Treatment with Apocynin Limits the Development of Acute Graft-versus-Host Disease in Mice.
Barbara Maximino RezendePriscila T T BernardesWilliam Antonio GonçalvesCarolina Braga de ResendeRayssa Maciel AthaydeThiago Vinicius ÁvilaDébora Gonzaga MartinsMarina G M CastorMauro Martins TexeiraVanessa PinhoPublished in: Journal of immunology research (2019)
Graft-versus-host disease (GVHD) is the most serious complication limiting the clinical utility of allogeneic hematopoietic stem cell transplantation (HSCT), in which lymphocytes of donors (graft) are activated in response to the host antigen. This disease is associated with increased inflammatory response through the release of inflammatory mediators such as cytokines, chemokines, and reactive oxygen species (ROS). In this study, we have evaluated the role of ROS in GVHD pathogenesis by treatment of recipient mice with apocynin (apo), an inhibitor of intracellular translocation of cytosolic components of NADPH oxidase complex. The pharmacological blockade of NADPH oxidase resulted in prolonged survival and reduced GVHD clinical score. This reduction in GVHD was associated with reduced levels of ROS and TBARS in target organs of GVHD in apocynin-treated mice at the onset of the mortality phase. These results correlated with reduced intestinal and liver injuries and decreased levels of proinflammatory cytokines and chemokines. Mechanistically, pharmacological blockade of the NADPH oxidase was associated with inhibition of recruitment and accumulation of leukocytes in the target organs. Additionally, the chimerism remained unaffected after treatment with apocynin. Our study demonstrates that ROS plays an important role in mediating GVHD, suggesting that strategies aimed at blocking ROS production may be useful as an adjuvant therapy in patients subjected to bone marrow transplantation.
Keyphrases
- allogeneic hematopoietic stem cell transplantation
- reactive oxygen species
- acute myeloid leukemia
- acute lymphoblastic leukemia
- cell death
- dna damage
- inflammatory response
- bone marrow
- high fat diet induced
- peripheral blood
- liver failure
- cardiovascular disease
- cardiovascular events
- adipose tissue
- coronary artery disease
- drug induced
- cell therapy