Methods to determine intestinal permeability and bacterial translocation during liver disease

Wang, Lirui; Llorente, Cristina; Hartmann, Phillipp; Yang, Anne Yuqing; Chen, Peng; Schnabl, Bernd

doi:10.1016/j.jim.2014.12.015

Cited by 211 publications

(206 citation statements)

References 101 publications

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“…Although a direct causal connection between winter fasting per se and these immune changes has not been shown, it is possible that some or all are adaptations to minimize deleterious effects of the increased gut permeability that accompanies hibernation (71,75). Elevated permeability can increase movement of bacterial products, such as lipopolysaccharide (LPS), across the epithelium and induce inflammation in the intestine and other organs (573). In support, hibernation is associated with increased epithelial expression of Toll-like receptor TLR5, and reduced expression of TLR4 (144).…”

Section: Fasting and The Immune Systemmentioning

confidence: 99%

Integrative Physiology of Fasting

Secor

Carey

2016

Comprehensive Physiology

135

144

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Extended bouts of fasting are ingrained in the ecology of many organisms, characterizing aspects of reproduction, development, hibernation, estivation, migration, and infrequent feeding habits. The challenge of long fasting episodes is the need to maintain physiological homeostasis while relying solely on endogenous resources. To meet that challenge, animals utilize an integrated repertoire of behavioral, physiological, and biochemical responses that reduce metabolic rates, maintain tissue structure and function, and thus enhance survival. We have synthesized in this review the integrative physiological, morphological, and biochemical responses, and their stages, that characterize natural fasting bouts. Underlying the capacity to survive extended fasts are behaviors and mechanisms that reduce metabolic expenditure and shift the dependency to lipid utilization. Hormonal regulation and immune capacity are altered by fasting; hormones that trigger digestion, elevate metabolism, and support immune performance become depressed, whereas hormones that enhance the utilization of endogenous substrates are elevated. The negative energy budget that accompanies fasting leads to the loss of body mass as fat stores are depleted and tissues undergo atrophy (i.e., loss of mass). Absolute rates of body mass loss scale allometrically among vertebrates. Tissues and organs vary in the degree of atrophy and downregulation of function, depending on the degree to which they are used during the fast. Fasting affects the population dynamics and activities of the gut microbiota, an interplay that impacts the host's fasting biology. Fasting-induced gene expression programs underlie the broad spectrum of integrated physiological mechanisms responsible for an animal's ability to survive long episodes of natural fasting.

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Section: Fasting and The Immune Systemmentioning

confidence: 99%

Integrative Physiology of Fasting

Secor

Carey

2016

Comprehensive Physiology

135

144

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“…a measure of health or infection-induced damage) against parasite load, where a steeper slope means lower tolerance [15]. We measured the effect of infection on host health/fitness in two ways: (i) relative weight change during the experiment, (ii) intestinal permeability to macromolecules (as an indication of tissue damage at the site of infection [16]; increased permeability impairs nutrient absorption and can lead to inflammatory disease [17,18]). Our aim was to test if nutritional status affected the slope of the relationship between each of these health measures and parasite load.…”

Section: Introductionmentioning

confidence: 99%

Effects of protein malnutrition on tolerance to helminth infection

2016

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Infection tolerance is the ability of a host to limit the health effects of a given parasite load. A few recent studies have demonstrated genetic variation for tolerance, but little is known about how environmental factors affect tolerance. Here, we used the intestinal nematode Heligmosomoides polygyrus in laboratory mice to test for effects of protein malnutrition on tolerance. We performed an experiment where two different mouse strains (CBA and BALB/c) were fed either adequate-protein food or low-protein food, and trickle-infected with different doses of H. polygyrus larvae during four weeks. We found that protein malnutrition decreases tolerance measured as intestinal barrier function, but only in one of the strains (BALB/c); that is, there was a host genotype-byenvironment interaction for tolerance. We conclude that nutritional status can affect tolerance and that sensitivity of tolerance to malnutrition may differ between host genotypes.

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“…Methodological problems should be taken into account when interpreting these conflicting results [76,81]. Some authors used sugars [69,70,82], whereas others used isotope probes [68,71,72,73]; the latter are considered to be the gold standard, since these probes are not synthesized or digested in the human body [68].…”

Section: Intestinal Hyperpermeabilitymentioning

confidence: 99%

Changes of Intestinal Functions in Liver Cirrhosis

2016

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Background: Understanding of the gut-liver axis is important for the up-to-date management of liver cirrhosis, and changes of intestinal functions form the core of this interesting research field. Summary: Most investigators noted small intestinal dysmotility in their patients with liver cirrhosis. Marked changes in the contraction pattern were observed in early manometric studies. The orocecal transit time, particularly small intestinal transit, has generally been reported to be prolonged, which has been demonstrated in multiple investigations to be related to the severity of the liver disease (e.g., Child-Pugh class), the presence of small intestinal bacterial overgrowth (SIBO) and hepatic encephalopathy (HE) as well as a history of spontaneous bacterial peritonitis. Bacteriologically proven SIBO in proximal jejunal aspiration has been reported to be present in up to 59% of cirrhotic patients and is associated with systemic endotoxemia. Clinical and experimental studies suggest that delayed small bowel transit in liver cirrhosis may lead to SIBO, which could contribute to the symptoms of abdominal pain and diarrhea. In addition to autonomic neuropathy, metabolic derangements and diabetic state, SIBO itself may delay intestinal transit in cirrhotic patients. Several studies, both from the West and the East, have shown that the gut microbiota is altered in cirrhotic patients and particularly those with HE. Further, a quantitative change in Bacteroides/Firmicutes ratio, with a prevalence of potentially pathogenic bacteria (e.g., Enterobacteriaceae) and reduction in specific commensals (e.g., Lachnospiraceae), has been described. Structural and functional changes in the intestinal mucosa that contribute to increases in intestinal permeability for bacteria and their products have been observed in patients with liver cirrhosis, which is considered as an important pathogenetic factor for several complications. The mechanism of intestinal barrier dysfunction in cirrhosis is multifactorial, including alcohol, portal hypertension (vascular congestion and dysregulation), endotoxemia, SIBO, local inflammation and, most likely, immunological factors and medications. Key Messages: This review summarizes major achievements regarding intestinal dysfunction in cirrhosis for future gastroenterology research. The question of whether this intestinal barrier dysfunction is accompanied and/or at least partly caused by structural and functional changes in the epithelial tight junction proteins is as yet unsolved. Development of new strategies to modulate gut-liver interaction is urgently needed.

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Methods to determine intestinal permeability and bacterial translocation during liver disease

Cited by 211 publications

References 101 publications

Integrative Physiology of Fasting

Integrative Physiology of Fasting

Effects of protein malnutrition on tolerance to helminth infection

Changes of Intestinal Functions in Liver Cirrhosis

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