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7. Role of curcumin and the inhibition of NF-kappaB in the onset of chemotherapy-induced mucosal barrier injury.

Author

Land, B. van 't, Blijlevens, N.M.A., Marteijn, J.A.F., Timal, S., Donnelly, J.P., Witte, T.J.M. de, Rabet, L. M', Land, B. van 't, Blijlevens, N.M.A., Marteijn, J.A.F., Timal, S., Donnelly, J.P., Witte, T.J.M. de, and Rabet, L. M'

Abstract

Contains fulltext : 59308.pdf (publisher's version ) (Closed access), The inhibition of nuclear factor kappa B (NF-kappaB) by, for instance, curcumin is becoming an important new approach in combination with chemotherapy or irradiation for the treatment of a variety of cancers including haematological malignancies. A dose-limiting side effect of anticancer therapy in the gastrointestinal tract is mucosal barrier injury. It is hypothesised that mucosal barrier injury is initiated and amplified by proinflammatory-and NF-kappaB-regulated mediators. Therefore, the effect of NF-kappaB inhibition was studied in the onset of mucosal barrier injury. In response to cytostatic drug treatment (arabinoside cytosine (Ara-C) and methotrexate (MTX)), NF-kappaB was activated in intestinal epithelial cells (IEC-6) resulting in an NF-kappaB-related induction of tumour necrosis factor alpha and monocyte chemoattractant protein-1. NF-kappaB inhibition increased the susceptibility of IEC-6 cells to Ara-C as well as MTX-induced cell death when obtained by the addition of caffeic acid phenethyl ester (CAPE), but not using curcumin. In an animal model for MTX-induced mucosal barrier injury, the induction of NF-kappaB-related cytokines and chemokines was detected upon treatment with MTX. Despite increased susceptibility shown in vitro, the inhibition of NF-kappaB resulted in a partial amelioration of villous atrophy normally seen in the small intestine upon MTX treatment. These results show that the inhibition of NF-kappaB does not increase intestinal side effects of the anticancer treatment, suggesting a safe use of curcumin and CAPE in combination with anticancer treatment.

Published
2004

8. Measuring mucosal damage induced by cytotoxic therapy.

Author

Blijlevens, N.M.A., Land, B. van 't, Donnelly, J.P., Rabet, L. M', Pauw, B.E. de, Blijlevens, N.M.A., Land, B. van 't, Donnelly, J.P., Rabet, L. M', and Pauw, B.E. de

Abstract

Contains fulltext : 57267.pdf (publisher's version ) (Closed access), We scored oral mucositis and gut toxicity and measured sugar permeability testing among 56 recipients of a haematopoietic stem cell transplant (HSCT) given myeloablative conditioning with idarubicin, cyclophosphamide and TBI, and a group of 18 patients given cytotoxic chemotherapy for newly diagnosed acute myeloid leukaemia (AML) or myelodysplastic syndrome (MDS). Gut integrity was already disturbed in the AML/MDS group as measured by the lactulose/rhamnose ratio (L/R ratio=0.09) before therapy and was severely perturbed (L/R ratio >0.13) for a month after HSCT. Oral mucositis and to a lesser extent gut toxicity was only significantly correlated with disturbed permeability in the transplant group. The data suggest that sugar permeability, oral mucositis and gut toxicity measure different features of mucosal damage after intensive cytotoxic therapy.

Published
2004

10. Emerging insights into early atherosclerosis in adolescents with chronic disease

Author

Ververs, Francesca Alexandra, Prakken, A.B.J., Garssen, J., Schipper, H.S., Land, B. van 't, and University Utrecht

Subjects
atherosclerosis, chronic disease, juvenile idiopathic arthritis, cystic fibrosis, obesity, coarctation of the aorta, adolescents, MRI, invariant Natural Killer T cell, dyslipidemia
Abstract

Atherosclerosis is a life-long disease process. It remains subclinical for years and presents only after the first decades of life as peripheral artery disease, ischemic heart disease (heart attack), or stroke, together known as cardiovascular disease (CVD). Chronic disease may accelerate atherogenesis due to the presence of inflammatory, metabolic, or hemodynamic risk factors. In the first part of the thesis the “Cardiovascular Disease in Adolescents with Chronic Disease” (CDACD) study results were presented. The cross-sectional study enrolled 114 adolescents 12-18 years old with chronic disorders including juvenile idiopathic arthritis, cystic fibrosis, obesity, corrected coarctation of the aorta, and healthy controls with a corrected atrial septal defect. The study showed that early vascular changes such as an increased pulse wave velocity and wall thickness can be detected in the aorta using MRI in adolescents with chronic disease. In addition, early cardiac changes were detected that suggested that the heart meets greater vascular resistance. These cardiac changes include early signs of relative left ventricular wall thickening in obese adolescents, and significant lower left ventricular global longitudinal strain (LVGLS) in multiple adolescent chronic disease groups. These findings emphasize the need for cardiovascular follow-up of children with chronic disease, and the importance of the aorta for assessment of preclinical atherosclerosis. In the second part of the thesis, iNKT cells were introduced as immune players that couple metabolic derangement to an inflammatory immune response, and in that manner may contribute to atherogenesis. However, we don’t know yet how iNKT cells are activated exactly. The thesis describes our efforts to identify activating antigens and environmental factors. We explored the use of sortase-mediated transpeptidation to isolate CD1d, the antigen-presenting molecule for iNKT cells, and were able to suggest a potential CD1d endogenous ligand. We also explored lipoproteins as potential carriers of iNKT cell antigens and found that the ratio of unhealthy LDL-cholesterol versus HDL-cholesterol may play a role in iNKT cell activation. Ultimately, iNKT cells may be potential immune targets to prevent or decelerate atherosclerosis, but first we must learn a lot more about iNKT cell function in health and disease.

Published
2022

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