IL-1β in bronchial lavage fluid is a non-invasive marker that predicts the viability of the pulmonary graft from the non-heart-beating donor

Non-heart-beating donation in Spain

“…So far no reliable way has been found to make that prediction. 37,38 Conclusion Uncontrolled NHBDs comprise one of the most reliable ways to ameliorate increasing death rates while waiting for an organ. Currently, however, the inherent limitations and complexity make it diffi cult to export the program in other countries.…”

The lectin-like domain of thrombomodulin protects against ischaemia–reperfusion lung injury

“…However, in the setting of ischaemia-reperfusion, it may also have pro-apoptotic effects, and thus contribute to tissue damage [37]. IL-1b plays a critical role in mediating the acute phase of the inflammatory response after ischaemia-reperfusion, and in a pig model of ischaemia-reperfusion injury, BALF levels of IL-1b correlate with graft function, suggesting that it may be a marker of graft viability [5]. Although the LLD of TM interferes with the activity of the proinflammatory HMGB1 [20], the present study did not detect differences in the subcellular pattern of expression of HMGB1 in the lung tissue sections of TM wt/wt versus TM LeD/LeD mice or treated versus sham-treated mice.…”

“…Nonetheless, major insights have recently been gained, and there are several well-defined features. These include: an influx of activated inflammatory cells; the release of pro-inflammatory cytokines [3][4][5]; local and systemic accumulation of chemokines and reactive oxygen species [6]; activation of complement [7]; increases in thromboxanes; cellular apoptosis; and reductions in nitric oxide (reviewed in [1]). Thus, therapeutic strategies have been devised to limit the severity of ischaemia-reperfusion injury with, for example: 1) complement inhibition; 2) neutralisation of interleukin (IL)-8 [8]; 3) use of antioxidants [8,9]; 4) use of vasodilators, such as nitric oxide; 5) inhibition of macrophage activation [10]; 6) interference with leukocyte adhesion [11,12]; 7) blocking generation of inflammatory arachidonic acid metabolites [13]; 8) suppression of the nuclear factor (NF)-kB pro-inflammatory signalling pathway [14]; and 9) promoting cell survival [15,16].…”

Donors after cardiocirculatory death and lung transplantation

“…They found a strong correlation between the increase of IL1beta concentration and the increase in pulmonary vascular resistance, mean airway pressure, and wet-to-dry weight ratio. They concluded that IL-1 beta in bronchial lavage fluid might be a useful, non-invasive marker that can predict the viability of the pulmonary graft from the DCD donors (40).…”