A recent research investigation, spearheaded by Luísa Figueiredo, who heads the team at the Instituto de Medicina Molecular João Lobo Antunes (iMM; Portugal), and published in Nature Microbiology, has discovered a fresh approach employed by the host organism to combat Trypanosoma brucei infection.
Trypanosoma brucei builds up in adipose tissue
Trypanosoma brucei, a parasite responsible for sleeping sickness in humans and nagana in cattle, poses a significant public health threat and economic burden in Sub-Saharan Africa. Studying the host’s response to infection is crucial for developing effective treatments. When transmitted through tsetse fly bites, these parasites occupy interstitial spaces in the host, potentially resulting in fatal consequences without intervention.
Leader of the lab where the study was carried Luisa Figueiredo sad a few years ago, they discovered that Trypanosoma brucei, the parasite responsible for sleeping sickness, gathers in unusually large quantities in adipose tissue. This discovery led them to focus their research on understanding how this colonization of adipose tissue influences the progression of the disease.
The build-up of parasites within these tissues coincides with a decrease in body mass. Figueiredo said that the research indicates that this weight reduction primarily results from the depletion of adipose tissue through lipolysis, which is a metabolic procedure responsible for breaking down triacylglycerols into their component compounds, including free fatty acids.
Immune response infection causes adipose tissue loss
Adipose tissue loss can result from various factors, and in this study, researchers discovered that a significant cause is the immune response to infection. The study’s first author, Henrique Machado, observed that when they infected immunocompromised mice and mice with impaired lipolysis, both groups experienced less body weight loss despite having more parasites.
The authors investigated whether lipolysis affects the progression of a disease and found that the loss of adipose tissue through lipolysis extends the lifespan of infected mice. Lipolysis also controls the number of parasites, suggesting a protective effect. This protection results from the release of toxic free fatty acids during lipolysis, leading to parasite death. Essentially, the host sacrifices fat mass to kill the parasites.
