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Saeed Khalili - One of the best experts on this subject based on the ideXlab platform.
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treatment for salivary gland hypofunction at both initial and advanced stages of sjogren like disease a comparative study of bone marrow therapy versus Spleen Cell therapy with a 1 year monitoring period
Cytotherapy, 2014Co-Authors: Saeed Khalili, Denise L Faustman, Yoshinori Sumita, David Blank, Alan C Peterson, Shohta Kodama, Simon D TranAbstract:Abstract Background aims Non-obese diabetic mice (NOD) exhibit autoimmune Sjogren-like disease (SS-like). We reported previously that a combined-therapy consisting of immuno- and Cell-based therapy rescued NOD from SS-like. However, therapies tested to date on NOD mice were aimed at the initial phase of SS-like. It is unknown whether therapies are effective in restoring salivary function when given at an advanced phase of SS-like. Methods The efficacy of two therapies (bone marrow versus Spleen Cells) was compared head-to-head for halting/reversing salivary hypofunction at two critical time points of SS-like (7-week-old NOD with normal saliva output and 20-week-old NOD with minimal saliva). NOD mice were divided into four groups: (i) control, (ii) complete Freund's adjuvant (CFA), (iii) bone marrow transplants with CFA or (iv) Spleen Cell transplants with CFA. Mice were monitored 8–12 months after therapy. Results Both Cell therapies were effective during the initial phase of SS-like; salivary flow rates were maintained between 80–100% of pre-symptomatic levels. Spleen Cell therapy was better than bone marrow when administered in the initial phase of SS-like. When Cell therapies were given at an advanced phase of SS-like (20 weeks and older), salivary flow rates improved but were at best 50% of pre-symptomatic levels. Both Cell therapies decreased tumor necrosis factor-α, transforming growth factor-β1 levels and T and B Cells while increasing epidermal growth factor and regulatory T Cells. Elevated serum epidermal growth factor levels were measured in Spleen-treated mice. Conclusions A therapeutic effect in advanced phase disease, albeit in mice, holds promise for humans in which Sjogren syndrome is generally not diagnosed until a late stage.
Simon D Tran - One of the best experts on this subject based on the ideXlab platform.
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treatment for salivary gland hypofunction at both initial and advanced stages of sjogren like disease a comparative study of bone marrow therapy versus Spleen Cell therapy with a 1 year monitoring period
Cytotherapy, 2014Co-Authors: Saeed Khalili, Denise L Faustman, Yoshinori Sumita, David Blank, Alan C Peterson, Shohta Kodama, Simon D TranAbstract:Abstract Background aims Non-obese diabetic mice (NOD) exhibit autoimmune Sjogren-like disease (SS-like). We reported previously that a combined-therapy consisting of immuno- and Cell-based therapy rescued NOD from SS-like. However, therapies tested to date on NOD mice were aimed at the initial phase of SS-like. It is unknown whether therapies are effective in restoring salivary function when given at an advanced phase of SS-like. Methods The efficacy of two therapies (bone marrow versus Spleen Cells) was compared head-to-head for halting/reversing salivary hypofunction at two critical time points of SS-like (7-week-old NOD with normal saliva output and 20-week-old NOD with minimal saliva). NOD mice were divided into four groups: (i) control, (ii) complete Freund's adjuvant (CFA), (iii) bone marrow transplants with CFA or (iv) Spleen Cell transplants with CFA. Mice were monitored 8–12 months after therapy. Results Both Cell therapies were effective during the initial phase of SS-like; salivary flow rates were maintained between 80–100% of pre-symptomatic levels. Spleen Cell therapy was better than bone marrow when administered in the initial phase of SS-like. When Cell therapies were given at an advanced phase of SS-like (20 weeks and older), salivary flow rates improved but were at best 50% of pre-symptomatic levels. Both Cell therapies decreased tumor necrosis factor-α, transforming growth factor-β1 levels and T and B Cells while increasing epidermal growth factor and regulatory T Cells. Elevated serum epidermal growth factor levels were measured in Spleen-treated mice. Conclusions A therapeutic effect in advanced phase disease, albeit in mice, holds promise for humans in which Sjogren syndrome is generally not diagnosed until a late stage.
Yoshinori Sumita - One of the best experts on this subject based on the ideXlab platform.
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treatment for salivary gland hypofunction at both initial and advanced stages of sjogren like disease a comparative study of bone marrow therapy versus Spleen Cell therapy with a 1 year monitoring period
Cytotherapy, 2014Co-Authors: Saeed Khalili, Denise L Faustman, Yoshinori Sumita, David Blank, Alan C Peterson, Shohta Kodama, Simon D TranAbstract:Abstract Background aims Non-obese diabetic mice (NOD) exhibit autoimmune Sjogren-like disease (SS-like). We reported previously that a combined-therapy consisting of immuno- and Cell-based therapy rescued NOD from SS-like. However, therapies tested to date on NOD mice were aimed at the initial phase of SS-like. It is unknown whether therapies are effective in restoring salivary function when given at an advanced phase of SS-like. Methods The efficacy of two therapies (bone marrow versus Spleen Cells) was compared head-to-head for halting/reversing salivary hypofunction at two critical time points of SS-like (7-week-old NOD with normal saliva output and 20-week-old NOD with minimal saliva). NOD mice were divided into four groups: (i) control, (ii) complete Freund's adjuvant (CFA), (iii) bone marrow transplants with CFA or (iv) Spleen Cell transplants with CFA. Mice were monitored 8–12 months after therapy. Results Both Cell therapies were effective during the initial phase of SS-like; salivary flow rates were maintained between 80–100% of pre-symptomatic levels. Spleen Cell therapy was better than bone marrow when administered in the initial phase of SS-like. When Cell therapies were given at an advanced phase of SS-like (20 weeks and older), salivary flow rates improved but were at best 50% of pre-symptomatic levels. Both Cell therapies decreased tumor necrosis factor-α, transforming growth factor-β1 levels and T and B Cells while increasing epidermal growth factor and regulatory T Cells. Elevated serum epidermal growth factor levels were measured in Spleen-treated mice. Conclusions A therapeutic effect in advanced phase disease, albeit in mice, holds promise for humans in which Sjogren syndrome is generally not diagnosed until a late stage.
Keina Maciele Dourado - One of the best experts on this subject based on the ideXlab platform.
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anonna muricata l soursop seed oil improves type 1 diabetes parameters in vivo and in vitro
PharmaNutrition, 2018Co-Authors: Laise Cedraz Pinto, Ana Tereza Cerqueiralima, Samara Dos Santos Suzarth, Rayane De Souza, Bruna Tosta, Hugo Da Silva, Anaque Oliveira Pires, Gerson De Almeida Queiroz, Tatiane Oliveira Teixeira, Keina Maciele DouradoAbstract:Abstract Annona muricata have many properties reported as antidiabetic, antitumor and antioxidant effects. However, studies on the use of fruit seeds are limited. In this study, we identified the immunomodulatory potential of A. muricata seed oil (AmSO) in streptozotocin (STZ)-induced in vivo and in vitro experimental model of T1D and whole blood Cell culture from diabetic patients. AmSO cytotoxicity was evaluated by MTT-tetrazolium and resazurin. AmSO was orally administered to BALB/c mice for 48 days and were divided into groups: control, STZ (diabetic), STZ–AmSO (diabetic, treated with 1.0 mg/kg AmSO), and AmSO groups (nondiabetic, treated with 1.0 mg/kg AmSO). T1D was induced with intraperitoneal administration of STZ (3 × 100 mg/kg). Biochemistry and histopathological analysis and area of pancreatic islets were evaluated. IL-10, IL-4, IL-17 production in Spleen Cell culture from diabetic mice exposed to AmSO and IFN-γ and IL-10 levels in whole blood Cell culture from diabetic patients exposed to AmSO was determined by ELISA. AmSO showed antihyperglycemic effect, preserved the area of pancreatic islets, preserved liver tissue, increased IL-4 and IL-10 levels in Spleen Cell culture, and decreased IFN-γ level in whole blood Cell culture. AmSO demonstrated immunomodulatory effect and therapeutic potential for the treatment and/or prevention of clinical T1D.
M. Goldman - One of the best experts on this subject based on the ideXlab platform.
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Spleen Cell cytokine secretion in Mycobacterium bovis BCG-infected mice
Infection and Immunity, 1992Co-Authors: Kris Huygen, J. P. Van Vooren, A. Drowart, Py Vandenbussche, JACQUELINE De Bruyn, Alain Kentos, Daniel Abramowicz, F. Jacobs, M. GoldmanAbstract:Three susceptible mouse strains, i.e., BALB/c (H-2d), C57BL/6 (H-2b), and major histocompatibility complex-congenic BALB.B10 (H-2b), were infected intravenously with 4 x 10(6) CFU of live Mycobacterium bovis BCG and analyzed 4 weeks later for in vitro Spleen Cell cytokine secretion in response to purified protein derivative (PPD), BCG culture filtrate (CF), BCG Cellular extract, total BCG, the purified extraCellular 30-32-kDa antigen (the fibronectin-binding antigen 85), or the intraCellular 65-kDa heat shock protein. C57BL/6 and BALB.B10 mice produced 5- to 10-fold more gamma interferon and interleukin-2 (IL-2) when stimulated with CF, PPD, and antigen 85 than BALB/c mice did. When stimulated with BCG extract and whole BCG, gamma interferon and IL-2 levels were generally lower and comparable in the three strains. IL-4 was detected in Spleen Cell culture supernatants from infected BALB/c mice but not from C57BL/6 or BALB.B10 mice. IL-5 could not be detected. C57BL/6 and BALB.B10 Spleen Cells also produced more tumor necrosis factor alpha and IL-6 after stimulation with PPD and CF than BALB/c Cells did. Finally, BCG vaccination generated efficient protective immunity in C57BL/6 and BALB.B10 mice but not in BALB/c mice. These data suggest that secreted mycobacterial CF antigens selectively induce a strong TH1 response in BCG-infected C57BL/6 and BALB.B10 mice, whereas in BALB/c mice this response is partly counterbalanced by TH2 Cells.