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Intestinal permeability induced by lipopolysaccharide and measured by lactulose, rhamnose and mannitol sugars in chickens

Published online by Cambridge University Press:  24 November 2016

S. Gilani*
Affiliation:
School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy Campus, Adelaide, SA 5371, Australia Poultry Cooperative Research Centre, University of New England, PO Box U242, Armidale, NSW 2351, Australia
G. S. Howarth
Affiliation:
School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy Campus, Adelaide, SA 5371, Australia
S. M. Kitessa
Affiliation:
PPPI Nutrition Research Laboratory, South Australian Research & Development Institute, Roseworthy, SA 5371, Australia Commonwealth Scientific and Industrial Research Organisation, Health and Bio-security, Adelaide, SA, Australia
C. D. Tran
Affiliation:
Commonwealth Scientific and Industrial Research Organisation, Health and Bio-security, Adelaide, SA, Australia School of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, SA 5005, Australia
R. E. A. Forder
Affiliation:
School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy Campus, Adelaide, SA 5371, Australia
R. J. Hughes
Affiliation:
School of Animal and Veterinary Sciences, University of Adelaide, Roseworthy Campus, Adelaide, SA 5371, Australia PPPI Nutrition Research Laboratory, South Australian Research & Development Institute, Roseworthy, SA 5371, Australia
*
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Abstract

Increased intestinal permeability (IP) can lead to compromised health. Limited in vivo IP research has been conducted in chickens. The objectives of the current study were to develop a model of increased IP utilizing lipopolysaccharide (LPS Escherichia coli O55:B5) and to evaluate IP changes using the lactulose, mannitol and rhamnose (LMR) sugar permeability test. In addition, fluorescein isothiocyanate dextran (FITC-d), d-lactate, zonula occludens (ZO-1) and diamine oxidase (DAO) permeability tests were employed. Male Ross chickens were reared until day 14 on the floor in an animal care facility and then transferred to individual cages in three separate experiments. In each of experiments 1 and 2, 36 chicks were randomly allocated to receive either saline (control) or LPS (n=18/group). Lactulose, mannitol and rhamnose sugar concentration in blood was measured at 0, 30, 60, 90, 120 and 180 min in experiment 1, at 60, 90 and 120 min in experiment 2 and at 90 min in experiment 3 (n=16/group). Lipopolysaccharide was injected intraperitoneally at doses of 0.5, 1 and 1 mg/kg BW in experiments 1, 2 and 3, respectively, on days 16, 18 and 20, whereas control received sterile saline. On day 21, only birds in experiments 1 and 2 were fasted for 19.5 h. Chicks were orally gavaged with the LMR sugars (0.25 gL, 0.05 gM, 0.05 gR/bird) followed by blood collection (from the brachial vein) as per time point for each experiment. Only in experiment 3, were birds given an additional oral gavage of FITC-d (2.2 mg/ml per bird) 60 min after the first gavage. Plasma d-lactate, ZO-1 and DAO concentrations were also determined by ELISA in experiment 3 (n=10). Administration of LPS did not affect IP as measured by the LMR sugar test compared with control. This was also confirmed by FITC-d and DAO levels in experiment 3 (P>0.05). The plasma levels of d-lactate were decreased (P<0.05). Plasma levels of ZO-1 were increased in the third experiment only and did not change in the first two experiments. Lipopolysaccharide at doses of 0.5 and 1 mg/kg did not increase IP in this model system. In conclusion, the LMR sugar can be detected in blood 90 min after the oral gavage. Further studies are needed for the applicability of LMR sugars tests.

Type
Research Article
Copyright
© The Animal Consortium 2016 

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