Published online Jun 29, 2020. doi: 10.5500/wjt.v10.i6.162
Peer-review started: February 24, 2020
First decision: April 22, 2020
Revised: May 9, 2020
Accepted: May 21, 2020
Article in press: May 21, 2020
Published online: June 29, 2020
Processing time: 120 Days and 3.8 Hours
Early microbial recognition by the innate immune system is accomplished by Toll-like receptors (TLRs), with resultant initiation of a pro-inflammatory response against infecting organisms. In spite of presence of an abundance of Toll-like receptors on the surface of the liver, gut bacteria does not elicit an inflammatory reaction in healthy individuals due to tolerance to these TLRs, suggesting that the inflammatory responses seen in the liver are the result of breakdown of this tolerance. While orthotopic liver transplantation is often life saving in many instances, death following this procedure is most commonly due to infection that occurs in up to 80% of transplant recipients, most commonly due to microbial causes in up to 70% of cases and viral infections in 20%, while fungal infections affect only 8% of cases. The probability of acquiring infection following hepatic transplantation is heightened due to affection of the innate immune defense mechanisms of the host following this procedure. Single nucleotide polymorphisms of TLRs have been associated with increased likelihood of either development of post-transplant infection or eradication of infecting organism. However, conflicting reports from other studies reveal that prevalence of this single nucleotide polymorphism is not increased in infected patients.
Core tip: Microbial recognition by the innate immunity is accomplished by Toll-like receptors (TLRs). In spite of presence of an abundance of TLRs on the surface of the liver, gut bacteria does not elicit an inflammatory reaction in healthy individuals due to tolerance to these TLRs suggesting that the inflammatory responses seen in the liver are the result of breakdown of this tolerance. The probability of acquiring infection following hepatic transplantation is heightened due to affection of the innate immunity of the host. There is controversy about the association between genetic polymorphism of TLRs with the development of post-transplant infection.