ABSTRACT
The Mycobacteriumabscessus complex (MABC) is a group of rapidly growing, nontuberculous mycobacteria that are ubiquitous in soil, urban water pipes, swimming pools, and drinking water. Members of the MABC are considered opportunistic pathogens. The aim of this study was to investigate the origins of MABC detected in broncho-lavage (BL) samples from asymptomatic cancer patients. We turned our attention to washing and disinfection procedures for bronchoscopes; we also assessed water and disinfectant samples. Of 10 BL and 34 environmental samples tested, four BL samples (40%) and seven environmental samples (20.6%) tested positive for MABC. We hypothesized that contamination could arise from the prewashing machine and/or the water used because no patient had clinical or radiological signs consistent with MABC respiratory tract infection. Our study highlights the importance of evaluating cleaning and disinfection procedures for endoscope channels to reduce the potential spread of microorganisms and artefactual results arising from contamination.
ABSTRACT
BACKGROUND: Bile salts (BSs) stimulate cholangiocyte proliferation in vitro and in vivo in normal rats. In this study, we evaluated the effects of BS-enriched diets on cholangiocyte proliferative activity already triggered by partial bile-duct ligation (pBDL), a surgical model that induces mild cholestatic conditions, focusing our attention on ursodeoxycholate (UDC). METHODS: Animals (n=45) were fed either a standard diet, or a 0.2% deoxycholate- or 0.2% UDC-enriched diet for 4 weeks. Then, in each group, ten animals underwent pBDL and five underwent sham operation. Serum and biliary BS levels, serum cholestasis and cytolysis indexes, as well as liver conventional histology, apoptosis and proliferative activity were evaluated 48 h after the operation. RESULTS: Animals that underwent pBDL showed sustained proliferative response compared with sham-operated rats. BS-enriched diets did not influence cholangiocyte proliferation in sham-operated rats. However, significantly increased proliferation was observed in pBDL rats fed a UDC-enriched diet. The evaluation of humoral and histological parameters excluded the possibility that the increased proliferation induced by UDC-enriched diet could be related to concomitant liver cell damage. CONCLUSION: A UDC-enriched diet is able to amplify the magnitude of the cholangiocyte hyperplastic process, which occurs by a stimulatory mechanism after partial bile-duct ligation.
Subject(s)
Bile Ducts/drug effects , Cholagogues and Choleretics/pharmacology , Cholestasis, Extrahepatic , Deoxycholic Acid/pharmacology , Ursodeoxycholic Acid/pharmacology , Administration, Oral , Animals , Bile Ducts/pathology , Bile Ducts/surgery , Cell Division/drug effects , Cholagogues and Choleretics/administration & dosage , Cholestasis, Intrahepatic/blood , Cholestasis, Intrahepatic/etiology , Cholestasis, Intrahepatic/pathology , Deoxycholic Acid/administration & dosage , Diet , Disease Models, Animal , Ligation , Liver/chemistry , Liver/drug effects , Liver/pathology , Liver Function Tests , Proliferating Cell Nuclear Antigen/analysis , Rats , Rats, Inbred F344 , Ursodeoxycholic Acid/administration & dosageABSTRACT
Hepatitis B virus (HBV) transgenic mice (official designation, Tg [Alb-1 HBV] Bri 44) invariably develop macroscopically evident tumors within the 20th month of life. Sustained proliferative activity seems to play an important role in the development of these lesions. We previously showed that ursodeoxycholate (UDC) stimulates hepatocyte proliferation in various experimental settings. Herein, we tested the assumption that biological factors able to further increase liver cell proliferation, such as UDC, could accelerate tumor development in this animal model. For this study, 22 eight-week-old male transgenic mice were divided into 2 groups; 11 animals received a standard diet, and 11 received a UDC-enriched diet. The 2 groups were further divided into 2 subgroups of 5 and 6 animals each and were sacrificed at 3 and 15 months of age, respectively. These different times were chosen to exclude diet-related toxicity (in 3-month-old mice) and evaluate tumor growth (in 15-month-old mice). In addition, hepatocyte proliferation was assessed in all animals. In 3-month-old mice receiving UDC, cholestatic and cytolytic indices as well as liver histology were comparable to those in controls. At 15 months, all UDC-treated mice showed large multinodular tumors whereas only 33% of controls developed smaller uninodular neoplasms. Hepatocyte proliferation was increased in all animals receiving UDC compared with controls. In conclusion, the increase in serum UDC (undetectable in mice fed a standard diet), in the absence of any toxic effect on the liver, suggests the involvement of this bile salt in the stimulation of hepatocyte proliferation and tumor growth.
