Pathogenesis of infection in surgical patients

PURPOSE OF REVIEW: Despite the application of prophylactic antimicrobial therapy and advanced technologies, infection remains one of the most common causes of morbidity and mortality in surgical patients. Understanding the pathogenesis of surgical infection would offer new insights into the development of biomarkers to predict and stratify infection in patients, and to explore specific strategies to minimize this serious postoperative complication. RECENT FINDINGS: The acute nonspecific inflammatory response triggered by endogenous danger signals evoked by surgical insult is beneficial, while paradoxically associated with reduced resistance to infection. There is growing evidence indicating that primed inflammation by surgical insult exaggerates the dysregulation of the immune-inflammatory response to the invasion of pathogens postoperatively. Innate immune receptors, such as Toll-like receptors (TLRs), contribute to detecting both pathogen-associated molecular patterns and endogenous damage-associated molecular patterns, and to further amplifying inflammatory responses to infection. Current evidence shows the fascinating role of non-TLRs in the process of infection. Non-TLRs, such as membrane-associated triggering receptor expressed on myeloid cells family, cytosolic nucleotide-binding oligomerization domain-like receptors and nuclear receptor nuclear family 4 subgroup A receptors, are also crucial in triggering the immune responses and mounting an effective defense against surgical insults and the second hit of infection. SUMMARY: Understanding the pivotal role of non-TLRs in sensing exogenous and endogenous molecules, and the influence of primed systemic inflammation and depressed immune status on the defense against pathogen after surgical insult, would be helpful to fully explore the relevant sophisticated phenomena of surgical infection, and to elucidate the occurrence of heterogeneous constellations of clinical signs and symptoms among this special population.