Bacterial Modulation of the Immune Response to Infection and its Consequences

Abstract

Infection begins when microorganisms overcome host barriers and multiply within host tissue. In an effort to contain infection, the host stages an inflammatory reaction to mobilize defense systems and kill the invading microorganisms. In most cases, the activated defense mechanisms lead to eradication of infection through a localized inflammatory reaction. However, when the infectious stimulus cannot be contained within tissues, infectious agents, their toxins, and host-derived mediators are released into the circulation leading to a systemic inflammatory response syndrome and remote organ dysfunction [1]. The pathogenesis of sepsis assumes that microorganisms lead to organ failure through a common pathway of injury. Over the past decade, a large number of host-derived inflammatory mediators have been discovered and implicated in the pathogenesis of sepsis. These mediators have pro-and/or anti-inflammatory efficacy and are interrelated through complex potentiating and inhibiting pathways with each other [2].