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Probiotics prevent intestinal barrier dysfunction in acute pancreatitis in rats via induction of ileal mucosal glutathione biosynthesis.
PLoS One. 2009; 4(2):e4512.Plos

Abstract

BACKGROUND

During acute pancreatitis (AP), oxidative stress contributes to intestinal barrier failure. We studied actions of multispecies probiotics on barrier dysfunction and oxidative stress in experimental AP.

METHODOLOGY/PRINCIPAL FINDINGS

Fifty-three male Spraque-Dawley rats were randomly allocated into five groups: 1) controls, non-operated, 2) sham-operated, 3) AP, 4) AP and probiotics and 5) AP and placebo. AP was induced by intraductal glycodeoxycholate infusion and intravenous cerulein (6 h). Daily probiotics or placebo were administered intragastrically, starting five days prior to AP. After cerulein infusion, ileal mucosa was collected for measurements of E. coli K12 and (51)Cr-EDTA passage in Ussing chambers. Tight junction proteins were investigated by confocal immunofluorescence imaging. Ileal mucosal apoptosis, lipid peroxidation, and glutathione levels were determined and glutamate-cysteine-ligase activity and expression were quantified. AP-induced barrier dysfunction was characterized by epithelial cell apoptosis and alterations of tight junction proteins (i.e. disruption of occludin and claudin-1 and up-regulation of claudin-2) and correlated with lipid peroxidation (r>0.8). Probiotic pre-treatment diminished the AP-induced increase in E. coli passage (probiotics 57.4+/-33.5 vs. placebo 223.7+/-93.7 a.u.; P<0.001), (51)Cr-EDTA flux (16.7+/-10.1 vs. 32.1+/-10.0 cm/s10(-6); P<0.005), apoptosis, lipid peroxidation (0.42+/-0.13 vs. 1.62+/-0.53 pmol MDA/mg protein; P<0.001), and prevented tight junction protein disruption. AP-induced decline in glutathione was not only prevented (14.33+/-1.47 vs. 8.82+/-1.30 nmol/mg protein, P<0.001), but probiotics even increased mucosal glutathione compared with sham rats (14.33+/-1.47 vs. 10.70+/-1.74 nmol/mg protein, P<0.001). Glutamate-cysteine-ligase activity, which is rate-limiting in glutathione biosynthesis, was enhanced in probiotic pre-treated animals (probiotics 2.88+/-1.21 vs. placebo 1.94+/-0.55 nmol/min/mg protein; P<0.05) coinciding with an increase in mRNA expression of glutamate-cysteine-ligase catalytic (GCLc) and modifier (GCLm) subunits.

CONCLUSIONS

Probiotic pre-treatment diminished AP-induced intestinal barrier dysfunction and prevented oxidative stress via mechanisms mainly involving mucosal glutathione biosynthesis.

Authors+Show Affiliations

Department of Clinical and Experimental Medicine, Division of Surgery, Linköping University, Linköping, Sweden.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19223985

Citation

Lutgendorff, Femke, et al. "Probiotics Prevent Intestinal Barrier Dysfunction in Acute Pancreatitis in Rats Via Induction of Ileal Mucosal Glutathione Biosynthesis." PloS One, vol. 4, no. 2, 2009, pp. e4512.
Lutgendorff F, Nijmeijer RM, Sandström PA, et al. Probiotics prevent intestinal barrier dysfunction in acute pancreatitis in rats via induction of ileal mucosal glutathione biosynthesis. PLoS One. 2009;4(2):e4512.
Lutgendorff, F., Nijmeijer, R. M., Sandström, P. A., Trulsson, L. M., Magnusson, K. E., Timmerman, H. M., van Minnen, L. P., Rijkers, G. T., Gooszen, H. G., Akkermans, L. M., & Söderholm, J. D. (2009). Probiotics prevent intestinal barrier dysfunction in acute pancreatitis in rats via induction of ileal mucosal glutathione biosynthesis. PloS One, 4(2), e4512. https://doi.org/10.1371/journal.pone.0004512
Lutgendorff F, et al. Probiotics Prevent Intestinal Barrier Dysfunction in Acute Pancreatitis in Rats Via Induction of Ileal Mucosal Glutathione Biosynthesis. PLoS One. 2009;4(2):e4512. PubMed PMID: 19223985.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Probiotics prevent intestinal barrier dysfunction in acute pancreatitis in rats via induction of ileal mucosal glutathione biosynthesis. AU - Lutgendorff,Femke, AU - Nijmeijer,Rian M, AU - Sandström,Per A, AU - Trulsson,Lena M, AU - Magnusson,Karl-Eric, AU - Timmerman,Harro M, AU - van Minnen,L Paul, AU - Rijkers,Ger T, AU - Gooszen,Hein G, AU - Akkermans,Louis M A, AU - Söderholm,Johan D, Y1 - 2009/02/18/ PY - 2008/08/02/received PY - 2009/01/18/accepted PY - 2009/2/19/entrez PY - 2009/2/19/pubmed PY - 2009/4/14/medline SP - e4512 EP - e4512 JF - PloS one JO - PLoS One VL - 4 IS - 2 N2 - BACKGROUND: During acute pancreatitis (AP), oxidative stress contributes to intestinal barrier failure. We studied actions of multispecies probiotics on barrier dysfunction and oxidative stress in experimental AP. METHODOLOGY/PRINCIPAL FINDINGS: Fifty-three male Spraque-Dawley rats were randomly allocated into five groups: 1) controls, non-operated, 2) sham-operated, 3) AP, 4) AP and probiotics and 5) AP and placebo. AP was induced by intraductal glycodeoxycholate infusion and intravenous cerulein (6 h). Daily probiotics or placebo were administered intragastrically, starting five days prior to AP. After cerulein infusion, ileal mucosa was collected for measurements of E. coli K12 and (51)Cr-EDTA passage in Ussing chambers. Tight junction proteins were investigated by confocal immunofluorescence imaging. Ileal mucosal apoptosis, lipid peroxidation, and glutathione levels were determined and glutamate-cysteine-ligase activity and expression were quantified. AP-induced barrier dysfunction was characterized by epithelial cell apoptosis and alterations of tight junction proteins (i.e. disruption of occludin and claudin-1 and up-regulation of claudin-2) and correlated with lipid peroxidation (r>0.8). Probiotic pre-treatment diminished the AP-induced increase in E. coli passage (probiotics 57.4+/-33.5 vs. placebo 223.7+/-93.7 a.u.; P<0.001), (51)Cr-EDTA flux (16.7+/-10.1 vs. 32.1+/-10.0 cm/s10(-6); P<0.005), apoptosis, lipid peroxidation (0.42+/-0.13 vs. 1.62+/-0.53 pmol MDA/mg protein; P<0.001), and prevented tight junction protein disruption. AP-induced decline in glutathione was not only prevented (14.33+/-1.47 vs. 8.82+/-1.30 nmol/mg protein, P<0.001), but probiotics even increased mucosal glutathione compared with sham rats (14.33+/-1.47 vs. 10.70+/-1.74 nmol/mg protein, P<0.001). Glutamate-cysteine-ligase activity, which is rate-limiting in glutathione biosynthesis, was enhanced in probiotic pre-treated animals (probiotics 2.88+/-1.21 vs. placebo 1.94+/-0.55 nmol/min/mg protein; P<0.05) coinciding with an increase in mRNA expression of glutamate-cysteine-ligase catalytic (GCLc) and modifier (GCLm) subunits. CONCLUSIONS: Probiotic pre-treatment diminished AP-induced intestinal barrier dysfunction and prevented oxidative stress via mechanisms mainly involving mucosal glutathione biosynthesis. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/19223985/Probiotics_prevent_intestinal_barrier_dysfunction_in_acute_pancreatitis_in_rats_via_induction_of_ileal_mucosal_glutathione_biosynthesis_ L2 - https://dx.plos.org/10.1371/journal.pone.0004512 DB - PRIME DP - Unbound Medicine ER -