gliadin/kansè

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Anticancer drug-loaded gliadin nanoparticles induce apoptosis in breast cancer cells.

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Nanoscale drug carriers play an important role in regulating the delivery, permeability, and retention of the drugs. Although various carriers have been used to encapsulate anticancer drugs, natural biomaterials are of great benefit for delivery and controlled release of drugs. We used the

Two Japanese cases of dermatitis herpetiformis associated each with lung cancer and autoimmune pancreatitis but showing no intestinal symptom or circulating immunoglobulin A antibodies to any known antigens.

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Dermatitis herpetiformis (DH) is common in some Caucasian populations but extremely rare in Japanese, probably because of different immunogenetic backgrounds. We report two Japanese DH cases with typical clinical, histological and direct immunofluorescence features. However, no symptom of

Expression of tumour necrosis factor-alpha, interleukin-6, and interleukin-2 mRNA in the jejunum of patients with coeliac disease.

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BACKGROUND A T-cell-mediated immune response may be responsible for the enteropathy seen in coeliac disease (CD), but it is unclear whether this is initiated in the epithelium or the lamina propria. We studied the site and number of cells expressing mRNA encoding the cytokines interleukin-2 (IL-2),

Dietary glycosaminoglycans interfere in bacterial adhesion and gliadin-induced pro-inflammatory response in intestinal epithelial (Caco-2) cells.

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Dietary components may have an important role in maintaining a balanced gut microbiota composition. Celiac disease is an autoimmune enteropathy caused by gliadins, and has been associated with a reduced proportion of Bifidobacterium in gut microbiota. This study evaluates the influence of

Involvement of gliadin, a component of wheat gluten, in increased intestinal permeability leading to non-steroidal anti-inflammatory drug-induced small-intestinal damage.

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Gliadin, a component of wheat gluten known to be an important factor in the etiology of celiac disease, is related to several other diseases through its enhancing effect on intestinal paracellular permeability. We investigated the significance of gliadin in non-steroidal anti-inflammatory drug

Immunomodulatory effects of Lactobacillus casei administration in a mouse model of gliadin-sensitive enteropathy.

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Coeliac disease (CD) is a very common food-sensitive enteropathy, which is triggered by gluten ingestion and is mediated by CD4(+) T cells. In addition, alterations in the intestinal microbiota that is normally involved in the homeostasis of GALT (gut-associated lymphoid tissue) seem to play a role

Identification of a novel immunomodulatory gliadin peptide that causes interleukin-8 release in a chemokine receptor CXCR3-dependent manner only in patients with coeliac disease.

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The autoimmune enteropathy, coeliac disease (CD), is triggered by ingestion of gluten-containing grains. We recently reported that the chemokine receptor CXCR3 serves as a receptor for specific gliadin peptides that cause zonulin release and subsequent increase in intestinal permeability. To explore

Bifidobacteria inhibit the inflammatory response induced by gliadins in intestinal epithelial cells via modifications of toxic peptide generation during digestion.

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Celiac disease (CD) is a chronic enteropathy triggered by intake of gliadin, the toxic component of gluten. This study aims at evaluating the capacity of different Bifidobacterium strains to counteract the inflammatory effects of gliadin-derived peptides in intestinal epithelial (Caco-2) cells. A

Improved Bioavailability of Curcumin in Gliadin-Protected Gold Quantum Cluster for Targeted Delivery.

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This study deals with the synthesis of a gliadin-stabilized gold quantum cluster (AuQC) for the encapsulation of curcumin (CUR) and its targeted delivery to the cancer cell. CUR is an anticancer drug containing a hydrophobic polyphenol derived from the rhizome of Curcuma longa. The

Gliadin stimulates human monocytes to production of IL-8 and TNF-alpha through a mechanism involving NF-kappaB.

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Wheat gliadin is the triggering agent in coeliac disease. In this study, we documented that proteolytic fragments of gliadin, in contrast to other food antigens, induced interleukin (IL)-8 and tumour necrosis factor-alpha (TNF-alpha) production and significantly increased interferon

Impact of Superoxide Dismutase-Gliadin on Radiation-induced Fibrosis: An Experimental Study.

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OBJECTIVE Radiation-induced fibrosis (RIF) has since long been considered as irreversible. Further understanding of its mechanisms has led to trials investigating RIF treatment and prevention. The effect of superoxide dismutase (SOD)-gliadin, an oral form of SOD that resists gastrointestinal

Immune profiling of breast milk from mothers with treated celiac disease.

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The protective effect of breastfeeding on celiac disease (CD) onset is controversial. We studied a wide range of milk components in milk produced by celiac mothers following long-term gluten-free diet (GFD) in comparison to milk produced by healthy

[Enteropathy-type T-cell lymphoma with CD8 and CD56 expression].

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A 54-year-old male presented at a previous hospital with abdominal pain, where the patient was diagnosed as having abdominal and retroperitoneal lymphadenopathies by CT scan, then, he was referred to our hospital for further examination. Upper gastrointestinal endoscopy showed a tumor formation in

Enteropathy associated T cell lymphoma.

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Enteropathy associated T cell lymphoma (EATCL) is the most serious complication of coeliac disease. HLA genotyping shows that patients with EATCL have the coeliac disease associated DQA1*0501, DQB1*0201 phenotype. Other HLA-DR/DQ alleles that may be associated with adult onset coeliac disease appear

Expression of cytotoxic proteins in peripheral T-cell and natural killer-cell (NK) lymphomas: association with extranodal site, NK or Tgammadelta phenotype, anaplastic morphology and CD30 expression.

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Most peripheral T-cell lymphomas (PTCL) express the alphabeta T-cell receptor (TCR) whereas rare PTCL express the gammadelta TCR. Most if not all gammadelta PTCL are extranodal lymphomas and among them, hepatosplenic gammadelta PTCL constitute a distinct clinicopathological entity. Besides alphabeta

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