The antihypoxia-adenosinergic pathogenesis as a result of collateral damage by overactive immune cells. Export

@article{citeulike:6031325, abstract = {Here, we attract attention to the possibility of iatrogenic exacerbation of immune-mediated tissue damage as a result of the unintended weakening of the tissue-protecting, hypoxia-adenosinergic pathway. These immunosuppressive, anti-inflammatory pathways play a critical and nonredundant role in the protection of normal tissues from collateral damage during an inflammatory response. We believe that it is the tissue hypoxia associated with inflammatory damage that leads to local inhibition of overactive immune cells by activating A2AR and A2BR and stabilizing HIF-1alpha. We show in an animal model of acute lung injury that oxygenation (i.e., inspiring supplemental oxygen) reverses tissue hypoxia and exacerbates ongoing inflammatory lung tissue damage. However, little has been done to carefully investigate and prevent this in a clinical setting. Similarly, the consumption of caffeine antagonizes A2ARs, resulting in exacerbation of ongoing acute inflammation. It is suggested that although the elimination of hypoxia-adenosinergic immunosuppression is desirable to improve vaccines, it is important to take into account the unintentional effects of supplemental oxygen and caffeine, which may increase collateral, inflammatory tissue damage.}, author = {Hatfield, Stephen and Belikoff, Bryan and Lukashev, Dmitriy and Sitkovsky, Michail and Ohta, Akio}, citeulike-article-id = {6031325}, citeulike-linkout-0 = {http://dx.doi.org/10.1189/jlb.0908577}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19564571}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19564571}, doi = {10.1189/jlb.0908577}, issn = {1938-3673}, journal = {Journal of leukocyte biology}, keywords = {adenosine, hypoxia, immunity}, month = {September}, number = {3}, pages = {545--548}, posted-at = {2009-10-29 06:04:34}, priority = {2}, title = {The antihypoxia-adenosinergic pathogenesis as a result of collateral damage by overactive immune cells.}, url = {http://dx.doi.org/10.1189/jlb.0908577}, volume = {86}, year = {2009} }

TY - JOUR ID - citeulike:6031325 L3 - citeulike-article-id:6031325 N2 - Here, we attract attention to the possibility of iatrogenic exacerbation of immune-mediated tissue damage as a result of the unintended weakening of the tissue-protecting, hypoxia-adenosinergic pathway. These immunosuppressive, anti-inflammatory pathways play a critical and nonredundant role in the protection of normal tissues from collateral damage during an inflammatory response. We believe that it is the tissue hypoxia associated with inflammatory damage that leads to local inhibition of overactive immune cells by activating A2AR and A2BR and stabilizing HIF-1alpha. We show in an animal model of acute lung injury that oxygenation (i.e., inspiring supplemental oxygen) reverses tissue hypoxia and exacerbates ongoing inflammatory lung tissue damage. However, little has been done to carefully investigate and prevent this in a clinical setting. Similarly, the consumption of caffeine antagonizes A2ARs, resulting in exacerbation of ongoing acute inflammation. It is suggested that although the elimination of hypoxia-adenosinergic immunosuppression is desirable to improve vaccines, it is important to take into account the unintentional effects of supplemental oxygen and caffeine, which may increase collateral, inflammatory tissue damage. IS - 3 JF - Journal of leukocyte biology SN - 1938-3673 EP - 548 TI - The antihypoxia-adenosinergic pathogenesis as a result of collateral damage by overactive immune cells. VL - 86 SP - 545 KW - adenosine KW - hypoxia KW - immunity AU - Hatfield, Stephen AU - Belikoff, Bryan AU - Lukashev, Dmitriy AU - Sitkovsky, Michail AU - Ohta, Akio PY - 2009/09// UR - http://dx.doi.org/10.1189/jlb.0908577 ER -