Editoriale

Non vi è dubbio che, nel bene come nel male, la mobilitazione popolare riveli sempre un potenziale trasformativo notevole, se non notevolissimo. Può esprimersi come potenza sublime e magmatica che – historia docet – non necessariamente porta caos e distruzione, neppure quando scuote le istituzioni alle fondamenta. Genera e nutre crisi; e «la crise de la démocratie – come rimarca il filosofo francese Paul Ricœur – est une crise double où se conjuguent un mouvement ascendant et un mouvement descendant, des menaces fécondes et des menaces ruineuses». Insomma, la crisi genera e nutre nuove energie e idee, fusione di orizzonti, rifondazione, nuovi slanci. In fin dei conti, la mobilitazione popolare è, già in quanto possibilità, un caposaldo della vita democratica. Ancora Ricœur evidenzia che «La démocratie est une idée en devenir et en combat. C’est une histoire commencée que nous avons la tâche de continuer. La crise (...) est un moment dans une histoire dont il faut retrouver l’élan». Di quel che accade in uno stato democratico, primo responsabile è il Popolo. E quando la politica si corrompe o è dirottata verso forme autoritarie, il potere a fortiori deve ritornare al Popolo.

Effect of a probiotic beverage consumption (Enterococcus faecium CRL 183 and Bifidobacterium longum ATCC 15707) in rats with chemically induced colitis.

BACKGROUND:Some probiotic strains have the potential to assist in relieving the symptoms of inflammatory bowel disease. The impact of daily ingestion of a soy-based product fermented by Enterococcus faecium CRL 183 and Lactobacillus helveticus 416 with the addition of Bifidobacterium longum ATCC 15707 on chemically induced colitis has been investigated thereof within a period of 30 days. METHODS:Colitis was induced by dextran sulfate sodium. The animals were randomly assigned into five groups: Group C: negative control; Group CL: positive control; Group CLF: DSS with the fermented product; Group CLP: DSS with the non-fermented product (placebo); Group CLS: DSS with sulfasalazine. The following parameters were monitored: disease activity index, fecal microbial analyses, gastrointestinal survival of probiotic microorganisms and short-chain fatty acids concentration in the feces. At the end of the protocol the animals' colons were removed so as to conduct a macroscopical and histopathological analysis, cytokines and nitrite quantification. RESULTS:Animals belonging to the CLF group showed fewer symptoms of colitis during the induction period and a lower degree of inflammation and ulceration in their colon compared to the CL, CLS and CLP groups (p<0.05). The colon of the animals in groups CL and CLS presented severe crypt damage, which was absent in CLF and CLP groups. A significant increase in the population of Lactobacillus spp. and Bifidobacterium spp. at the end of the protocol was verified only in the CLF animals (p<0.05). This group also showed an increase in short-chain fatty acids (propionate and acetate). Furthermore, the intestinal survival of E. faecium CRL 183 and B. longum ATCC 15707 in the CLF group has been confirmed by biochemical and molecular analyzes. CONCLUSIONS:The obtained results suggest that a regular intake of the probiotic product, and placebo to a lesser extent, can reduce the severity of DSS-induced colitis on rats

Representative photomicrographs from the different experimental colon groups, stained with hematoxylin/eosin.

<p><b>Group C:</b> healthy animals that did not receive the products under study. <b>Group C:</b> negative control–healthy animals; <b>Group CL:</b> positive control—DSS; <b>Group CLF:</b> DSS with the fermented product; <b>Group CLP:</b> DSS with the non-fermented product (placebo); <b>Group CLS:</b> DSS with sulfasalazine. (100x and 400x). <b>1:</b> healthy epithelium; <b>2 and 5</b>: epithelium with severe crypt damage, featuring as ulceration area; <b>3 e 4:</b> inflammatory cell infiltrated areas, however with no crypt alteration. n = 10.</p

Agarose gel electrophoresis of PCR products obtained from colonies isolated from feces in different groups of animals.

<p>Column 1: 1kb DNA ladder; column 2: <i>B</i>. <i>longum</i> ATCC 15707; column 3: T0 CLF group (before products administration), column 4: T1 CLF group (after 2 weeks of products administration); column 5: T2 CLF group (after 4 weeks of products administration); column 6: group C; column 7: group CL; column 8: group CLP; column 9: group CLS. <b>Group C:</b> negative control–healthy animals; <b>Group CL:</b> positive control—DSS; <b>Group CLF:</b> DSS with the fermented product; <b>Group CLP:</b> DSS with the non-fermented product (placebo); <b>Group CLS:</b> DSS with sulfasalazine.</p

Cytokines production in colon from different groups after 30 days of experimental protocol.

<p><b>Cytokine in colon.</b> Concentrations of TNF-α (A); IL-1β (B); IL-6 (C); TGF-β (D); IL-10 (E) and NO (F) were measured by ELISA in colon supernatants. Data are presented as mean ± SD. Means with the same letter in the same graphic do not differ (p<0.05) <b>Group C:</b> negative control–healthy animals; <b>Group CL:</b> positive control—DSS; <b>Group CLF:</b> DSS with the fermented product; <b>Group CLP:</b> DSS with the non-fermented product (placebo); <b>Group CLS:</b> DSS with sulfasalazine. n = 10.</p

Colitis induction and products administration during the experimental protocol.

<p>Colitis induction and products administration during the experimental protocol.</p

Fecal SCFA concentration (mM/g) from different groups throughout the experimental period.

<p>Same lowercase letters indicate that there was no difference when comparing times. Same capital letters indicate that there was no difference when comparing groups (Tukey test, p<0.05). <b>Group C:</b> healthy animals that did not receive the products under study. <b>Group C:</b> negative control–healthy animals; <b>Group CL:</b> positive control—DSS; <b>Group CLF:</b> DSS with the fermented product; <b>Group CLP:</b> DSS with the non-fermented product (placebo); <b>Group CLS:</b> DSS with sulfasalazine. <b>T0</b> = before products administration, <b>T1</b> = one week after products administration, <b>T2</b> = colitis induction period, <b>T3</b> = one week after the end of the induction <b>T4</b> = at the end of the experiment. <b>A</b> = acetate, <b>B</b> = propionate, <b>C</b> = butyrate.</p

Plate counts for different microbial groups expressed in logCFU/g.

<p>Plate counts for different microbial groups expressed in logCFU/g.</p