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Hydrolysates of glycated and heat‐treated peanut 7 S globulin ( A ra h 1) modulate human gut microbial proliferation, survival and adhesion
Author(s) -
Teodorowicz M.,
Świątecka D.,
Savelkoul H.,
Wichers H.,
Kostyra E.
Publication year - 2014
Publication title -
journal of applied microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.889
H-Index - 156
eISSN - 1365-2672
pISSN - 1364-5072
DOI - 10.1111/jam.12358
Subject(s) - library science , biology , microbiology and biotechnology , computer science
Aims Evaluation of an effect of glycation of A ra h 1 on proliferation and survival rate and adhesion of intestinal E nterococcus faecalis , E scherichia coli and L actobacillus acidophilus . Methods and Results Pure Ara h 1 heated at three different temperature conditions (G37, G60 and C145°C) in the presence or absence of glucose was subjected to enzymatic hydrolysis. Impacts of A ra h 1 hydrolysates on the bacterial proliferation, survival rate and adhesion to Caco‐2 cells in mono and heterogeneous cultures were studied with fluorescent techniques: DAPI , LIVE / DEAD staining and FISH . Examined hydrolysates hindered proliferation of E . coli and E nt. faecalis with simultaneous decrease in their survival. Maillard reaction ( MR , glycation) of A ra h 1 did not alter the effect of hydrolysates on bacterial proliferation rate. Hydrolysates modified at 60 and 145°C with glucose altered the profile of immobilized bacteria, mostly by lowering the number of adhering E . coli and promoting the adhesion of bacteria from genera L actobacillus and E nterococcus . Conclusions Ara h1 hydrolysates processed in various ways demonstrated their strong modulatory effect on bacterial proliferation, survival rate and adhesion. Significance and Impact of the Study Reducing the adhesion of opportunistic bacteria by hydrolysates of A ra h 1 glycated at 60 and 145°C, together with modulation of immobilization of beneficial lactobacilli and enterococci, may be of relevance in terms of the physiological status of the intestinal barrier.