Evaluation and Treatment Urosepsis

Ureteral stent-associated infection and sepsis: pathogenesis and prevention: a review

“…These PRRs come in many forms, such as Toll-like receptors (TLRs), CD14, CD18, and selectin, which are typically present on the surface of neutrophils, macrophages, endothelial cells, and urothelial cells. As a result, intracellular messengers, such as nuclear factor-jB and protein-kinase C, are activated, inducing the transcription of important pro-inflammatory cytokines, which include tumor necrosis factor (TNF)-a, interferon gamma (IFNc), interleukin (IL)-1, IL-6, IL-8 and platelet activating factor (PAF) (Farias et al 2015). These factors act cooperatively or antagonistically on target organs, incorporating other mediators such as chemokines, thromboxane, prostaglandins, leukotriene, and endogenous vasodilators such as nitric oxide (NO) (Wagenlehner et al 2013).…”

“…As sepsis persists, a TH2 anti-inflammatory response can take place, which is characterized by immunosuppression, a state which promotes cell healing and recovery, but also predisposes patients to nosocomial infections, which account for the mortality in the longer course of sepsis seen in hospitalized patients (Farias et al 2015). Patients with a suppressed immune system may experience a shift to production of anti-inflammatory cytokines, an absence of normal immune responses to PAMPS, and the death of immune cells.…”