Lactobacillus acidophilus protects tight junctions from aspirin damage in HT-29 cells.
OBJECTIVE
Non-steroidal anti-inflammatory drugs cause enterocyte damage inducing an increase of intestinal permeability. Tight junctions are the key structures in the permeability of the intestinal mucosa. ZO-1 is a tight junction associated protein considered a good marker of their integrity. It has been suggested that probiotics could play a protective role in the intestinal barrier function. We determined, in vitro, whether the heat-killed Lactobacillus acidophilus strain LB (LaLB) with its spent culture supernatant protects tight junctions of HT-29 cells from aspirin (ASA) damage.


METHODS
HT-29 cells were treated with ASA alone or ASA and LaLB with its spent culture supernatant together. Morphological alterations of tight junctions were evaluated by immunofluorescence using an anti-ZO-1 antibody. Moreover, a semiquantitative assay for ZO-1 was performed by Western blot.


RESULTS
Immunofluorescence analysis showed a fragmented and granulous ZO-1 staining, after ASA treatment. Using both ASA and LaLB with its spent culture supernatant together, we found a fine continuous linear web at cell-cell contacts similarly to control. Western blot revealed that ASA inhibited ZO-1 expression and LaLB with its spent culture supernatant counteracted this effect.


CONCLUSIONS
This pilot study shows, for the first time, the protective effect of LaLB with its spent culture supernatant on tight junctions from ASA damage. These results suggest that probiotics could play a role in the prevention of ASA-induced alterations of intestinal permeability.
Montalto
Massimo
M
Institute of Internal Medicine, Catholic University, Rome, IT-00168 Italy. mmontalto@rm.unicatt.it
Maggiano
Nicola
N
Ricci
Riccardo
R
Curigliano
Valentina
V
Santoro
Luca
L
Di Nicuolo
Fiorella
F
Vecchio
Fabio Maria
FM
Gasbarrini
Antonio
A
Gasbarrini
Giovanni
G
D000230:Adenocarcinoma / Q000473:pathology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001241:Aspirin / Q000009:adverse effects*; D003110:Colonic Neoplasms / Q000473:pathology; D006801:Humans; D007413:Intestinal Mucosa / Q000473:pathology; D007779:Lactobacillus acidophilus / Q000502:physiology*; D019108:Tight Junctions / Q000502:physiology*; D014407:Tumor Cells, Cultured
D000894:Anti-Inflammatory Agents, Non-Steroidal; D001241:Aspirin