The results indicate that HIV infection leads to increased production of free radicals and decreased production of GCLC resulting in depletion of rGSH and this may lead, in part, to the loss of innate immune function observed in HIV patients.
The results indicate that GSH by its direct antimycobacterial activity inhibits the growth of intracellular M. tb inside DCs (dendritic cells).
We report that L-GSH supplementation for 3 months in people with T2DM was able to reduce the levels of oxidative stress in all blood components and prevent depletion of glutathione (GSH) in this population known to be GSH deficient.
Our results show that the supplementation of mice with L-GSH led to increased levels of total GSH, which is associated with reduced oxidative stress, increased levels of granuloma-promoting cytokines, and decreased M. tb burden in the lung. PMID: Read the Article
These findings suggest potential therapeutic benefits of L-GSH supplementation in conjunction with first-line antibiotic therapy against M. tb infection in individuals with T2DM.
They characterized the functions of neutrophils in response to Mycobacterium tuberculosis (M. tb) infection, with particular reference to glutathione (GSH).