Sentence examples for protracted inflammation from inspiring English sources

ARDS is a condition characterized by excessive and protracted inflammation.

However, there might be a disruption of this communication between the brain and the immune system in the course of protracted inflammation, as shown in an arthritis model in rats [ 10].

Production of a diverse repertoire of antigen-specific CD4+ T lymphocytes is essential for a host to respond to emerging microbial threats to create memory for heightened secondary responses to previously encountered pathogens and to suppress immune responses after microbial clearance to avoid tissue damage resulting from excessive or protracted inflammation [ 1].

There is growing evidence that sepsis induces long lasting alterations of transcriptional programs through epigenetic mechanisms that may lead to protracted inflammation, organ failure, sepsis-induced immune suppression (SIIS), secondary infections and death.

The former is represented by a protracted inflammation, characterized by both destruction and healing of the tissue involved in the inflammatory process.

First described in 1967 [ 2, 3], ARDS is an acute life threatening condition characterized by excessive and protracted systemic inflammation.

This supports that protracted Giardia infection, and possibly protracted intestinal inflammation, may have induced PI-IBS and fatigue in this cohort.

He postulates that cytokines secreted by the host during ARDS may favor the growth of some strains of bacteria and consequently explain the association between exaggerated and protracted systemic inflammation and the development of nosocomial infections [ 1].

We hypothesized that cytokines secreted by the host during acute respiratory distress syndrome may indeed favor the growth of bacteria and explain the association between exaggerated and protracted systemic inflammation and the frequent development of nosocomial infections.

In analogy to the situation found in humans, protracted injury and inflammation lead to HCC development in virtually 100% of Mdr2−/− mice by 16 months [14].

Antioxidant treatment in oxidant-induced lung injury has been widely observed to suppress NF-κB activation and the protracted neutrophilic lung inflammation [ 7, 10, 11].