Viable and Heat-Inactivated Bifidobacterium bifidum MIMBb75 Protect the Intestinal Barrier

Irritable bowel syndrome (IBS) is a common disorder of gut–brain interaction (DGBI) of multifactorial genesis. Studies consistently show a disrupted intestinal barrier with increased permeability in IBS patients, regardless of subtype. This allows facultative pathogenic bacteria to translocate into underlying body tissue and to initiate or exacerbate IBS symptoms. Protecting the intestinal barrier is therefore a primary therapeutic target. Bifidobacterium bifidum MIMBb75 has proven its efficacy in IBS both in its viable and heat-inactivated forms. Its efficacy is thought to be mediated by the physical adhesion of B. bifidum MIMBb75 to intestinal epithelial cells, thereby protecting the intestinal barrier. In the present study, we show—using a Caco-2 model—that this strain-specific adhesion is facilitated by the high cell surface hydrophobicity of B. bifidum MIMBb75, which is retained following heat inactivation. In line with these adhesive properties, both viable and heat-inactivated B. bifidum MIMBb75 protect the epithelial barrier, as indicated by an increased transepithelial electrical resistance in Caco-2 monolayers. Together, these findings strongly support a physical mode of action in which both viable and heat-inactivated B. bifidum MIMBb75 adhere to the epithelial surface and act, figuratively, as a protective plaster on the epithelial barrier.