Use of Wild Type or Recombinant Lactic Acid Bacteria as an Alternative Treatment for Gastrointestinal Inflammatory Diseases: A Focus on Inflammatory Bowel Diseases and Mucositis

Abstract

The human gastrointestinal tract (GIT) is highly colonized by bacterial communities, which live in a symbiotic relationship with the host in normal conditions. It has been shown that a dysfunctional interaction between the intestinal microbiota and the host immune system, known as dysbiosis, is a very important factor responsible for the development of different inflammatory conditions of the GIT, such as the idiopathic inflammatory bowel diseases (IBD), a complex and multifactorial disorder of the GIT. Dysbiosis has also been implicated in the pathogenesis of other GIT inflammatory diseases such as mucositis usually caused as an adverse effect of chemotherapy. As both diseases have become a great clinical problem, many research groups have been focusing on developing new strategies for the treatment of IBD and mucositis. In this review, we show that lactic acid bacteria (LAB) have been capable in preventing and treating both disorders in animal models, suggesting they may be ready for clinical trials. In addition, we present the most current studies on the use of wild type or genetically engineered LAB strains designed to express anti-inflammatory proteins as a promising strategy in the treatment of IBD and mucositis.

Keywords: Lactococcus lactis; genetic engineering; inflammatory bowel diseases; lactic acid bacteria; mucositis.

FIGURE 1

Probiotic LAB anti-inflammatory mechanisms on the intestinal mucosa. (A) Intestinal homeostasis provided by the healthy microbiota role in stimulating ephitelial barrier components such as mucus, Paneth cells activity and eliciting protective immune responses such as IgA. (B) The overgrowth of pro-inflammatory mucin-degrading pathobionts induces inflammation in the mucosa. Administration of probiotics prevents inflammatory responses by inhibiting the growth of pathogens directly; increases mucus secretion by goblet cells and the secretion of defensins by Paneth cells; fortificates tight junction stability; stimulates mucosal immunity by inducing IgA production by B cells to the intestinal lumen, limiting harmful microbe adherence and colonization.