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Hepatocellular carcinoma and food contamination: Ochratoxin A as a great prompter

World Journal of Gastroenterology 2013年第24期19卷 3723-3725页

作者： Raphael JF Felizardo niels os.cmara Division of Nephrology Department of Medicine Federal University of Sao PauloSao Paulo CEP 05508-900 Brazil Department of Immunology Institute of Biomedical Sciences University of S o PauloSao Paulo CEP 05508-900 Brazil

Ochratoxin A (OTA) is a secondary metabolite of Asper-gillus and Penicillium, microorganisms that can be haz-ardous to health when present as food contaminants. OTA is a potent member of a group of mycotoxins. Prolonged exposure to mycotoxins in the diet is related to cancer, among other diseases. Hepatocellular car-cinoma (Hcc) accounts for 70%-90% of primary liver cancers and is the third leading cause of cancer-related deaths worldwide. In a recent study, Ibrahim et al proposed a correlation between the incidence of Hcc and contamination with OTA. Analysis of OTA in serum samples showed that Hcc patients had the highest incidence of OTA of the subjects examined (5-fold higher than that of the control group). OTA levels were significantly increased in Hcc patients. This study demonstrates that chronic exposure to high levels of OTA may be associated with a high risk of liver cancer development. Future epidemiologic studies of Hcc should focus on good practices in food preparation, food storage and the consumption of OTA-containing foods.

关键词： Ochratoxin A Mycotoxin Food contamination Hepatocellular carcinoma Liver cancer Egypt

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cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

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World Journal of Hepatology 2013年第10期5卷 541-549页

作者： clarice Silvia Taemi Origassa niels Olsen Saraiva cmara Laboratory of Experimental and clinical Immunology Nephrology Division Medicine DepartmentFederal University of So Paulo Laboratory of Transplantation Immunobiology Department of Immunology Institute of Biomedical Science ⅣUniversity of So Paulo

The activation of heme oxygenase-1(HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide(cO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and *** addition, the products of the HO-catalyzed reaction, particularly cO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis c and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the cO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of low concentrations of exogenous cO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload(with signs of a chronic hepatitis) and iron deficiency anemia(with paradoxical increased levels of ferritin).Hypoxia induces HO-1 expression in multiple rodent,bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types(endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and cO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury.

关键词： Heme oxygenases Bilirubin Hepatitis c Kupffer cells Polymorphisms Immunoregulatory Hypoxia Liver ischemia

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Intestinal barrier: A gentlemen's agreement between microbiota and immunity

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World Journal of Gastrointestinal Pathophysiology 2014年第1期5卷 18-32页

作者： Andrea Moro caricilli Angela castoldi niels Olsen Saraiva cmara Department of Immunology University of Sao Paulo Department of Medicine Federal University of Sao Paulo

Our body is colonized by more than a hundred trillion commensals, represented by viruses, bacteria and fungi. This complex interaction has shown that the microbiome system contributes to the host's adaptation to its environment, providing genes and functionality that give flexibility of diet and modulate the immune system in order not to reject these symbionts. In the intestine,specifically, the microbiota helps developing organ structures, participates of the metabolism of nutrients and induces immunity. certain components of the microbiota have been shown to trigger inflammatory responses, whereas others, anti-inflammatory *** diversity and the composition of the microbiota,thus, play a key role in the maintenance of intestinal homeostasis and explain partially the link between intestinal microbiota changes and gut-related disorders in humans. Tight junction proteins are key molecules for determination of the paracellular permeability. In the context of intestinal inflammatory diseases, the intestinal barrier is compromised, and decreased expression and differential distribution of tight junction proteins is observed. It is still unclear what is the nature of the luminal or mucosal factors that affect the tight junctionproteins function, but the modulation of the immune cells found in the intestinal lamina propria is hypothesized as having a role in this modulation. In this review,we provide an overview of the current understanding of the interaction of the gut microbiota with the immune system in the development and maintenance of the intestinal barrier.

关键词： Microbiota Immune system Lamina propria Intestinal barrier

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