**Abstract**

Sepsis, as a complex entity, comprises multiple pathophysiological mechanisms which bring about high morbidity and mortality. The previous studies showed that the gastrointestinal tract is damaged during sepsis, and its main symptoms include increased permeability, bacterial translocation (BT), and malabsorption. BT is the invasion of indigenous intestinal bacteria via the gut mucosa to other tissues. It occurs in pathological conditions such as disruption of the intestine's ecological balance and mucosal barrier permeability, immunosuppression, and oxidative stress through transcellular/paracellular pathways and initiate an excessive systemic inflammatory response. Thereby, recent clinical and preclinical studies focus on the association between sepsis and intestinal barrier dysfunction. This chapter overviews the current knowledge about the molecular basis of BT of the intestine, its role in the progress of sepsis, detection of BT, and actual therapeutic approaches.

**Keywords:** bacterial translocation, intestinal barrier, inflammation, sepsis, multiple organ failure

### **1. Introduction**

Sepsis has been announced to be a global health priority by the World Health Organization as in 2017, 48.9 million sepsis cases and 11 million sepsis-related deaths were reported worldwide [1, 2]. However, although significant progress has been made regarding the mechanism of sepsis, treatment modalities still have not gone beyond fluid resuscitation, vasopressors, antibiotics, and palliative care, after all [1, 3].

Sepsis is a perilous condition caused by the dysregulated and hyperactive host response to the pathogen. This response leads to an inflammation out of control and eventually multiple organ dysfunction syndrome (MODS), which is the primary cause of sepsis-related deaths. The propulsive force of the severe consequences of sepsis, such as MODS, is the intestines due to its potential to provoke systemic immune response via the injured intestinal epithelia losing its barrier function, and cannot prevent the pathogens and toxins to confined intraluminally and secreting and releasing the pro-inflammatory cytokines into the circulation [1, 3–9]. In this chapter, we aimed to cover the fate of the intestinal barrier (IB) and bacterial translocation (BT) during sepsis along with diagnostic methods and potential therapeutic options for IB dysfunction in the light of this information.
