The Experts below are selected from a list of 9204 Experts worldwide ranked by ideXlab platform
John B. Hay - One of the best experts on this subject based on the ideXlab platform.
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Cyclosporine A inhibits Lymphocyte Migration into ovine peripheral nerve allografts.
Microsurgery, 1996Co-Authors: Gregory M. T. Hare, Susan E. Mackinnon, Rajiv Midha, Pui-yeun Wong, Catherine A. Munro, William Andrade, Daniel A. Hunter, John B. HayAbstract:Lymphocyte Migration into nerve allografts was measured to estimate the cyclosporine A (CsA) dose required to suppress rejection. Twelve outbred sheep received daily subcutaneous CsA at 0, 5, 10, or 15 mg/kg/day for 2 weeks prior to implantation of multiple heterotopic subcutaneous nerve grafts. Lymphocyte Migration was determined after 7 days by an intravenous pulse of autologous 111 indium-labeled Lymphocytes and subsequent quantitation of gamma radioactivity in nerve tissue (CPM/g, mean ± SEM). Measurement by radioimmunoassay revealed a dose-dependent increase in blood cyclosporine levels. Lymphocyte Migration into autografts (404 ± 44) was significantly less than Migration into allografts (16,554 ± 2,049), in control animals (P < 0.01). A dose-dependent inhibition of Lymphocyte Migration into nerve allografts was observed with counts of 7,662 ± 1,692, 4,083 ± 1,112, and 1,561 < 232 in sheep receiving 5, 10, or 15 mg/kg/day of CsA, respectively. Daily CsA administration produced effective blood levels and immunosuppression sufficient to inhibit Lymphocyte Migration into nerve allografts.
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Effect of cold preservation on Lymphocyte Migration into peripheral nerve allografts in sheep.
Transplantation, 1993Co-Authors: Gregory M. T. Hare, Susan E. Mackinnon, P. J. Evans, Yasushi Nakao, R. Midha, J. A. Wade, D. A. Hunter, John B. HayAbstract:Lymphocyte Migration into fresh and preserved peripheral nerve allografts was quantitated to assess the effect of cold preservation and freeze-thawing pretreatment on the local immunological response to nerve allografts. Out-bred ewes received multiple 1.5-cm subcutaneous heterotopic peroneal nerve autografts, fresh allografts, and pretreated allografts, implanted within the same recipient. Lymphocyte Migration was studied at 7 days by injecting autologous 111indium-labeled Lymphocytes intravenously. After 3 hr of recirculation, Lymphocyte Migration into graft tissue was quantitated by a gamma counter (epm/g, mean +/- SEM). Lymphocyte traffic into fresh nerve allografts (21,623 +/- 3783) increased an average 9.4-fold over the autograft value (2918 +/- 377, P < 0.04). Histologic studies illustrated a marked lymphocytic infiltrate of CD4+ and CD8+ cells and enhanced class I and II MHC expression in fresh allografts, but not in autografts. Short-term cold preservation, for 6 and 12 hr (5 degrees C), enhanced Lymphocyte entry into pretreated allograft tissue. Conversely, cold preservation for longer periods (1 and 3 weeks) dramatically reduced Lymphocyte Migration to values below corresponding autograft levels (783 +/- 100 and 1,252 +/- 120, respectively, P < 0.01). A comparable reduction in Lymphocyte Migration into nerve allografts was observed after freeze-thawing pretreatment (P < 0.01). Cold preservation of donor allogeneic Lymphocytes inhibited their capacity to induce intradermal host Lymphocyte Migration, implicating passenger Lymphocytes as a potential cold-sensitive allogeneic component of the nerve allograft. Assessment of the local response to ovine peripheral nerve allografts, utilizing radiolabeled autologous Lymphocytes, demonstrated that cold preservation and freeze-thawing pretreatment significantly reduced Lymphocyte Migration into nerve allografts. The mechanism(s) of reduced Lymphocyte Migration may involve inactivation or death of antigen-presenting cells, including passenger Lymphocytes.
Gregory M. T. Hare - One of the best experts on this subject based on the ideXlab platform.
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Cyclosporine A inhibits Lymphocyte Migration into ovine peripheral nerve allografts.
Microsurgery, 1996Co-Authors: Gregory M. T. Hare, Susan E. Mackinnon, Rajiv Midha, Pui-yeun Wong, Catherine A. Munro, William Andrade, Daniel A. Hunter, John B. HayAbstract:Lymphocyte Migration into nerve allografts was measured to estimate the cyclosporine A (CsA) dose required to suppress rejection. Twelve outbred sheep received daily subcutaneous CsA at 0, 5, 10, or 15 mg/kg/day for 2 weeks prior to implantation of multiple heterotopic subcutaneous nerve grafts. Lymphocyte Migration was determined after 7 days by an intravenous pulse of autologous 111 indium-labeled Lymphocytes and subsequent quantitation of gamma radioactivity in nerve tissue (CPM/g, mean ± SEM). Measurement by radioimmunoassay revealed a dose-dependent increase in blood cyclosporine levels. Lymphocyte Migration into autografts (404 ± 44) was significantly less than Migration into allografts (16,554 ± 2,049), in control animals (P < 0.01). A dose-dependent inhibition of Lymphocyte Migration into nerve allografts was observed with counts of 7,662 ± 1,692, 4,083 ± 1,112, and 1,561 < 232 in sheep receiving 5, 10, or 15 mg/kg/day of CsA, respectively. Daily CsA administration produced effective blood levels and immunosuppression sufficient to inhibit Lymphocyte Migration into nerve allografts.
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Effect of cold preservation on Lymphocyte Migration into peripheral nerve allografts in sheep.
Transplantation, 1993Co-Authors: Gregory M. T. Hare, Susan E. Mackinnon, P. J. Evans, Yasushi Nakao, R. Midha, J. A. Wade, D. A. Hunter, John B. HayAbstract:Lymphocyte Migration into fresh and preserved peripheral nerve allografts was quantitated to assess the effect of cold preservation and freeze-thawing pretreatment on the local immunological response to nerve allografts. Out-bred ewes received multiple 1.5-cm subcutaneous heterotopic peroneal nerve autografts, fresh allografts, and pretreated allografts, implanted within the same recipient. Lymphocyte Migration was studied at 7 days by injecting autologous 111indium-labeled Lymphocytes intravenously. After 3 hr of recirculation, Lymphocyte Migration into graft tissue was quantitated by a gamma counter (epm/g, mean +/- SEM). Lymphocyte traffic into fresh nerve allografts (21,623 +/- 3783) increased an average 9.4-fold over the autograft value (2918 +/- 377, P < 0.04). Histologic studies illustrated a marked lymphocytic infiltrate of CD4+ and CD8+ cells and enhanced class I and II MHC expression in fresh allografts, but not in autografts. Short-term cold preservation, for 6 and 12 hr (5 degrees C), enhanced Lymphocyte entry into pretreated allograft tissue. Conversely, cold preservation for longer periods (1 and 3 weeks) dramatically reduced Lymphocyte Migration to values below corresponding autograft levels (783 +/- 100 and 1,252 +/- 120, respectively, P < 0.01). A comparable reduction in Lymphocyte Migration into nerve allografts was observed after freeze-thawing pretreatment (P < 0.01). Cold preservation of donor allogeneic Lymphocytes inhibited their capacity to induce intradermal host Lymphocyte Migration, implicating passenger Lymphocytes as a potential cold-sensitive allogeneic component of the nerve allograft. Assessment of the local response to ovine peripheral nerve allografts, utilizing radiolabeled autologous Lymphocytes, demonstrated that cold preservation and freeze-thawing pretreatment significantly reduced Lymphocyte Migration into nerve allografts. The mechanism(s) of reduced Lymphocyte Migration may involve inactivation or death of antigen-presenting cells, including passenger Lymphocytes.
Ryota Hokari - One of the best experts on this subject based on the ideXlab platform.
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involvement of autotaxin lysophospholipase d expression in intestinal vessels in aggravation of intestinal damage through Lymphocyte Migration
Laboratory Investigation, 2013Co-Authors: Hideaki Hozumi, Ryota Hokari, Chie Kurihara, Kazuyuki Narimatsu, Hirokazu Sato, Shingo Sato, Toshihide Ueda, Masaaki Higashiyama, Yoshikiyo Okada, Chikako WatanabeAbstract:Involvement of autotaxin/lysophospholipase D expression in intestinal vessels in aggravation of intestinal damage through Lymphocyte Migration
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Involvement of autotaxin/lysophospholipase D expression in intestinal vessels in aggravation of intestinal damage through Lymphocyte Migration.
Laboratory investigation; a journal of technical methods and pathology, 2013Co-Authors: Hideaki Hozumi, Ryota Hokari, Chie Kurihara, Kazuyuki Narimatsu, Hirokazu Sato, Shingo Sato, Toshihide Ueda, Masaaki Higashiyama, Yoshikiyo Okada, Chikako WatanabeAbstract:Lysophosphatidic acid (LPA) has a critical role in Lymphocyte Migration to secondary lymphoid organs. Autotaxin (ATX)/lysophospholipase D, in the vascular endothelium, is the main enzyme involved in LPA production. Whether ATX is involved in pathological Lymphocyte Migration to the inflamed mucosa has not been studied. We investigated the involvement of ATX in inflammatory bowel disease patients and two murine models of colitis. Tissue samples were obtained by intestinal biopsies from patients with Crohn's disease and those with ulcerative colitis with informed consent. ATX immunoreactivity was colocalized with MAdCAM-1-positive high-endothelial-like vessels, close to sites of Lymphocyte infiltration. Enhanced expression of ATX mRNA was observed in the inflamed mucosa from Crohn's disease and ulcerative colitis patients. ATX mRNA expression level was remarkably higher in the actively inflamed mucosa than in the quiescent mucosa in the same patient. In the T-cell-transferred mouse model, ATX mRNA expression level gradually increased as colitis developed. In the dextran sodium sulfate mouse model, the expression level was considerably higher in colonic mucosa of chronically developed colitis than in colonic mucosa of acute colitis. Administration of an ATX inhibitor, bithionol, remarkably decreased Lymphocyte Migration to the intestine and ameliorated both dextran sodium sulfate-induced colitis and CD4-induced ileocolitis. In transwell assays, administration of bithionol or 1-bromo-3(s)-hydroxy-4-(palmitoyloxy) butylphosphonate (BrP-LPA) significantly decreased transMigration of splenocytes through high-endothelial-like vessels induced by TNF-α. We conclude that enhanced expression of ATX in the active mucosa has been implicated in the pathophysiology of inflammatory bowel disease through enhancing aberrant Lymphocyte Migration to the inflamed mucosa.
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Chronic allergy to dietary ovalbumin induces Lymphocyte Migration to rat small intestinal mucosa that is inhibited by MAdCAM-1.
American journal of physiology. Gastrointestinal and liver physiology, 2003Co-Authors: Toshiko Ogawa, Ryota Hokari, Chikako Watanabe, Soichiro Miura, Yoshikazu Tsuzuki, Takashi Ogino, Ken Teramoto, Toshiaki Inamura, Hiroshi Nagata, Hiromasa IshiiAbstract:Few models have described a chronic food allergy with morphological changes in the intestinal mucosa. Here we established an ovalbumin (OVA)-induced, cell-mediated, allergic rat model and examined Lymphocyte Migration in the gut. Brown Norway rats were intraperitoneally sensitized to OVA and then given 10 mg OVA/day by gastric intubation for 6 wk. Lymphocyte subsets and adhesion molecules were examined immunohistochemically, and the Migration of T Lymphocytes to microvessels of Peyer's patches and villus mucosa was observed by using an intravital microscope. Serum OVA-specific IgG and IgE levels were increased in animals repeatedly exposed to OVA. Significant villus atrophy and increased crypt depth was accompanied by increased infiltration of T Lymphocytes in the small intestinal mucosa of the group given OVA. Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups. The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T Lymphocyte infiltration. Intravital observation demonstrated that in rats with a chronic allergy, T Lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process. Our model of chronic food allergy revealed that Lymphocyte Migration was increased with MAdCAM-1 upregulation.
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Nitric oxide modulates T-Lymphocyte Migration in Peyer's patches and villous submucosa of rat small intestine
Gastroenterology, 1998Co-Authors: Ryota Hokari, Soichiro Miura, Hiroshi Serizawa, Yoshikazu Tsuzuki, Iwao Kurose, Hajime Higuchi, Takeharu Shigematsu, Hiroyuki Kimura, Hitoshi Fujimori, Makoto SuematsuAbstract:Abstract Background & Aims: Although nitric oxide (NO) is known to influence the recruitment of neutrophils in inflamed tissue, its role in Lymphocyte-endothelial cell interactions remains poorly understood. The objectives of this study were to assess the effects of NO synthesis inhibition on T-Lymphocyte Migration in microvessels of rat small intestine and to define the role of adhesion molecules in this process. Methods: T Lymphocytes collected from rat intestinal lymph were labeled with carboxyfluorescein diacetate succinimidyl ester and injected into the jugular vein of recipient rats. The Migration of T Lymphocytes into normal and N G -nitro-L-arginine methyl ester (L-NAME)-treated intestinal microvessels was monitored by using an intravital microscope. Results: L-NAME significantly increased rolling and adherence of Lymphocytes in postcapillary venules of Peyer's patches and submucosal venules without significantly decreasing red blood cell velocity. The subsequent appearance of Lymphocytes in the initial lymphatics was also accelerated by L-NAME. Anti–α4-integrin antibody markedly inhibited the L-NAME–induced Lymphocyte-endothelial cell interaction. Anti–P-selectin monoclonal antibody also significantly attenuated these adhesive interactions in both vascular regions. Conclusions: These data suggest that NO is an important modulator of Lymphocyte Migration in Peyer's patches and in nonlymphoid regions of the intestine. GASTROENTEROLOGY 1998;115:618-627
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Vasoactive intestinal peptide modulates T Lymphocyte Migration in Peyer's patches of rat small intestine
American Journal of Physiology-Gastrointestinal and Liver Physiology, 1997Co-Authors: Soichiro Miura, Ryota Hokari, Hiroshi Serizawa, Yoshikazu Tsuzuki, Iwao Kurose, Makoto Suematsu, Hajime Higuchi, Takeharu Shigematsu, Masahiko Hirokawa, Hiroyuki KimuraAbstract:Although vasoactive intestinal peptide (VIP) has been postulated to function in modulation of T cell trafficking, the exact mechanism has not been elucidated in vivo. In the present study, the effects of VIP on T Lymphocyte Migration were examined in rat Peyer's patches. T Lymphocytes collected from intestinal lymph of rats were labeled with carboxyfluorescein diacetate succinimidyl ester and injected into the jugular vein. Peyer's patches of the recipient rats were observed with intravital fluorescence microscopy. In vivo intra-arterial infusion of or in vitro incubation with VIP did not affect the initial Lymphocyte interaction with postcapillary venules of Peyer's patches. However, these treatments with VIP significantly inhibited transendothelial Migration and also significantly blocked the interstitial Migration of T cells and inhibited their subsequent appearance in the interfollicular lymphatics. Treatment with adenosine 3',5'-cyclic monophosphate (cAMP)-inducing agents resulted in similar inhibitory effect on T Lymphocyte Migration in Peyer's patches. In conclusion, VIP has significant inhibitory effects on T Lymphocyte Migration in Peyer's patches, possibly mediated by elevation of the intracellular cAMP concentrations.
Susan E. Mackinnon - One of the best experts on this subject based on the ideXlab platform.
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Cyclosporine A inhibits Lymphocyte Migration into ovine peripheral nerve allografts.
Microsurgery, 1996Co-Authors: Gregory M. T. Hare, Susan E. Mackinnon, Rajiv Midha, Pui-yeun Wong, Catherine A. Munro, William Andrade, Daniel A. Hunter, John B. HayAbstract:Lymphocyte Migration into nerve allografts was measured to estimate the cyclosporine A (CsA) dose required to suppress rejection. Twelve outbred sheep received daily subcutaneous CsA at 0, 5, 10, or 15 mg/kg/day for 2 weeks prior to implantation of multiple heterotopic subcutaneous nerve grafts. Lymphocyte Migration was determined after 7 days by an intravenous pulse of autologous 111 indium-labeled Lymphocytes and subsequent quantitation of gamma radioactivity in nerve tissue (CPM/g, mean ± SEM). Measurement by radioimmunoassay revealed a dose-dependent increase in blood cyclosporine levels. Lymphocyte Migration into autografts (404 ± 44) was significantly less than Migration into allografts (16,554 ± 2,049), in control animals (P < 0.01). A dose-dependent inhibition of Lymphocyte Migration into nerve allografts was observed with counts of 7,662 ± 1,692, 4,083 ± 1,112, and 1,561 < 232 in sheep receiving 5, 10, or 15 mg/kg/day of CsA, respectively. Daily CsA administration produced effective blood levels and immunosuppression sufficient to inhibit Lymphocyte Migration into nerve allografts.
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Effect of cold preservation on Lymphocyte Migration into peripheral nerve allografts in sheep.
Transplantation, 1993Co-Authors: Gregory M. T. Hare, Susan E. Mackinnon, P. J. Evans, Yasushi Nakao, R. Midha, J. A. Wade, D. A. Hunter, John B. HayAbstract:Lymphocyte Migration into fresh and preserved peripheral nerve allografts was quantitated to assess the effect of cold preservation and freeze-thawing pretreatment on the local immunological response to nerve allografts. Out-bred ewes received multiple 1.5-cm subcutaneous heterotopic peroneal nerve autografts, fresh allografts, and pretreated allografts, implanted within the same recipient. Lymphocyte Migration was studied at 7 days by injecting autologous 111indium-labeled Lymphocytes intravenously. After 3 hr of recirculation, Lymphocyte Migration into graft tissue was quantitated by a gamma counter (epm/g, mean +/- SEM). Lymphocyte traffic into fresh nerve allografts (21,623 +/- 3783) increased an average 9.4-fold over the autograft value (2918 +/- 377, P < 0.04). Histologic studies illustrated a marked lymphocytic infiltrate of CD4+ and CD8+ cells and enhanced class I and II MHC expression in fresh allografts, but not in autografts. Short-term cold preservation, for 6 and 12 hr (5 degrees C), enhanced Lymphocyte entry into pretreated allograft tissue. Conversely, cold preservation for longer periods (1 and 3 weeks) dramatically reduced Lymphocyte Migration to values below corresponding autograft levels (783 +/- 100 and 1,252 +/- 120, respectively, P < 0.01). A comparable reduction in Lymphocyte Migration into nerve allografts was observed after freeze-thawing pretreatment (P < 0.01). Cold preservation of donor allogeneic Lymphocytes inhibited their capacity to induce intradermal host Lymphocyte Migration, implicating passenger Lymphocytes as a potential cold-sensitive allogeneic component of the nerve allograft. Assessment of the local response to ovine peripheral nerve allografts, utilizing radiolabeled autologous Lymphocytes, demonstrated that cold preservation and freeze-thawing pretreatment significantly reduced Lymphocyte Migration into nerve allografts. The mechanism(s) of reduced Lymphocyte Migration may involve inactivation or death of antigen-presenting cells, including passenger Lymphocytes.
Soichiro Miura - One of the best experts on this subject based on the ideXlab platform.
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Chronic allergy to dietary ovalbumin induces Lymphocyte Migration to rat small intestinal mucosa that is inhibited by MAdCAM-1.
American journal of physiology. Gastrointestinal and liver physiology, 2003Co-Authors: Toshiko Ogawa, Ryota Hokari, Chikako Watanabe, Soichiro Miura, Yoshikazu Tsuzuki, Takashi Ogino, Ken Teramoto, Toshiaki Inamura, Hiroshi Nagata, Hiromasa IshiiAbstract:Few models have described a chronic food allergy with morphological changes in the intestinal mucosa. Here we established an ovalbumin (OVA)-induced, cell-mediated, allergic rat model and examined Lymphocyte Migration in the gut. Brown Norway rats were intraperitoneally sensitized to OVA and then given 10 mg OVA/day by gastric intubation for 6 wk. Lymphocyte subsets and adhesion molecules were examined immunohistochemically, and the Migration of T Lymphocytes to microvessels of Peyer's patches and villus mucosa was observed by using an intravital microscope. Serum OVA-specific IgG and IgE levels were increased in animals repeatedly exposed to OVA. Significant villus atrophy and increased crypt depth was accompanied by increased infiltration of T Lymphocytes in the small intestinal mucosa of the group given OVA. Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups. The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T Lymphocyte infiltration. Intravital observation demonstrated that in rats with a chronic allergy, T Lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process. Our model of chronic food allergy revealed that Lymphocyte Migration was increased with MAdCAM-1 upregulation.
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Nitric oxide modulates T-Lymphocyte Migration in Peyer's patches and villous submucosa of rat small intestine
Gastroenterology, 1998Co-Authors: Ryota Hokari, Soichiro Miura, Hiroshi Serizawa, Yoshikazu Tsuzuki, Iwao Kurose, Hajime Higuchi, Takeharu Shigematsu, Hiroyuki Kimura, Hitoshi Fujimori, Makoto SuematsuAbstract:Abstract Background & Aims: Although nitric oxide (NO) is known to influence the recruitment of neutrophils in inflamed tissue, its role in Lymphocyte-endothelial cell interactions remains poorly understood. The objectives of this study were to assess the effects of NO synthesis inhibition on T-Lymphocyte Migration in microvessels of rat small intestine and to define the role of adhesion molecules in this process. Methods: T Lymphocytes collected from rat intestinal lymph were labeled with carboxyfluorescein diacetate succinimidyl ester and injected into the jugular vein of recipient rats. The Migration of T Lymphocytes into normal and N G -nitro-L-arginine methyl ester (L-NAME)-treated intestinal microvessels was monitored by using an intravital microscope. Results: L-NAME significantly increased rolling and adherence of Lymphocytes in postcapillary venules of Peyer's patches and submucosal venules without significantly decreasing red blood cell velocity. The subsequent appearance of Lymphocytes in the initial lymphatics was also accelerated by L-NAME. Anti–α4-integrin antibody markedly inhibited the L-NAME–induced Lymphocyte-endothelial cell interaction. Anti–P-selectin monoclonal antibody also significantly attenuated these adhesive interactions in both vascular regions. Conclusions: These data suggest that NO is an important modulator of Lymphocyte Migration in Peyer's patches and in nonlymphoid regions of the intestine. GASTROENTEROLOGY 1998;115:618-627
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Vasoactive intestinal peptide modulates T Lymphocyte Migration in Peyer's patches of rat small intestine
American Journal of Physiology-Gastrointestinal and Liver Physiology, 1997Co-Authors: Soichiro Miura, Ryota Hokari, Hiroshi Serizawa, Yoshikazu Tsuzuki, Iwao Kurose, Makoto Suematsu, Hajime Higuchi, Takeharu Shigematsu, Masahiko Hirokawa, Hiroyuki KimuraAbstract:Although vasoactive intestinal peptide (VIP) has been postulated to function in modulation of T cell trafficking, the exact mechanism has not been elucidated in vivo. In the present study, the effects of VIP on T Lymphocyte Migration were examined in rat Peyer's patches. T Lymphocytes collected from intestinal lymph of rats were labeled with carboxyfluorescein diacetate succinimidyl ester and injected into the jugular vein. Peyer's patches of the recipient rats were observed with intravital fluorescence microscopy. In vivo intra-arterial infusion of or in vitro incubation with VIP did not affect the initial Lymphocyte interaction with postcapillary venules of Peyer's patches. However, these treatments with VIP significantly inhibited transendothelial Migration and also significantly blocked the interstitial Migration of T cells and inhibited their subsequent appearance in the interfollicular lymphatics. Treatment with adenosine 3',5'-cyclic monophosphate (cAMP)-inducing agents resulted in similar inhibitory effect on T Lymphocyte Migration in Peyer's patches. In conclusion, VIP has significant inhibitory effects on T Lymphocyte Migration in Peyer's patches, possibly mediated by elevation of the intracellular cAMP concentrations.
