Zileuton is a member of the class of 1-benzothiophenes that is 1-benzothiophene in which the hydrogen at position 2 is replaced by a 1-[carbamoyl(hydroxy)amino]ethyl group. A selective 5-lipoxygenase inhibitor, it inhibits the formation of leukotrienes LTB4, LTC4, LDT4, and LTE4. It is used for the management of chronic asthma. It has a role as an EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor, a non-steroidal anti-inflammatory drug, an anti-asthmatic drug, a leukotriene antagonist and a ferroptosis inhibitor. It is a member of ureas and a member of 1-benzothiophenes. It derives from a hydride of a 1-benzothiophene.
Related Questions and Answers
A: At 5 days post-infection, Zileuton treatment increased the number of CD8+ T cells in the spleen. The treatment also promoted a shift towards a more anti-inflammatory profile, with increased numbers of IL-10-producing and FOXP3+ T regulatory cells (Tregs) among both CD4+ and CD8+ T cells. This suggests that Zileuton helps regulate the immune response to prevent excessive inflammation.
A: Zileuton treatment maintained lung compliance closer to that of control mice, as measured by pressure-volume (PV) curves. Additionally, treated mice exhibited milder cardiac alterations compared to untreated infected mice, as shown by electrocardiogram (ECG) analysis.
A: Zileuton treatment led to higher levels of IL-10 and IFN-γ, while reducing levels of pro-inflammatory cytokines like CXCL-2, IL-1β, and CXCL-1. The treatment also increased the number of IL-10-producing neutrophils and reduced TNF-producing dendritic cells in the lungs. At 5 days post-infection, treated mice showed increased numbers of Th2, Treg CD4+, and Treg CD8+ cells producing IL-10, and reduced Th1 infiltrating cells.
A: Zileuton treatment significantly improved survival rates, delayed mortality, reduced weight loss, and improved clinical scores in MHV-3-infected mice. The treatment also maintained lung function and reduced inflammatory scores in the lungs, independent of viral load control.
A: Zileuton modulates host immune responses by reducing pro-inflammatory cytokines and increasing anti-inflammatory cytokines like IL-10, thereby improving lung function and survival rates without affecting the host's ability to clear the virus.