmunology of the digestive tract.

The epithelium of the gastrointestinal tract is continuously exposed to the external environment containing food antigens, microbes and other pathogens. Immunologic and nonimmunologic mechanisms contribute to the neutralization and elimination of these foreign antigens. The immune system of the intestine is the most extensive in the organism and involves diffuse populations of immune cells, lymphoid aggregates and intraepithelial lymphocytes. On the other hand, the functions of the digestive tract contribute to the overall host defense (mucus secretion, gastric acid secretion, water and electrolyte secretion and peristaltism). These functions are regulated by intrinsic and extrinsic nervous systems. It is currently recognized that the physiological and pathological responses of the intestine require an integrate neuroimmune network. Such neuroimmune regulation is based on anatomical and biochemical supports. Indeed, there are membrane-to-membrane contacts between axonal varicosities and the immune cells. Specific receptors for neurotransmitters such as substance P, vasoactive intestinal polypeptide and somatostatin have been identified in many immune cells. Nerve profile change has been described under pathological conditions such as parasitic infections and acute phase of inflammation. In addition to supporting the growth and survival of several populations of nerves the classical nerve growth factor (NGF) has been shown to affect an immune cell population by inducing mast cell hyperplasia. Furthermore the NGF can induce mast cell degranulation, acting directly on mast cell membrane NGF receptors or indirectly by NGF-mediated release of substance P by peripheral extrinsic or intrinsic nerves. Moreover, non-immune cells such as epithelial and smooth muscle cells can produce immunologic messengers under pathological conditions such as infectious diseases or inflammation. Besides the local regulation of gut functions, neuroimmune control can be exerted at extra-intestinal sites. During physiological and pathological conditions, gastrointestinal secretions and motor events are strongly regulated by the central nervous system. Moreover, infectious agents can induce cytokine and particularly interleukin-1 release by the brain astrocytes and microglial cells which have been shown to play a pivotal role in fever induction and modifications of the gastrointestinal functions. Visceral afferent fibers play a pivotal role in 'cross-communication' between central sites and immune response. Recent studies evoke, more specifically, the role of vagus as a key modulatory participant in the close relationship between the extraintestinal nerves and the immune system. Future work in this field will clarify the role of the different participants in the intimate communication between the gastrointestinal tract, immune system and central nervous system.

Animals↗
PubMed2007

Vasoactive intestinal peptide balances pro- and anti-inflammatory cytokines in the Pseudomonas aeruginosa-infected cornea and protects against corneal perforation.

Corneal infection with Pseudomonas aeruginosa perforates the cornea in susceptible C57BL/6 (B6), but not resistant BALB/c, mice. To determine whether vasoactive intestinal peptide (VIP) played a role in development of the resistant response, protein expression levels were tested by immunocytochemistry and enzyme immunoassay in BALB/c and B6 corneas. Both mouse strains showed constitutive expression of corneal VIP protein and nerve fiber distribution. However, disparate expression patterns were detected in the cornea after infection. VIP protein was elevated significantly in BALB/c over B6 mice at 5 and 7 days postinfection. Therefore, B6 mice were injected with rVIP and subsequently demonstrated decreased corneal opacity and resistance to corneal perforation compared with PBS controls. rVIP- vs PBS-treated B6 mice also demonstrated down-regulation of corneal mRNA and/or protein levels for proinflammatory cytokines/chemokines: IFN-gamma, IL-1beta, MIP-2, and TNF-alpha, whereas anti-inflammatory mediators, IL-10 and TGF-beta1, were up-regulated. Treatment with rVIP decreased NO levels and polymorphonuclear neutrophil (PMN) number. To further define the role of VIP, peritoneal macrophages (Mphi) and PMN from BALB/c and B6 mice were stimulated with LPS and treated with rVIP. Treatment of LPS-stimulated Mphi from both mouse strains resulted in decreased IL-1beta and MIP-2 protein levels; PMN responded similarly. Both cell types also displayed a strain-dependent differential response to rVIP, whereby B6 Mphi/PMN responded only to a higher concentration of VIP compared with cells from BALB/c mice. These data provide evidence that neuroimmune regulation of the cytokine network and host inflammatory cells functions to promote resistance against P. aeruginosa corneal infection.

Animals↗
PubMed2004

Consequences of alcohol-induced early dysregulation of responses to trauma/hemorrhage.

Acute alcohol intoxication is a frequent underlying condition associated with traumatic injury. Studies from our laboratory have been designed to examine the early hemodynamic, proinflammatory, and neuroendocrine alterations in responses to hemorrhagic shock in surgically catheterized, conscious, unrestrained, male Sprague-Dawley rats during acute alcohol intoxication (1.75-g/kg bolus, followed by a constant 15-h infusion at a rate of 250-300 mg/kg/h). With both fixed-pressure (40 mm Hg) and fixed-volume (50%) hemorrhagic shock, followed by fluid resuscitation with Ringer's lactate, acute (15 h) alcohol intoxication has been shown to impair significantly the immediate hemodynamic, metabolic, and inflammatory counterregulatory responses to hemorrhagic shock. Alcohol intoxication enhanced hemodynamic instability during blood loss and impaired the recovery of mean arterial blood pressure during fluid resuscitation. Activation of neuroendocrine pathways involved in restoring hemodynamic stability was significantly attenuated in alcohol-intoxicated hemorrhaged animals. The hemodynamic and neuroendocrine impairment is associated with enhanced expression of lung and spleen tumor necrosis factor, and it suppressed circulating neutrophil function. In addition, neuroimmune regulation of cytokine production by spleen-derived macrophages obtained from alcohol-intoxicated hemorrhaged animals was impaired when examined in vitro. We hypothesize that impaired neuroendocrine activation contributes to hemodynamic instability, which, in turn, prolongs tissue hypoperfusion and enhances risk for tissue injury. Specifically, the early dysregulation in counterregulatory responses is hypothesized to affect host defense mechanisms during the recovery period. We examined host response to systemic (cecal ligation and puncture) and localized (pneumonia) infectious challenge in animals recovering from hemorrhage during acute alcohol intoxication. Increased morbidity and mortality from infection were observed in alcohol-intoxicated hemorrhaged animals. Our results indicate that alcohol-induced alterations in early hemodynamic and neuroimmune responses to shock have an impact on susceptibility to an infectious challenge during the early recovery period.

Alcoholic Intoxication↗
PubMed1994

Ionizing radiation reduces neurally evoked electrolyte transport in rat ileum through a mast cell-dependent mechanism.

BACKGROUND/AIMS: Mechanisms of neuroimmune regulation of intestinal electrolyte transport under pathophysiological conditions are unclear. This study investigated the effect of ionizing radiation on ileal electrolyte transport. METHODS: Rats were exposed to 10 Gy gamma-radiation and were killed 2, 24, and 48 hours later. Ileal segments were either mounted in Ussing chambers and exposed to electrical field stimulation, prostaglandin E2, leukotriene D4, or theophylline, or they were assayed for biochemical indices of inflammation. Other segments were processed for routine histological screening, mast cell counts, or immunohistochemical analysis of the distribution of vasoactive intestinal polypeptide or substance P immunoreactivity. RESULTS: Basal short-circuit current was unchanged 2, 24, or 48 hours postirradiation. However, there was a reduction of tissue responsiveness to electrical field stimulation, prostaglandin E2, and theophylline but not to leukotriene D4. Decreased responsiveness at 2-hours postirradiation was blocked by pretreatment with the H1 antagonist pyrilamine. Tissue myeloperoxidase activity and 5-hydroxytryptamine content were not altered postirradiation, but tissue histamine and mucosal mast cells were significantly reduced at 24 and 48 hours. There were no significant changes in villus-crypt architecture until 48 hours postirradiation. There was no significant alteration in the distribution of immunoreactive vasoactive intestinal polypeptide or substance P. CONCLUSIONS: Ionizing radiation reduced the transport response to neural stimulation. The effect correlated temporally with decreased mast cells and histamine, suggesting a functional role for previously reported mast cell-nerve interactions.

Animals↗
PubMed2004

High nitric oxide production in autistic disorder: a possible role for interferon-gamma.

BACKGROUND: Neuroimmune regulation abnormalities have been implicated in the pathophysiology of autistic disorder. Nitric oxide (NO) is involved in immune reactivity and is known to affect brain neurodevelopmental processes. Recent evidence indicates that NO, and cytokines involved in NO production, may be high in children with autism. The purpose of this study was to verify that plasma NO is high in children with autism and determine whether this elevation is related to plasma levels of cytokines involved in NO production. METHODS: The metabolites of NO, nitrite, and nitrate (NOx), along with the cytokines interferon-gamma (IFN-gamma), tumor necrosis factor-alpha, and interleukin-1beta, were measured in plasma of 29 children with autism (mean age +/- SD = 6.1 +/- 2.8 years) and 27 age- and gender-matched healthy comparison subjects using commercially available assay kits. RESULTS: Plasma levels of NOx were significantly higher in the autistic subjects (p =.006); plasma levels of the cytokines did not differ between groups. NOx and IFN-gamma levels were positively correlated in the autistic subjects (r =.51; p =.005). CONCLUSIONS: These results confirm that plasma NO is high in some children with autism and suggest that this elevation may be related to IFN-gamma activity.

Autistic Disorder↗
PubMed1998

Hypothalamic GABA-ergic activity and T-cell proliferation in aged mammal: effect of dietary protein.

Short-term supplementation of low protein diet (LPD) or high protein diet (HPD) to the aged (18 months old) rats did not change the hypothalamic GABAergic activity and immune response. Long-term supplementation of LPD on the other hand, enhanced hypothalamic GABAergic activity with an immunopotentiation by increasing the T-cell proliferating activity and peripheral blood lymphocyte count in the same age group of rats. Unlike LPD, HPD under long-term supplementation to the aged rats reduced the hypothalamic GABAergic activity with immunosuppression. These results thus suggest that (i) hypothalamic GABAergic activity is a regulatory index of immune response in aged mammals and (ii) long-term consumption of protein-poor or protein-rich diet may be an exogenous modulator of neuroimmune regulation in relation to central GABAergic activity and immune response.

4-Aminobutyrate Transaminase↗
PubMed1994

Neuroimmune signaling in regulation of intestinal ion transport.

Complex interactions between the enteric nervous system, the immune system, and the epithelium govern the transport rates of salt and water across the intestinal lining. Luminal antigens or bacterial products are detected by the immune system, which triggers a cascade of events associated with the release of inflammatory mediators. These mediators, by lowering the response threshold for transmission in some neural circuits, augment ongoing neural reflexes that promote secretion. Associated with these effects is a dampening of responses in other neural circuits innervating the mucosal effectors. Selective excitation and inhibition of the neural reflex circuitry coupled with direct actions of inflammatory mediators on epithelial cells result in stereotypical motility and secretory patterns that are characterized by strong muscular contractions, copious secretion, and diarrhea.

Animals↗