Effect of oral supplementation of lactobacilli on bacterial translocation in acute liver injury induced by d-galactosamine

Kasravi, F. Behzad; Adawi, Diya; Molin, Göran; Bengmark, S; Jeppsson, Bengt

doi:10.1016/s0168-8278(97)80060-8

Cited by 49 publications

(43 citation statements)

References 37 publications

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“…We have previously shown similar effects for L. plantarum but that was seen after rectal administration (46). In oral administration (47) there was an effect for L. plantarum but not for the other tested strain (L. reuteri ). The mechanisms by which probiotics work and affect bacterial translocation and hepatocellular injury are not fully understood.…”

Section: Aerobicsupporting

confidence: 65%

Probiotic strains ofLactobacillusandBifidobacteriumaffect the translocation and intestinal load ofEnterobacteriaceaedifferently after D-galactosamine-induced liver injury in rats

Osman

Adawi

Ahrné

et al. 2005

Microbial Ecology in Health and Disease

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Department of Surgery, University Hospital Malmö , Lund University, Sweden AbstractIn an acute liver injury model we compared the effects of different Lactobacillus and Bifidobacterium strains on bacterial translocation, intestinal load of Enterobacteriaceae and the extent of liver injury. This was an experimental study carried out in an university hospital in Sweden. Sprague-Dawley rats were divided into six groups: liver injury control and five groups of liver injury with administration of three different Lactobacillus and two Bifidobacterium strains (orally twice daily for 8 days). Liver injury was induced on the eighth day by intraperitoneal injection of D-galactosamine (1.1 g/kg body weight). The main outcome measures were samples collected 24 h after injury. Liver enzymes and bilirubin serum levels, bacterial translocation (to arterial and portal blood, liver and mesenteric lymph nodes), intestinal load of Enterobacteriaceae in relation to lactobacilli and the total bacterial load were evaluated and randomly amplified polymorphic DNA (RAPD) analysis of translocating bacteria was carried out. Lactobacillus plantarum DSM 9843, Lactobacillus gasseri 5B3 and Bifidobacterium infantis DSM 15158 decreased bacterial translocation to the liver compared with the liver injury control group. Lactobacillus paracasei DSM 13434 translocated to the liver. The Enterobacteriaceae count in the caecum decreased in the L. plantarum DSM 9843, L. gasseri 5B3, Bifidobacterium 'urinalis' 3B1 and B. infantis DSM 15158 groups, while all the administered probiotics decreased it in the colon. The levels of alanine aminotransferase (ALT) and bilirubin were significantly lower in the L. plantarum DSM 9843 and B. infantis DSM 15158 groups compared with the liver injury control group. All test strains except L. paracasei DSM 13434 inhibited translocation to the liver. Instead, L. paracasei was found in the liver and it also failed to decrease the load of Enterobacteriaceae in caecum. The best strains in protecting the liver during injury were L. plantarum DSM 9843 and B. infantis DSM 15158, as reflected by bilirubin and liver enzymes. Thus, there are major effectual differences between strains/species. In contrast, the phylogenetically most diverse strains, L. plantarum DSM 9843 and B. infantis DSM 15158, exercised the same effects.

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Section: Aerobicsupporting

confidence: 65%

Probiotic strains ofLactobacillusandBifidobacteriumaffect the translocation and intestinal load ofEnterobacteriaceaedifferently after D-galactosamine-induced liver injury in rats

Osman

Adawi

Ahrné

et al. 2005

Microbial Ecology in Health and Disease

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“…This phenomenon has recently been corroborated by experimental studies with induced pancreatitis [10, 11]. It is known, for instance, that Lactobacilli and fibre either alone or in combination, are capable of modulating the immune response and preventing microbial translocation in chemically induced hepatitis [12]. Lactobacillus plantarum 299v ( Lp 299v) can colonise the mucosa of the human gut after oral administration and possesses a pronounced ability to adhere to enterocytes of the human intestinal mucosa, as demonstrated in vitro [13].…”

Section: Introductionmentioning

confidence: 77%

Lactobacillus plantarum Reduces Infection of Pancreatic Necrosis in Experimental Acute Pancreatitis

Mangiante¹,

Colucci²,

Canepari³

et al. 2001

Dig Surg

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Background: Infection is the commonest cause of death in acute pancreatitis. Early reduction of commensal flora (particularly Lactobacillus species) and, at the same time, overgrowth of Enterobacteriaceae, especially Escherichia coli, have recently been described during acute pancreatitis. Lactobacillus plantarum has been shown to be effective in reducing the egress of endotoxin and microbial translocation in several experimental models such as chemically induced hepatitis and ulcerative colitis. Aim: The aim of the study was to determine whether L. plantarum 299v (Lp 299v) is capable of effectively reducing microbial translocation in experimental pancreatitis. Methods: Acute pancreatitis was induced by isolation and ligation of the biliopancreatic duct in Lewis rats weighing 250–350 g. The animals were divided into 3 groups: group A, sham operation; group B, induction of pancreatitis and no further treatment, and group C, induction of pancreatitis + daily administration by gavage of a 5-ml/day suspension of Lp 299v at 0.5–1.0 × 10⁹ bacteria/ml for 8 days, 4 days before and 4 days after induction of pancreatitis. All animals were sacrificed after 96 h. Histological studies and microbiological analyses were performed. Results: At sacrifice, 40/55 animals showed signs of severe pancreatitis. Since acute pancreatitis was the specific disease investigated, only these animals were subjected to further study. In group B, we found pathogenic micro-organisms in the mesenteric lymph nodes in 14/20 animals and in the pancreatic tissue in 10/20. The bacterial flora consisted predominantly of E. coli, Enterococcus faecalis, Pseudomonas and Proteus species. In contrast, when the animals were kept under an ’umbrella’ of Lp 299v, growth of E. faecalis or E. coli were detected only in 4/20 mesenteric lymph node cultures and in 3/20 pancreatic tissue cultures. Conclusions:Lp 299v is effective in reducing microbial translocation in experimental pancreatitis. Treatment with probiotic bacteria seems to be a promising alternative to antibiotic therapy.

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“…The most important of these mechanisms are intestinal colonization resistance, intestinal mucosal barrier, and body reticuloendothelial system function (Wells et al, 1987). Previous studies showed that these mechanisms are severely impaired in some serious diseases, such as acute liver injury, cirrhosis, severe scalding injury and hemorrhagic shock, which could lead to excessive growth of gram negative aerobic bacteria, bacteria and endotoxin translocation, and aggravated liver injury (Li et al, 2004;Chiva et al, 2002;Kasravi et al, 1997;Wang et al, 2002). But data on the relationship between intestinal microflora status and ischemia/reperfusion (I/R) liver injury are not available.…”

Section: Introductionmentioning

confidence: 99%

Intestinal microflora in rats with ischemia/reperfusion liver injury

Xing

Li²,

Xu³

et al. 2005

J Zheijang Univ Sci B

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Abstract:Objectives: To investigate the intestinal microflora status related to ischemia/reperfusion (I/R) liver injury and explore the possible mechanism. Methods: Specific pathogen free grade Sprague-Dawley rats were randomized into three groups: Control group (n=8), sham group (n=6) and I/R group (n=10). Rats in the control group did not receive any treatment, rats in the I/R group were subjected to 20 min of liver ischemia, and rats in the sham group were only subjected to sham operation. Twenty-two hours later, the rats were sacrificed and liver enzymes and malondialdehyde (MDA), superoxide dismutase (SOD), serum endotoxin, intestinal bacterial counts, intestinal mucosal histology, bacterial translocation to mesenteric lymph nodes, liver, spleen, and kidney were studied. Results: Ischemia/reperfusion increased liver enzymes, MDA, decreased SOD, and was associated with plasma endotoxin elevation in the I/R group campared to those in the sham group. Intestinal Bifidobacteria and Lactobacilli decreased and intestinal Enterobacterium and Enterococcus, bacterial translocation to kidney increased in the I/R group compared to the sham group. Intestinal microvilli were lost, disrupted and the interspace between cells became wider in the I/R group. Conclusion: I/R liver injury may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function, which contributes to endotoxemia and bacterial translocation to kidney.

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Effect of oral supplementation of lactobacilli on bacterial translocation in acute liver injury induced by d-galactosamine

Cited by 49 publications

References 37 publications

Probiotic strains ofLactobacillusandBifidobacteriumaffect the translocation and intestinal load ofEnterobacteriaceaedifferently after D-galactosamine-induced liver injury in rats

Probiotic strains ofLactobacillusandBifidobacteriumaffect the translocation and intestinal load ofEnterobacteriaceaedifferently after D-galactosamine-induced liver injury in rats

Lactobacillus plantarum Reduces Infection of Pancreatic Necrosis in Experimental Acute Pancreatitis

Intestinal microflora in rats with ischemia/reperfusion liver injury

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