Alterations in Intestinal Microbial Flora and Human Disease

Mohamed Othman; Roberto Agüero; Henry C. Lin


Curr Opin Gastroenterol. 2008;24(1):11-16. 

In This Article

Abstract and Introduction

Purpose of review: To highlight the evidence supporting the role of altered commensal gut flora in human disease. While the contribution of the indigenous gut microbial community is widely recognized, only recently has there been evidence pointing to indigenous flora in disease.
Recent findings: This review discusses recent evidence pointing to the role of altered commensal gut flora in such common conditions as irritable bowel syndrome and inflammatory bowel disease. Recent studies document the intricate relationship between the vast population of microbes that live in our gut and the human host. Since increased intestinal permeability and immune activation are consequences of an altered host-gut microbial relationship, what are the clinical effects of this shift in relationship?
Summary: We focus on the example of an abnormal expansion of gut microbial flora into the small bowel or small intestinal bacterial overgrowth and discuss the effects of bacterial overgrowth on the human host in acute pancreatitis, bacterial gastroenteritis, irritable bowel syndrome, inflammatory bowel disease, hepatic encephalopathy, and fibromyalgia and burn injury. The identification of the underlying role of altered commensal gut microbiota in these and other human diseases could lead to novel diagnostic and therapeutic strategies that would improve clinical outcome.

Our intestinal microbial flora includes a variety of microorganisms, predominantly bacteria, which colonize the gut of all living organisms. Colonization of the gut begins at birth with the first exposure to the flora of the birth canal. Shortly after birth, hundreds of species of bacteria and archaea establish themselves in the human gastrointestinal tract.[1,2] For decades the importance in human health of gut microbes, commonly referred to as commensal flora, despite advanced knowledge of the microbial world, has been underappreciated. The adult human intestine is home to more than 400 species of microbes, which normally remain confined to the distal gut where the concentration of organisms is approximately 1011 organisms per gram of content (colon) but surprisingly just 100-2 organisms per gram of content in the proximal small intestine.[3] The gut microflora is essential for the development of both the digestive tract itself as well as our immune system, required for the development of tissues such as Peyer's patches and the production of immunoglobulin A.[4] The gut microflora is physically separated from the host by a thin intestinal epithelial barrier. The 'tight junctions' between the cells of the intestinal barrier precisely regulate the transport of molecules while prohibiting the migration of microorganisms;[5,6] however, this selective permeability can be altered directly by bacteria or indirectly via cytokines produced by the immune response of the host.[6,7] One example of the effect of gut microbes on the host is small intestinal bacterial overgrowth (SIBO), described as a proliferation of the distal gut bacterial population, proximally, into the small intestine. SIBO may permit or facilitate translocation of those bacteria or bacterial components (antigen) across the intestinal barrier, with negative consequences to health. In this review, we focus on the effect of altered gut microbiota, as exemplified by SIBO, on the human host in the settings of acute pancreatitis, bacterial gastroenteritis, irritable bowel syndrome, inflammatory bowel disease, hepatic encephalopathy, fibromyalgia and burn injury.


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