A study published in the Journal of Leukocyte Biology found that THC reduced several inflammatory responses and helped preserve a structural component of lung tissue in mice infected with a parasitic worm.
The research, conducted by scientists at the University of California, Riverside, examined how THC affects immune activity during infection and whether those changes influence damage to lung tissue.
Researchers used mice infected with Nippostrongylus brasiliensis, a parasitic worm that travels through the lungs before reaching the intestines. The animals received daily doses of THC at 5 milligrams per kilogram of body weight for 14 days before infection, with treatment later resumed during the infection period.
THC significantly altered several immune responses. Treated mice showed reduced infection-induced increases in circulating eosinophils and monocytes, two types of white blood cells involved in inflammation. Researchers also observed increased regulatory T cells, which help control excessive immune activity.
Additional testing found that immune cells from THC-treated mice produced lower levels of two inflammatory signaling molecules, tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ), following laboratory stimulation.
Researchers also examined gene activity in eosinophils and macrophages collected from the lungs. THC shifted these cells away from several inflammatory and tissue-remodeling pathways while increasing activity associated with cellular metabolism and responses to stress.
One notable finding involved collagen VI, a protein that helps maintain the structural framework of lung tissue. Infected mice that did not receive THC showed a significant reduction in collagen VI staining compared with uninfected controls. THC-treated infected mice, however, retained collagen VI levels that were not significantly reduced compared with their uninfected counterparts.
The findings suggest that THC’s effects on immune activity may help limit certain changes associated with inflammation-related lung damage.
