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Neurogenic control of the cutaneous stress response: A yin and yang example for neuro-immune interaction
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Abstracts / Brain, Behavior, and Immunity 24 (2010) S1–S71
cytokine levels in patients and controls. Moreover, to improve the statistical power, Pearson’s correlation, was conducted investigating the relationship between pro-inflammatory cytokines and cognition in the entire sample. Results: As expected, patients scored significantly worse on all the cognitive tasks presented compared to controls (p < 0.05), together with a trend for higher levels of pro-inflammatory cytokine IL-8 (p = 0.069). Particularly, high levels of IL-8, and IL-6 were related to significantly (p < 0.05) worse cognitive performance on perception and visuospatial domain (r = 0.37, p = 0.03), executive function/working memory domain (r = 0.38, p = 0.02), and verbal memory (r = 0.42, p = 0.02) in the entire sample. Conclusions: Our data demonstrate that pro-inflammation in first-episode psychosis may be one possible mechanism behind cognitive dysfunction in psychosis. doi:10.1016/j.bbi.2010.07.089
Abstract # 314 Effects of the chronic treatment of 5-HT4 receptor agonist (RS 67333) in subjects with different coping in response to social stress E. Gómez-Lázaro, A. Arregi, G. Beitia, O. Vegas, A. Azpiroz, L. Garmendia Department of Basic Psychological Processes and their Development, Avda, Tolosa 70, Basque Country University, San Sebastián, Guipuzcoa 20018, Spain The aim of this study was to analyze the effect of a chronic treatment with a potential antidepressant on the changes produced by social-stress in function of the strategy adopted by subjects. Male mice were socially stressed by repeated experiences of defeat using a sensorial contact model, for 26 consecutive days. Two subgroups, active or passive, were established after the 18 social-stress session in accordance with the behavioural coping. The levels of corticosterone measured at this time showed that passive subjects had higher levels of corticosterone than active and controls. After 26 days of social-stress all animals were subjected to the forced swimming test (FST) for 2 days and 24 h after the animals were sacrificed. The pharmacological treatment was applied during the last 10 days of experiment. The results showed that drug treated passive subjects had lower immobility in social confrontation than non-treated passive subjects. There were no significant differences in the behaviours measured in FST. Active and passive subjects had higher levels of IL-6 and TNF-a, and lower levels of corticosterone than controls. The drug did not affect these variables. Active subjects had higher levels of BDNF and 5-HT1A receptor mRNA in the hippocampus than passive and controls. The drug reduced BDNF levels in all groups. The results indicate that the drug treatment was effective in reversing only some of the variables measured. doi:10.1016/j.bbi.2010.07.090
Abstract # 317 Peripheral administration of LPS exacerbates spontaneous relapse in experimental autoimmune encephalomyelitis S. Mardiguian a, S. Patel a, N.R. Sibson a, G. Watt b, D.C. Anthony a a University of Oxford, Department of Pharmacology, Mansfield Road, Oxford, Great Britain and Northern Ireland, UK b UCB Celltech, UK
There has been considerable interest in the role of infectious agents in the development of MS. Several studies have shown the accentuation of EAE following the peripheral inoculation with live bacteria, however most of these studies have focused on the acute phase of the disease. In this study, we sought to investigate whether a peripheral challenge would exacerbate spontaneous relapse in CREAE. To this end, we have injected 30 lg of LPS intraperitoneally in Biozzi ABH mice during the remission period. The animals were scored daily and an inverted screen was used to assess hind-limb strength. We found that peripheral administration of LPS in EAE mice brings forward and exacerbates the relapse phase. It is of interest to note that there was a still delay of 5 days from the time of the LPS administration to the appearance of the first clinical signs. In behavioural tests LPS-treated mice spent less time on the inverted screen than the saline-treated mice. Disease exacerbation by LPS challenge was also associated with an increase in mRNA expression of hepatic acute phase proteins and chemokines and an increase in neutrophil recruitment to the liver. In non-EAE animals, LPS had no effect on hepatic chemokine production. Thus, our findings provide evidence that bacterial infection can exacerbate spontaneous relapse in EAE, which may be underpinned by a persistent increase in circulating chemokines. doi:10.1016/j.bbi.2010.07.091
Abstract # 318 Neurogenic control of the cutaneous stress response: A yin and yang example for neuro-immune interaction E.M. Peters a,b, W. Snaga a, C. Liezmann a a University-Medicine Charité, Charité Center 12 for Internal Medicine and Dermatology, Psycho-Neuro-Immunology, Campus Virchow, Berlin, Germany b University Giessen, Department of Psychosomatic Medicine, PsychoNeuro-Immunolgy, Giessen, Germany
At the border between our environment and our body/self – the skin – a multitude of challenges are met by a complex neuroimmune–endocrine network. Numerous deteriorating effects on cutaneous health maintenance and inflammatory disease have been described for most challenges under scrutiny, among them allergen provocation as an example of inflammatory stress and noise exposure as an example for perceived stress. However, clinical observation has long suggested that stress can be beneficial and recent publications suggest neuro-immune control of regulatory mechanisms in inflammation. We here summarize work that point at a pro-inflammatory effect of acute activation of neurogenic inflammation versus control of inflammation by repeated stress-experience during inflammation development obtained in a mouse model for atopic dermatitis-like allergic dermatitis (AlD) combined with noise stress exposure. We found that a singular stress exposure prior to AlD provocation worsened neurogenic inflammation and AlD severity in a Substance P (SP) and mast cell dependent manner. By contrast, repeated stress exposure prior to AlD sensitization reduced AlD severity involving alterated dendritic cell activation and induction of Tregs in a SP dependent fashion. Together these data suggest that the capacity of the skin to effectively meet a given challenge depends on the stressors involved and their timing of encounter and can be targeted in two ways: blockade of exacerbating stress paradigms versus therapeutic exploitation of beneficial stress paradigms. doi:10.1016/j.bbi.2010.07.092
Abstracts / Brain, Behavior, and Immunity 24 (2010) S1–S71
cytokine levels in patients and controls. Moreover, to improve the statistical power, Pearson’s correlation, was conducted investigating the relationship between pro-inflammatory cytokines and cognition in the entire sample. Results: As expected, patients scored significantly worse on all the cognitive tasks presented compared to controls (p < 0.05), together with a trend for higher levels of pro-inflammatory cytokine IL-8 (p = 0.069). Particularly, high levels of IL-8, and IL-6 were related to significantly (p < 0.05) worse cognitive performance on perception and visuospatial domain (r = 0.37, p = 0.03), executive function/working memory domain (r = 0.38, p = 0.02), and verbal memory (r = 0.42, p = 0.02) in the entire sample. Conclusions: Our data demonstrate that pro-inflammation in first-episode psychosis may be one possible mechanism behind cognitive dysfunction in psychosis. doi:10.1016/j.bbi.2010.07.089
Abstract # 314 Effects of the chronic treatment of 5-HT4 receptor agonist (RS 67333) in subjects with different coping in response to social stress E. Gómez-Lázaro, A. Arregi, G. Beitia, O. Vegas, A. Azpiroz, L. Garmendia Department of Basic Psychological Processes and their Development, Avda, Tolosa 70, Basque Country University, San Sebastián, Guipuzcoa 20018, Spain The aim of this study was to analyze the effect of a chronic treatment with a potential antidepressant on the changes produced by social-stress in function of the strategy adopted by subjects. Male mice were socially stressed by repeated experiences of defeat using a sensorial contact model, for 26 consecutive days. Two subgroups, active or passive, were established after the 18 social-stress session in accordance with the behavioural coping. The levels of corticosterone measured at this time showed that passive subjects had higher levels of corticosterone than active and controls. After 26 days of social-stress all animals were subjected to the forced swimming test (FST) for 2 days and 24 h after the animals were sacrificed. The pharmacological treatment was applied during the last 10 days of experiment. The results showed that drug treated passive subjects had lower immobility in social confrontation than non-treated passive subjects. There were no significant differences in the behaviours measured in FST. Active and passive subjects had higher levels of IL-6 and TNF-a, and lower levels of corticosterone than controls. The drug did not affect these variables. Active subjects had higher levels of BDNF and 5-HT1A receptor mRNA in the hippocampus than passive and controls. The drug reduced BDNF levels in all groups. The results indicate that the drug treatment was effective in reversing only some of the variables measured. doi:10.1016/j.bbi.2010.07.090
Abstract # 317 Peripheral administration of LPS exacerbates spontaneous relapse in experimental autoimmune encephalomyelitis S. Mardiguian a, S. Patel a, N.R. Sibson a, G. Watt b, D.C. Anthony a a University of Oxford, Department of Pharmacology, Mansfield Road, Oxford, Great Britain and Northern Ireland, UK b UCB Celltech, UK
There has been considerable interest in the role of infectious agents in the development of MS. Several studies have shown the accentuation of EAE following the peripheral inoculation with live bacteria, however most of these studies have focused on the acute phase of the disease. In this study, we sought to investigate whether a peripheral challenge would exacerbate spontaneous relapse in CREAE. To this end, we have injected 30 lg of LPS intraperitoneally in Biozzi ABH mice during the remission period. The animals were scored daily and an inverted screen was used to assess hind-limb strength. We found that peripheral administration of LPS in EAE mice brings forward and exacerbates the relapse phase. It is of interest to note that there was a still delay of 5 days from the time of the LPS administration to the appearance of the first clinical signs. In behavioural tests LPS-treated mice spent less time on the inverted screen than the saline-treated mice. Disease exacerbation by LPS challenge was also associated with an increase in mRNA expression of hepatic acute phase proteins and chemokines and an increase in neutrophil recruitment to the liver. In non-EAE animals, LPS had no effect on hepatic chemokine production. Thus, our findings provide evidence that bacterial infection can exacerbate spontaneous relapse in EAE, which may be underpinned by a persistent increase in circulating chemokines. doi:10.1016/j.bbi.2010.07.091
Abstract # 318 Neurogenic control of the cutaneous stress response: A yin and yang example for neuro-immune interaction E.M. Peters a,b, W. Snaga a, C. Liezmann a a University-Medicine Charité, Charité Center 12 for Internal Medicine and Dermatology, Psycho-Neuro-Immunology, Campus Virchow, Berlin, Germany b University Giessen, Department of Psychosomatic Medicine, PsychoNeuro-Immunolgy, Giessen, Germany
At the border between our environment and our body/self – the skin – a multitude of challenges are met by a complex neuroimmune–endocrine network. Numerous deteriorating effects on cutaneous health maintenance and inflammatory disease have been described for most challenges under scrutiny, among them allergen provocation as an example of inflammatory stress and noise exposure as an example for perceived stress. However, clinical observation has long suggested that stress can be beneficial and recent publications suggest neuro-immune control of regulatory mechanisms in inflammation. We here summarize work that point at a pro-inflammatory effect of acute activation of neurogenic inflammation versus control of inflammation by repeated stress-experience during inflammation development obtained in a mouse model for atopic dermatitis-like allergic dermatitis (AlD) combined with noise stress exposure. We found that a singular stress exposure prior to AlD provocation worsened neurogenic inflammation and AlD severity in a Substance P (SP) and mast cell dependent manner. By contrast, repeated stress exposure prior to AlD sensitization reduced AlD severity involving alterated dendritic cell activation and induction of Tregs in a SP dependent fashion. Together these data suggest that the capacity of the skin to effectively meet a given challenge depends on the stressors involved and their timing of encounter and can be targeted in two ways: blockade of exacerbating stress paradigms versus therapeutic exploitation of beneficial stress paradigms. doi:10.1016/j.bbi.2010.07.092