- Email: [email protected]
Systemic parthenolide treatment attenuates LPS-induced fever, circulating cytokines and markers of brain inflammation in rats
PNIRS meeting abstracts / Brain, Behavior, and Immunity 25 (2011) S179–S242
IL-7 receptor (IL7R) is expressed on synovial B cells but the role of these cells in arthritis is unclear. Results: Activation of naı¨ve splenic murine B cells with CD40L and IL-4 in vitro increases IL7R expression on these cells. To determine the role of IL-7R+ B cells in arthritis we treated arthritic mice with B cells that have been activated and stimulated with IL-7. Mice treated with IL-7 stimulated B cells developed more severe arthritis than controls. We know from former experiments that norepinephrine treated B cells show anti-inflammatory potential in arthritis. Therefore B cells were activated in the presence of norepinehphrine and then stimulated with IL-7. Treatment of mice with these B cells did not show different severity of arthritis as compared to controls. As possible explanation for this observation we show that proper IL-7 signaling via STAT5 is inhibited in B cells pretreated with norepinephrine. Conclusion: Taken together, these data indicate that IL7R+ B cells have a proinflammatory role in arthritis, which can be inhibited by the sympathetic neurotransmitter norepinephrine via inhibition of IL-7R signaling.
doi:10.1016/j.bbi.2011.07.045
43. Intravenous neural stem cells abolish hypersensitivity in the mouse chronic constriction injury neuropathic pain model: Focus on cytokines and nerve repair S. Franchi a, D. Ferrari b, E. Borsani c, P. Procacci d, A. Vescovi b, A.E. Panerai a, M. Colleoni a, P. Sacerdote a a Dipartimento di Farmacologia, Università degli Studi Milano, University of Milano, Milano, Italy b Dipartimento di Biotecnologie e Bioscienze, Università di MilanoBicocca, Milano, Italy c Dipartimento di Scienze Biomediche e Biotecnologie, Università di Brescia, Brescia, Italy d Dipartimento di Scienze Morfologiche, Università di Milano, Milano, Italy
We investigated the effect of mouse adult neural stem cells (NSC) systemic administration on neuropathic pain symptoms, allodynia and hyperalgesia in the sciatic nerve chronic constriction injury (CCI) model. The effect on pain was correlated to the biochemical and morphological changes. NSC from mice subventricular region, expressing the GFP protein, were injected into caudal vein at a dose ranging from 1 to 3 million. The cell injections started at day 7 since CCI. At different times since NSC administration we evaluated their presence at the lesion site and their effect on: painful symptoms; sciatic nerve pro and anti-inflammatory cytokines; cFos, SP and CGRP in the spinal cord and nerve repair. 24 h after administration, cells were selectively localized in the injured nerve where they remained up to 7 days. NSC dose-dependently decreased painful behaviour starting 3 days after injection and with an effect still present after 21 days. NSC decreased the pro-inflammatory cytokines IL-1 and IL-6, increased by the pathology, and modulated IL-10 levels. Cells were also able to restore the alterations in cFos and SP induced by CCI in the spinal cord. The biochemical changes induced by NSC and their effect on pain remission seem to be independent from their reparative effect and possibly due to a bidirectional interaction between NSC and the lesioned inflamed nerve.
doi:10.1016/j.bbi.2011.07.046
S191
44. Predictors of immune recovery following hematopoietic stem cell transplantation E.S. Costanzo, M.B. Juckett, D. Sheerar, T.L. Becker, A.M. Nelson, K. Schell, P. Hematti, C.L. Coe University of Wisconsin-Madison, Department of Psychiatry, Carbone Cancer Center, 6001 Research Park Blvd., Madison, WI 53719, USA For cancer patients undergoing hematopoietic stem cell transplantation (HSCT), timely immune recovery is critical to prevent recurrence and protect against pathogens. We examined effects of psychosocial factors on immune reconstitution following autologous HSCT. Participants (N = 36) completed measures of psychological symptoms (IDAS), cancer-related distress (IES), and social support (SPS) before HSCT. Leukocyte profiles were assessed 30 and 100 days post-HSCT. Lymphocytes, monocytes, and plasmacytoid and myeloid dendritic cells (pDC and mDC) were immunophenotyped and analyzed by multicolor flow cytometry. Linear regression models covarying for treatment, diagnosis, and age indicated that depression predicted poorer recovery of lymphocytes and DC, including lower B cell (z = 2.1, p = .04), CD4+ T cell (z = 1.9, p = .05), pDC (z = 2.0, p = .04), and mDC (z = 2.8, p = .006) counts. Anxiety was also associated with lower numbers of lymphocytes and DC, including NK cells (z = 3.1, p = .002), CD4+ T cells (z = 2.5; p = .01), and pDC (z = 2.9, p = .003). Cancer-related distress predicted lower B cell (z = 2.7, p = .007) and monocyte counts (z = 2.3, p = .02). In contrast, social support was associated with higher NK cell (z = 3.1; p = .002) and CD4+ T cell numbers (z = 3.1, p = .002) but lower B cell counts (z = 2.1, p = .04). Social support also predicted better recovery of pDC (z = 2.4, p = .02) and mDC (z = 2.9, p = .003). Findings suggest psychological distress may delay immune reconstitution while social support has a protective influence. The pre-transplant period may provide a window of opportunity during which psychosocial interventions can improve recovery. doi:10.1016/j.bbi.2011.07.047
45. Systemic parthenolide treatment attenuates LPS-induced fever, circulating cytokines and markers of brain inflammation in rats C. Rummel, R. Gerstberger, J. Roth, T. Hübschle Institute of Veterinary-Physiology and -Biochemistry, Justus-LiebigUniversity Gießen, Frankfurter Str. 100, Giessen 35392, Germany Parthenolide (P) a sesquiterpene lactone derived from Mexican India medical plants has been reported to exhibit a variety of antiinflammatory, immunomodulatory effects including the peripheral inhibition of the nuclear factor (NF)-kappaB- or signal transducer and activator of transcription (STAT3)-pathway. To test the effect of P on LPS-induced systemic inflammation, the accompanying brain inflammatory response and fever, we treated rats with parthenolide (1 mg/kg), simultaneously or 1 h prior to a systemic challenge with a moderate (100 lg/kg) dose of lipopolysaccharide (LPS). Only in Ppretreated animals the initial hypothermia, the second phase of the LPS-induced fever and circulating interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) were significantly attenuated. In the hypothalamus, markers of NFkappaB/NF-IL6 pathway activation namely inhibitor kappaBalpha, NF-IL6 and the serin/threonin kinase-like protein mRNA expression and NFkappaB immunoreactivity were significantly reduced while NF-IL6 immunoreactivity and suppressor of cytokine signaling 3 mRNA expression remained
S192
PNIRS meeting abstracts / Brain, Behavior, and Immunity 25 (2011) S179–S242
unaltered 8 h after LPS-stimulation by P pretreatment. Importantly, this response was accompanied by decreased mRNA expression of the rate limiting enzyme in prostaglandin synthesis cyclooxygenase 2 (COX2) known for its critical role in fever induction pathways. In summary, P attenuates the febrile response during LPS-induced systemic inflammation by reducing the circulating cytokines IL-6 and TNFalpha and decreasing the hypothalamic NFkappaB/NF-IL6 activation and expression of COX2 suggesting a therapeutic potential for P to reduce brain inflammation. doi:10.1016/j.bbi.2011.07.048
46. Stress and surgery reduce baseline plasma IL-12 levels in rats: Mediation by prostaglandins and corticosterone, but not catecholamines L. Shaashua a, L. Sominsky a, G. Page b, S. Ben-Eliyahu a a
Neuroimmunology Research Unit, Department of Psychology, Tel Aviv University, Tel Aviv 69978, Israel b School of Nursing, Johns Hopkins University, Baltimore, MD, USA IL-12 is a major pro-inflammatory/pro-CMI cytokine that drives Th1 differentiation. Suppression of IL-12 production by numerous stress factors was reported in-vitro, but mainly in artificially stimulated leukocytes. In-vivo effects of natural stress conditions in rats without prior immune stimulation are largely unknown, and were the focus of the current study, which also sought to elucidate neuroendocrine mediating mechanisms. Wet-cage exposure, social confrontation, and laparotomy, all reduced baseline plasma IL-12 levels. Administration of apparently physiologically relevant doses of prostaglandin-E2, epinephrine, or corticosterone, had similar impacts, the latter two hormones exerting significantly greater impacts in males. The GR blocker, RU-486, and the COX-2 inhibitor, etodolac, attenuated the effects of stress and surgery, but surprisingly different aand/or b-adrenergic blockers had no beneficial effects. A simultaneous blockade of CORT and prostaglandins completely abolished the effects of surgery. To decipher the paradox in which epinephrine administration reduced IL-12, but catecholamine blockade had no prophylactic impact in stressed animals, adrenalectomized and sham-operated rats were subjected to epinephrine and/or CORT administration. While CORT reduced IL-12 levels in both conditions, epinephrine did so only in sham operated animals, indicating that its effects are mediated through elevation of endogenous CORT levels, which were indeed observed following epinephrine administration in normal rats. Overall, corticosterone and prostaglandins, but not catecholamines, have a significant role in mediating stress- and surgery-induced reduction in plasma IL-12 baseline levels. doi:10.1016/j.bbi.2011.07.049
47. Isolating mice slows wound healing L. Yang a, P.T. Marucha a,b, C.G. Engeland a,b
the effects of isolation stress on wound healing and gene expression in dermal tissues. One-hundred and sixty female and male SKH-1 mice were divided into two groups: isolate-housed (ISO), and group-housed controls (GRO). ISO mice were individually housed from 3 weeks before wounding. Under anesthesia, two 3.5 mm biopsy punch wounds were placed dorsally on each mouse and harvested at day 1, 3, 5 or 7 post-wounding. Wound closure was assessed through daily pictures. Biopsies were analyzed by RT-PCR for gene expression including KGF, which is important in re-epithelialization, and a-SMA which correlates with fibroblast contractile ability. Isolation stress significantly delayed wound closure rates (p < .001 each sex). Female ISO mice had lower KGF gene expression at days 1 and 3. Male ISO mice had lower gene expression for KGF at days 1 and 3, and a-SMA at days 3 and 5. Surprisingly, ISO mice had less bacteria in the wounds than controls (p < .01). Thus, a high bacterial burden was not necessary to induce stress-impaired healing in this relatively naturalistic model. These findings suggest that isolation impairs wound healing through alterations in re-epithelialization and wound contraction independent of infection. doi:10.1016/j.bbi.2011.07.050
48. Role of Hsp70 in lung inflammation after chronic stress M. Pannacci, V. Lucini, S. Dugnani, F. Scaglione Dept. Pharmacology, University of MIlan, via Vanvitelli 32, Milan 20129, USA Exercise induces a range of stressors that stimulate synthesis of heat shock protein (HSPs) which acts as molecular chaperones to maintain cellular homeostasis. In particular, an increased of Hsp 70 is associated with tolerance to stressors and cytoprotective effects. Moreover Hsp70 is well described in whole lungs in response to stressors during lung inflammation and injury. Our work evaluated a correlation between expression of proinflammatory cytokines (TNFa; IL1b; ICAM1; MCP1) and expression of Hsp70 in a murine model of physical stress also considering the susceptibility to respiratory tract infection (RTI). Mice Balb/C were subjected to swimming for 1 h/day for 4 weeks; after chronic exercise, animals were infected with 1 108 CFU of S. Pneumoniae. Changes in gene expression of proinflammatory cytokines and Hsp70 were evaluated by Real Time PCR on RNA extracted from lungs. Hsp70 expression increased significantly during 4 week of exercise (p < .05), additionally this expression showed to attenuate proinflammatory cytokines release (p < .05) in stressed animals. In chronic stressed group, this decrease is maintained even 24 h or 48 h after infection with S. Pneumoniae. Bacterial size was significantly higher (p< 0.001) in chronic stressed animals vs controls (7 106 ± 3.5 CFU/lung vs 3.5 104 ± 1.5 CFU/lung). Data obtained confirmed that in chronic exercise increased levels of Hsp70, but the contemporary decrease of proinflammatory cytokines is associated to an increased risk of RTI. doi:10.1016/j.bbi.2011.07.051
a
University of Illinois at Chicago (UIC), 801 S Paulina St., M/C 859, Chicago, IL 60612, USA b Center for Wound Repair and Tissue Regeneration (UIC), USA Wound healing in humans and rodents is impaired by exposure to chronic psychological stress. Isolation stress, which is akin to loneliness/isolation in humans, can negatively affect immunity. This is important, as mice are often separated in scientific studies to prevent potentially confounding interactions. This study investigated
49. The impact of whole body proton radiation on immune-CNS communication M.J. Pecaut, E. Bayeta, X. Luo-Owen, C. Perez, S. Rightnar, G. Harding, P. Gifford, D.S. Gridley Loma Linda University, Dept. of Radiation Medicine (Radiobiology Research Laboratories), 11175 Campus St. CSP A-1010, Loma Linda, CA 92354, USA
IL-7 receptor (IL7R) is expressed on synovial B cells but the role of these cells in arthritis is unclear. Results: Activation of naı¨ve splenic murine B cells with CD40L and IL-4 in vitro increases IL7R expression on these cells. To determine the role of IL-7R+ B cells in arthritis we treated arthritic mice with B cells that have been activated and stimulated with IL-7. Mice treated with IL-7 stimulated B cells developed more severe arthritis than controls. We know from former experiments that norepinephrine treated B cells show anti-inflammatory potential in arthritis. Therefore B cells were activated in the presence of norepinehphrine and then stimulated with IL-7. Treatment of mice with these B cells did not show different severity of arthritis as compared to controls. As possible explanation for this observation we show that proper IL-7 signaling via STAT5 is inhibited in B cells pretreated with norepinephrine. Conclusion: Taken together, these data indicate that IL7R+ B cells have a proinflammatory role in arthritis, which can be inhibited by the sympathetic neurotransmitter norepinephrine via inhibition of IL-7R signaling.
doi:10.1016/j.bbi.2011.07.045
43. Intravenous neural stem cells abolish hypersensitivity in the mouse chronic constriction injury neuropathic pain model: Focus on cytokines and nerve repair S. Franchi a, D. Ferrari b, E. Borsani c, P. Procacci d, A. Vescovi b, A.E. Panerai a, M. Colleoni a, P. Sacerdote a a Dipartimento di Farmacologia, Università degli Studi Milano, University of Milano, Milano, Italy b Dipartimento di Biotecnologie e Bioscienze, Università di MilanoBicocca, Milano, Italy c Dipartimento di Scienze Biomediche e Biotecnologie, Università di Brescia, Brescia, Italy d Dipartimento di Scienze Morfologiche, Università di Milano, Milano, Italy
We investigated the effect of mouse adult neural stem cells (NSC) systemic administration on neuropathic pain symptoms, allodynia and hyperalgesia in the sciatic nerve chronic constriction injury (CCI) model. The effect on pain was correlated to the biochemical and morphological changes. NSC from mice subventricular region, expressing the GFP protein, were injected into caudal vein at a dose ranging from 1 to 3 million. The cell injections started at day 7 since CCI. At different times since NSC administration we evaluated their presence at the lesion site and their effect on: painful symptoms; sciatic nerve pro and anti-inflammatory cytokines; cFos, SP and CGRP in the spinal cord and nerve repair. 24 h after administration, cells were selectively localized in the injured nerve where they remained up to 7 days. NSC dose-dependently decreased painful behaviour starting 3 days after injection and with an effect still present after 21 days. NSC decreased the pro-inflammatory cytokines IL-1 and IL-6, increased by the pathology, and modulated IL-10 levels. Cells were also able to restore the alterations in cFos and SP induced by CCI in the spinal cord. The biochemical changes induced by NSC and their effect on pain remission seem to be independent from their reparative effect and possibly due to a bidirectional interaction between NSC and the lesioned inflamed nerve.
doi:10.1016/j.bbi.2011.07.046
S191
44. Predictors of immune recovery following hematopoietic stem cell transplantation E.S. Costanzo, M.B. Juckett, D. Sheerar, T.L. Becker, A.M. Nelson, K. Schell, P. Hematti, C.L. Coe University of Wisconsin-Madison, Department of Psychiatry, Carbone Cancer Center, 6001 Research Park Blvd., Madison, WI 53719, USA For cancer patients undergoing hematopoietic stem cell transplantation (HSCT), timely immune recovery is critical to prevent recurrence and protect against pathogens. We examined effects of psychosocial factors on immune reconstitution following autologous HSCT. Participants (N = 36) completed measures of psychological symptoms (IDAS), cancer-related distress (IES), and social support (SPS) before HSCT. Leukocyte profiles were assessed 30 and 100 days post-HSCT. Lymphocytes, monocytes, and plasmacytoid and myeloid dendritic cells (pDC and mDC) were immunophenotyped and analyzed by multicolor flow cytometry. Linear regression models covarying for treatment, diagnosis, and age indicated that depression predicted poorer recovery of lymphocytes and DC, including lower B cell (z = 2.1, p = .04), CD4+ T cell (z = 1.9, p = .05), pDC (z = 2.0, p = .04), and mDC (z = 2.8, p = .006) counts. Anxiety was also associated with lower numbers of lymphocytes and DC, including NK cells (z = 3.1, p = .002), CD4+ T cells (z = 2.5; p = .01), and pDC (z = 2.9, p = .003). Cancer-related distress predicted lower B cell (z = 2.7, p = .007) and monocyte counts (z = 2.3, p = .02). In contrast, social support was associated with higher NK cell (z = 3.1; p = .002) and CD4+ T cell numbers (z = 3.1, p = .002) but lower B cell counts (z = 2.1, p = .04). Social support also predicted better recovery of pDC (z = 2.4, p = .02) and mDC (z = 2.9, p = .003). Findings suggest psychological distress may delay immune reconstitution while social support has a protective influence. The pre-transplant period may provide a window of opportunity during which psychosocial interventions can improve recovery. doi:10.1016/j.bbi.2011.07.047
45. Systemic parthenolide treatment attenuates LPS-induced fever, circulating cytokines and markers of brain inflammation in rats C. Rummel, R. Gerstberger, J. Roth, T. Hübschle Institute of Veterinary-Physiology and -Biochemistry, Justus-LiebigUniversity Gießen, Frankfurter Str. 100, Giessen 35392, Germany Parthenolide (P) a sesquiterpene lactone derived from Mexican India medical plants has been reported to exhibit a variety of antiinflammatory, immunomodulatory effects including the peripheral inhibition of the nuclear factor (NF)-kappaB- or signal transducer and activator of transcription (STAT3)-pathway. To test the effect of P on LPS-induced systemic inflammation, the accompanying brain inflammatory response and fever, we treated rats with parthenolide (1 mg/kg), simultaneously or 1 h prior to a systemic challenge with a moderate (100 lg/kg) dose of lipopolysaccharide (LPS). Only in Ppretreated animals the initial hypothermia, the second phase of the LPS-induced fever and circulating interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) were significantly attenuated. In the hypothalamus, markers of NFkappaB/NF-IL6 pathway activation namely inhibitor kappaBalpha, NF-IL6 and the serin/threonin kinase-like protein mRNA expression and NFkappaB immunoreactivity were significantly reduced while NF-IL6 immunoreactivity and suppressor of cytokine signaling 3 mRNA expression remained
S192
PNIRS meeting abstracts / Brain, Behavior, and Immunity 25 (2011) S179–S242
unaltered 8 h after LPS-stimulation by P pretreatment. Importantly, this response was accompanied by decreased mRNA expression of the rate limiting enzyme in prostaglandin synthesis cyclooxygenase 2 (COX2) known for its critical role in fever induction pathways. In summary, P attenuates the febrile response during LPS-induced systemic inflammation by reducing the circulating cytokines IL-6 and TNFalpha and decreasing the hypothalamic NFkappaB/NF-IL6 activation and expression of COX2 suggesting a therapeutic potential for P to reduce brain inflammation. doi:10.1016/j.bbi.2011.07.048
46. Stress and surgery reduce baseline plasma IL-12 levels in rats: Mediation by prostaglandins and corticosterone, but not catecholamines L. Shaashua a, L. Sominsky a, G. Page b, S. Ben-Eliyahu a a
Neuroimmunology Research Unit, Department of Psychology, Tel Aviv University, Tel Aviv 69978, Israel b School of Nursing, Johns Hopkins University, Baltimore, MD, USA IL-12 is a major pro-inflammatory/pro-CMI cytokine that drives Th1 differentiation. Suppression of IL-12 production by numerous stress factors was reported in-vitro, but mainly in artificially stimulated leukocytes. In-vivo effects of natural stress conditions in rats without prior immune stimulation are largely unknown, and were the focus of the current study, which also sought to elucidate neuroendocrine mediating mechanisms. Wet-cage exposure, social confrontation, and laparotomy, all reduced baseline plasma IL-12 levels. Administration of apparently physiologically relevant doses of prostaglandin-E2, epinephrine, or corticosterone, had similar impacts, the latter two hormones exerting significantly greater impacts in males. The GR blocker, RU-486, and the COX-2 inhibitor, etodolac, attenuated the effects of stress and surgery, but surprisingly different aand/or b-adrenergic blockers had no beneficial effects. A simultaneous blockade of CORT and prostaglandins completely abolished the effects of surgery. To decipher the paradox in which epinephrine administration reduced IL-12, but catecholamine blockade had no prophylactic impact in stressed animals, adrenalectomized and sham-operated rats were subjected to epinephrine and/or CORT administration. While CORT reduced IL-12 levels in both conditions, epinephrine did so only in sham operated animals, indicating that its effects are mediated through elevation of endogenous CORT levels, which were indeed observed following epinephrine administration in normal rats. Overall, corticosterone and prostaglandins, but not catecholamines, have a significant role in mediating stress- and surgery-induced reduction in plasma IL-12 baseline levels. doi:10.1016/j.bbi.2011.07.049
47. Isolating mice slows wound healing L. Yang a, P.T. Marucha a,b, C.G. Engeland a,b
the effects of isolation stress on wound healing and gene expression in dermal tissues. One-hundred and sixty female and male SKH-1 mice were divided into two groups: isolate-housed (ISO), and group-housed controls (GRO). ISO mice were individually housed from 3 weeks before wounding. Under anesthesia, two 3.5 mm biopsy punch wounds were placed dorsally on each mouse and harvested at day 1, 3, 5 or 7 post-wounding. Wound closure was assessed through daily pictures. Biopsies were analyzed by RT-PCR for gene expression including KGF, which is important in re-epithelialization, and a-SMA which correlates with fibroblast contractile ability. Isolation stress significantly delayed wound closure rates (p < .001 each sex). Female ISO mice had lower KGF gene expression at days 1 and 3. Male ISO mice had lower gene expression for KGF at days 1 and 3, and a-SMA at days 3 and 5. Surprisingly, ISO mice had less bacteria in the wounds than controls (p < .01). Thus, a high bacterial burden was not necessary to induce stress-impaired healing in this relatively naturalistic model. These findings suggest that isolation impairs wound healing through alterations in re-epithelialization and wound contraction independent of infection. doi:10.1016/j.bbi.2011.07.050
48. Role of Hsp70 in lung inflammation after chronic stress M. Pannacci, V. Lucini, S. Dugnani, F. Scaglione Dept. Pharmacology, University of MIlan, via Vanvitelli 32, Milan 20129, USA Exercise induces a range of stressors that stimulate synthesis of heat shock protein (HSPs) which acts as molecular chaperones to maintain cellular homeostasis. In particular, an increased of Hsp 70 is associated with tolerance to stressors and cytoprotective effects. Moreover Hsp70 is well described in whole lungs in response to stressors during lung inflammation and injury. Our work evaluated a correlation between expression of proinflammatory cytokines (TNFa; IL1b; ICAM1; MCP1) and expression of Hsp70 in a murine model of physical stress also considering the susceptibility to respiratory tract infection (RTI). Mice Balb/C were subjected to swimming for 1 h/day for 4 weeks; after chronic exercise, animals were infected with 1 108 CFU of S. Pneumoniae. Changes in gene expression of proinflammatory cytokines and Hsp70 were evaluated by Real Time PCR on RNA extracted from lungs. Hsp70 expression increased significantly during 4 week of exercise (p < .05), additionally this expression showed to attenuate proinflammatory cytokines release (p < .05) in stressed animals. In chronic stressed group, this decrease is maintained even 24 h or 48 h after infection with S. Pneumoniae. Bacterial size was significantly higher (p< 0.001) in chronic stressed animals vs controls (7 106 ± 3.5 CFU/lung vs 3.5 104 ± 1.5 CFU/lung). Data obtained confirmed that in chronic exercise increased levels of Hsp70, but the contemporary decrease of proinflammatory cytokines is associated to an increased risk of RTI. doi:10.1016/j.bbi.2011.07.051
a
University of Illinois at Chicago (UIC), 801 S Paulina St., M/C 859, Chicago, IL 60612, USA b Center for Wound Repair and Tissue Regeneration (UIC), USA Wound healing in humans and rodents is impaired by exposure to chronic psychological stress. Isolation stress, which is akin to loneliness/isolation in humans, can negatively affect immunity. This is important, as mice are often separated in scientific studies to prevent potentially confounding interactions. This study investigated
49. The impact of whole body proton radiation on immune-CNS communication M.J. Pecaut, E. Bayeta, X. Luo-Owen, C. Perez, S. Rightnar, G. Harding, P. Gifford, D.S. Gridley Loma Linda University, Dept. of Radiation Medicine (Radiobiology Research Laboratories), 11175 Campus St. CSP A-1010, Loma Linda, CA 92354, USA