Effect of Maillard reaction on biochemical properties of peanut 7S globulin (Ara h 1) and its interaction with a human colon cancer cell line (Caco-2)

Abstract

PurposeThe purpose of this study was to determine the influence of Maillard reaction (MR, glycation) on biochemical and biological properties of the major peanut allergen Ara h 1.MethodsThree different time/temperature conditions of treatment were applied (37, 60, and 145 °C). The extent of MR was assessed by SDS-PAGE, loss of free amino groups, fluorescence intensity, content of bound sugar and fructosamine. The Caco-2 model system was applied to study effects of hydrolysed and non-hydrolysed Ara h 1 on proliferation and interleukin-8 (IL-8) secretion from Caco-2 cells.ResultsWe demonstrated significant differences in the biochemical properties of Ara h 1 glycated at different time/temperature conditions. Glycation of Ara h 1 at 37 °C was shown to cause least biochemical changes, not limiting pepsin hydrolysis. Loss of free amino groups, increase of fluorescence and brown colour of Ara h 1 glycated at 60 and 145 °C indicated advanced and final stages of MR. Non-treated Ara h 1 inhibited Caco-2 cell proliferation and stimulated IL-8 secretion. This effect was less pronounced for glycated Ara h 1. Incubation of Caco-2 cells with non-hydrolysed Ara h 1, glycated at the temperature of 37 and 60 °C, did not stimulate IL-8 secretion.ConclusionEach applied time/temperature-treatment combination caused different biochemical changes of Ara h 1, underlining diversity of formed MRPs. MR, independently of temperature/time conditions, reduced the pro-inflammatory properties of native Ara h 1, reflected in stimulation of IL-8 secretion from intestinal epithelial cells.

Peanut Allergens Alter Intestinal Barrier Permeability and Tight Junction Localisation in Caco-2 Cell Cultures1

“…Therefore, if the redistribution or loss of JAM-A homodimerisation at the TJ results in increased epithelial proliferation, then it is likely that peanut lectin is not the cause but may be the additional constituents contained within the PE treatment. In contrast to this, Ara h 1 has recently been observed to prevent cell proliferation [56], therefore any proliferative response as a result of decreased JAM-A homodimerisation may be ameliorated by the preventative action of Ara h 1. This remains an area for more extensive research to ascertain the role of JAM-A in intestinal epithelial barrier integrity reduction and cellular proliferation after exposure to peanut.…”

“…Movement of JAM-A to the apical membrane in response to inflammatory mediators has also been observed in brain endothelial cells [55]. It is possible that the inflammatory response produced after exposure of Caco-2 cells to peanut allergens Ara h 1 [56] and Ara h 2 [10] may be the cause of the redistribution of JAM-A within the cell.…”

Effect of boiling on the structure and immunoreactivity of recombinant peanut protein Ara h 1

“…However, several studies have testified that thermal processing can enhance or reduce the immunoreactivity of peanuts (Rao et al, 2016;Shen et al, 2015;Teodorowicz et al, 2013). Boiling has been proved by researches that can reduce the allergenicity of peanut allergens mainly because the low-molecular-weight allergens that existed inside of the peanut kernel would transfer into the cooking water (Schmitt, Nesbit, Hurlburt, Cheng, & Maleki, 2010;Starkl, 2011), and thus produce a relatively low sensitivity peanut maintaining decreased content of allergen.…”

“…Allergy to peanut is a common, severe and generally persistent medical disorder, affecting more than 1% of children all over the world (Sicherer & Sampson, 2014;Teodorowicz, Fiedorowicz, Kostyra, Wichers, & Kostyra, 2013). There are currently no effective therapies for peanut allergy; peanut-free diet is the only option for patients (Burks et al, 2015;Hurlburt, McBride, Nesbit, Ruan, & Maleki, 2014).…”

The Molecular Basis of Peanut Allergy

“…Further studies in Caco-2 cells, which are a model for intestinal epithelia, demonstrated that RAGE activation by AGEs stimulated MAP-kinases [67]. More recently, AGE-modified Ara h 1 was demonstrated to influence the proliferation of Caco-2 cells, in a manner dependent on the incubation time and temperature, indicating the possibility that specific AGE modifications may be important for influencing the pro-inflammatory network [68]. …”