IMMUNOMODULATION AND SEPSIS: IMPACT OF THE PATHOGEN

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Abstract
Infection begins when microorganisms overcome host barriers and multiply within host tissues. To contain the infection, the host mounts an inflammatory response that mobilizes defense systems and kills the invading microorganisms. A focal inflammatory response is usually sufficient to eradicate the organisms. However, when it fails to contain the infection, the organisms, their toxins, and numerous host mediators are released into the bloodstream, producing a systemic inflammatory response and organ failure. Microorganisms have coevolved with their hosts, thereby acquiring means of overcoming host defense mechanisms or even taking advantage of innate host responses. Many pathogens avoid recognition by the host or dampen host immune responses via sophisticated pathogen–host interactions. Some pathogens benefit from the inflammatory response. According to current hypotheses regarding the pathogenesis of sepsis, the host generates both an innate immune response identical for all pathogens and an adaptive pathogen-specific response. Determining whether the innate response benefits the pathogen or the host is essential for understanding host–pathogen interactions. In this review, we discuss how pathogens interfere with innate and adaptive immune responses to escape eradication by the host.