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155. Bifidobacterium bifidum strain BB1 inhibits TNF-α-induced increase in intestinal epithelial tight junction permeability via TLR-2/TLR-6 receptor complex-dependent stimulation of PPAR-γ and suppression of NF-kB p65

Author

Abdulqadir, Raz, Al-Sadi, Rana, Haque, Mohammad, Gupta, Yash, Rawat, Manmeet, and Ma, Thomas Y.

Abstract

Bifidobacterium bifidum(BB) strain BB1 causes a strain-specific enhancement in intestinal epithelial tight junction (TJ) barrier. TNF-α induces an increase in intestinal epithelial TJ permeability and promotes intestinal inflammation. The major purpose of this study was to delineate the protective effect of BB1 against the TNF-α induced increase in intestinal TJ permeability and to unravel the intracellular mechanisms involved. Previously reported, TNF-α produces an increase in intestinal epithelial TJ permeability in Caco-2 monolayers and in mice. The addition of BB1 inhibited the TNF-α increase in Caco-2 intestinal TJ permeability and mouse intestinal permeability in a strain-specific manner. BB1 inhibited the TNF-α induced increase in intestinal TJ permeability by interfering the with TNF-α induced enterocyte NF-κB p50/p65 and MLCK gene activation. The BB1 protective effect against the TNF-α induced increase in intestinal permeability was mediated by TLR-2/TLR-6 heterodimer complex activation of PPAR-γ and PPAR-γ pathway inhibition of TNF-α induced IKK-α activation, which in turn resulted in a step-wise inhibition of NF-κB p50/p65, MLCK gene, MLCK kinase activity, MLCK-induced opening of the TJ barrier. In conclusion, these studies unravel novel intracellular mechanisms of BB1 protection against the TNF-α induced increase in intestinal TJ permeability. Our data show that BB1 protects against the TNF-α induced increase in intestinal epithelial TJ permeability via a PPAR-γ dependent inhibition of NF-κB p50/p65 and MLCK gene activation.

Published
2024
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156. Cytochalasin B modulation of Caco-2 tight junction barrier: role of myosin light chain kinase

Author

MA, THOMAS Y., HOA, NEIL T., TRAN, DANIEL D., BUI, VUONG, PEDRAM, ALI, MILLS, SUSAN, and MERRYFIELD, MARGARET

Subjects
Permeability -- Research, Protein kinases -- Research, Actin -- Research, Biological sciences
Abstract

Ma, Thomas Y., Neil T. Hoa, Daniel D. Tran, Vuong Bui, Ali Pedram, Susan Mills, and Margaret Merryfield. Cytochalasin B modulation of Caco-2 tight junction barrier: role of myosin light chain kinase. Am J Physiol Gastrointest Liver Physiol 279: G875-G885, 2000.--The intracellular mechanisms that mediate cytochalasin-induced increase in intestinal epithelial tight junction (TJ) permeability are unclear. In this study, we examined the involvement of myosin light chain kinase (MLCK) in this process, using the filter-grown Caco-2 intestinal epithelial monolayers. Cytochalasin B (Cyto B) (5 [micro] g/ml) produced an increase in Caco-2 MLCK activity, which correlated with the increase in Caco-2 TJ permeability. The inhibition of Cyto B-induced MLCK activation prevented the increase in Caco-2 TJ permeability. Additionally, myosin-[Mg.sup.2+] -ATPase inhibitor and metabolic inhibitors (which inhibit MLCK induced actinmyosin contraction) also prevented the Cyto B-induced increase in Caco-2 TJ permeability. Cyto B caused a late-phase (15-30 min) aggregation of actin fragments into large actin clumps, which was also inhibited by MLCK inhibitors. Cyto B produced a morphological disturbance of the ZO-1 TJ proteins, visually correlating with the functional increase in Caco-2 TJ permeability. The MLCK and myosin- [Mg.sup.2+] -ATPase inhibitors prevented both the functional increase in TJ permeability and disruption of ZO-1 proteins. These findings suggested that Cyto B-induced increase in Caco-2 TJ permeability is regulated by MLCK activation. paracellular permeability; myosin light chain kinase; actin filaments; ZO-1 protein.

Published
2000

163. Treatment Plan Adherence to Guidelines in Senior Adult Oncology Patients

Author

Mackenzie, MD, Amy R., Barsevick, PhD, Andrea M., Myers, PhD, Ronald, Koch, MD, Ludmila De Oliveira, Keith, PhD, Scott W., Wolf, MA, Thomas, Cocroft, MA, James, Schoppe, MPH, Joshua, Williams III, Ulysses, Chapman, DO, Andrew, Mackenzie, MD, Amy R., Barsevick, PhD, Andrea M., Myers, PhD, Ronald, Koch, MD, Ludmila De Oliveira, Keith, PhD, Scott W., Wolf, MA, Thomas, Cocroft, MA, James, Schoppe, MPH, Joshua, Williams III, Ulysses, and Chapman, DO, Andrew

Abstract

Materials & Methods: Review of 287 records Patients ≥ 65 years old with new diagnosis of cancer Seen by 6, dual-boarded hematologists/ oncologists practicing in an urban academic cancer center Treatment plans compared to national guidelines to determine plan adherence status Patients were recommended: Adherent plan (AP) or Non-adherent plan (N-AP)

Published
2015

165. Expression of Programmed Death-Ligand 1 by Human Colonic CD90+ Stromal Cells Differs Between Ulcerative Colitis and Cohn's Disease and Determines Their Capacity to Suppress Th1 Cells.

Author

Beswick, Ellen J., Grim, Carl, Singh, Abinav, Aguirre, Jose E., Tafoya, Marissa, Suimin Qiu, Rogler, Gerhard, McKee, Rohini, Samedi, Von, Ma, Thomas Y., Reyes, Victor E., Powell, Don W., Pinchuk, Irina V., Bemark, Mats, Bimczok, Diane, and Griffin, Matthew

Subjects
PROGRAMMED cell death 1 receptors, CROHN'S disease, STROMAL cells
Abstract

Background and Aims: The role of programmed cell death protein 1 (PD-1) and its ligands in the dysregulation of T helper immune responses observed in the inflammatory bowel disease (IBD) is unclear. Recently, a novel concept emerged that CD90+ colonic (myo)fibroblasts (CMFs), also known as stromal cells, act as immunosuppressors, and are among the key regulators of acute and chronic inflammation. The objective of this study was to determine if the level of the PD-1 ligands is changed in the IBD inflamed colonic mucosa and to test the hypothesis that changes in IBD-CMF-mediated PD-1 ligand-linked immunosuppression is a mechanism promoting the dysregulation of Th1 cell responses. Methods: Tissues and cells derived from Crohn's disease (CD), ulcerative colitis (UC), and healthy individuals (N) were studied in situ, ex vivo, and in culture. Results: A significant increase in programmed death-ligand 1 (PD-L1) was observed in the inflamed UC colonic mucosa when compared to the non-inflamed matched tissue samples, CD, and healthy controls. UC-CMFs were among the major populations in the colonic mucosa contributing to the enhanced PD-L1 expression. In contrast, PD-L1 expression was decreased in CD-CMFs. When compared to CD-CMFs and N-CMFs, UC-CMFs demonstrated stronger suppression of IL-2, Th1 transcriptional factor Tbet, and IFN-γ expression by CD3/CD28-activated CD4+ T cells, and this process was PD-L1 dependent. Similar observations were made when differentiated Th1 cells were cocultured with UC-CMFs. In contrast, CD-CMFs showed reduced capacity to suppress Th1 cell activity and addition of recombinant PD-L1 Fc to CD-CMF:T cell cocultures partially restored the suppression of the Th1 type responses. Conclusion: We present evidence showing that increased PD-L1 expression suppresses Th1 cell activity in UC. In contrast, loss of PD-L1 expression observed in CD contributes to the persistence of the Th1 inflammatory milieu in CD. Our data suggest that dysregulation of the Th1 responses in the inflamed colonic mucosa of IBD patients is promoted by the alterations in PD-L1 expression in the mucosal mesenchymal stromal cell compartment. [ABSTRACT FROM AUTHOR]

Published
2018
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167. Spinal cord stimulation and the pregnant patient-specific considerations for management: A case series and review of the literature

Author

Stephen D. Pratt, MA Thomas T. Simopoulos Md, Donald J. Bernardini, and Tamara C. Takoudes

Subjects
Pregnancy, integumentary system, business.industry, Chronic pain, General Medicine, medicine.disease, Spinal cord stimulator, Neuromodulation (medicine), law.invention, Anesthesiology and Pain Medicine, medicine.anatomical_structure, Neurology, Quality of life, law, Anesthesia, medicine, Abdomen, Gestation, Neurology (clinical), Peripartum Period, business
Abstract

Objectives: The use of spinal cord stimulation (SCS) is a form of neuromodulation used to treat chronic pain in those patients who are refractory to conventional medical management. Not uncommonly, SCS can dramatically improve a patient’s quality of life, and those who are in the childbearing years may go on to become pregnant. The purpose of this case series is to describe: 1) implantation considerations in women of childbearing age; 2) use of rechargeable systems; 3) the obstetric and anesthetic concerns in patients with spinal cord stimulators; 4) risks of using SCS in the peripartum period. Materials and Methods: Two female patients with complex regional pain syndrome I (CRPS I) who were well managed with SCS became pregnant. In both patients, the leads were placed through the T12/L1 interspace and the generator was placed in the buttock region. In the first patient, the device was deactivated prior to conception and maintained off for the duration of the pregnancy. The second patient became pregnant on two separate occasions, with active SCS for a portion of the first trimester. During her second pregnancy, the patient elected to use of SCS at 30 weeks’ gestation. Results: The developing fetuses with intrauterine exposure to SCS were followed out for a minimum of two years and are developmentally normal. The physical presence of the device did not complicate obstetric or anesthetic care. Rechargeable SCS systems were not adversely affected when turned off for the duration of the pregnancy. Conclusion: Implantation of SCS devices in women of childbearing years should take into account the future needs of both obstetric and anesthetic care by avoiding the abdomen and lower lumbar spine whenever possible. There was no appreciable decline of battery capacity in present day constant current rechargeable generators when deactivated for the duration of pregnancy.

Published
2011

175. IL-1β Causes an Increase in Intestinal Epithelial Tight Junction Permeability1

Author

Al-Sadi, Rana M. and Ma, Thomas Y.

Subjects
Curcumin, Pyrrolidines, Interleukin-1beta, NF-kappa B, Membrane Proteins, Apoptosis, Article, Permeability, Tight Junctions, Thiocarbamates, Occludin, Humans, RNA, Messenger, Caco-2 Cells, Intestinal Mucosa
Abstract

IL-1beta is a prototypical proinflammatory cytokine that plays a central role in the intestinal inflammation amplification cascade. Recent studies have indicated that a TNF-alpha- and IFN-gamma-induced increase in intestinal epithelial paracellular permeability may be an important mechanism contributing to intestinal inflammation. Despite its central role in promoting intestinal inflammation, the role of IL-1beta on intestinal epithelial tight junction (TJ) barrier function remains unclear. The major aims of this study were to determine the effect of IL-1beta on intestinal epithelial TJ permeability and to elucidate the mechanisms involved in this process, using a well-established in vitro intestinal epithelial model system consisting of filter-grown Caco-2 intestinal epithelial monolayers. IL-1beta (0-100 ng/ml) produced a concentration- and time-dependent decrease in Caco-2 transepithelial resistance. Conversely, IL-1beta caused a progressive time-dependent increase in transepithelial permeability to paracellular marker inulin. IL-1beta-induced increase in Caco-2 TJ permeability was accompanied by a rapid activation of NF-kappaB. NF-kappaB inhibitors, pyrrolidine dithiocarbamate and curcumin, prevented the IL-1beta-induced increase in Caco-2 TJ permeability. To further confirm the role of NF-kappaB in the IL-1beta-induced increase in Caco-2 TJ permeability, NF-kappaB p65 expression was silenced by small interfering RNA transfection. NF-kappaB p65 depletion completely inhibited the IL-1beta-induced increase in Caco-2 TJ permeability. IL-1beta did not induce apoptosis in the Caco-2 cell. In conclusion, our findings show for the first time that IL-1beta at physiologically relevant concentrations causes an increase in intestinal epithelial TJ permeability. The IL-1beta-induced increase in Caco-2 TJ permeability was mediated in part by the activation of NF-kappaB pathways but not apoptosis.

Published
2007

189. Francia y el conflicto del Líbano

Author

Clara Mª. Thomas de Antonio

Subjects
Romanic languages, PC1-5498, French literature - Italian literature - Spanish literature - Portuguese literature, PQ1-3999
Abstract

No hay resumen

Published
1989
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