Chagas disease (CD), also known as American trypanosomiasis, is a neglected tropical disease (NTD) caused by the protozoan parasite Trypanosoma cruzi. The disease is endemic in 21 Latin American countries, and according the World Health Organization (WHO), 8 million of people are infected worldwide [1]. Benznidazole (Bdz) and Nifurtimox (NF) are the reference drugs available to the treatment of CD, however, both drugs are toxic and not very effective in chronic patients [2].

In endemic countries, T. cruzi is transmitted through various species of blood-sucking triatomine insects [3]. However, outbreaks by oral contamination have been reported in several Brazilian regions [4], and due to migration, CD is increasingly diagnosed also in non-endemic countries, which include European and North American countries [5].

In the mammalian host, trypomastigotes forms of the parasite infect macrophages, fibroblasts and muscle cells [6], and turns into intracellular form, which are amastigotes. These amastigotes will turn into trypomastigotes, that promotes the cell rupture, and spread the infection in the host. Clinically, CD has two clinical phases: acute and chronic. Most acute infections are asymptomatic, and is characterized by microscopically detectable parasitemia and non-specific symptoms, such as myocarditis, pericardial effusion or meningoencephalitis [7]. The parasitemia becomes undetectable after 4–8 weeks, and in the absence of an effective treatment, the individual passes into the chronic phase [8]. An estimated 20–30% of infected individuals progress to cardiac and/or gastrointestinal disease [9].

The innate and acquired immune response are essential to controlling T. cruzi infection. The innate immune system comprises several cells type, such as dendritic cells (DCs), monocytes/macrophages (Mo) and natural killer cells (NK) [10], [11]. The recognition of pathogens by these cell types leads to phagocytosis and the production of pro-inflammatory cytokines, instructing the development of a specific adaptive immune response, which include the T-helper type 1 (Th1) response [6], important to inhibition of intracellular parasites. On the other hand, the T-helper type 2 response (Th2) promotes the parasite’s replication [12].

Due to the intense inflammatory response observed in CD, especially in chronic cardiac patients (CCC), an ideal therapeutic intervention should not only comprise phagocytic mechanisms, to kill the parasite, but also reducing the inflammation, to prevent the tissue damage [13]. In this context, photosynthetic microorganisms, such as microalgae, are promising candidates for CD therapy, due to its biological properties, which include anti-inflammatory and antiparasitic activities [14], [15]. Studies carried out with Chlorophyta microalgae have demonstrated that these microorganisms can modulate the immune response, as well as led to inhibition of T. cruzi trypomastigotes in low concentrations [16], [17], [18].

Currently, microalgae have attracted attention as new sources of bioactives for therapeutic use. Chlorella sp. are widely used as a source of nutritional ingredients while Tetradesmus obliquus (oldest species known as Scenedesmus obliquus) are still little known. Both microalgae are of commercial importance due to the composition of bioactive compounds such as polyunsaturated fatty acids (PUFAs), polysaccharides, photosynthetic pigments, protein and phenolic compounds [19], [20]. Several studies reported that these bioactive compounds have potential therapeutic activities, such as antioxidant, antimicrobial, anti-thrombolytic, antihypertensive, anti-inflammatory, anti-cancer, and anti-hyperglycemia [21], [22]. However, the effects of C. vulgaris or T. obliquus extracts on the immune response of human cell infected with of T. cruzi are still unknow.

Therefore, this study aimed to evaluate, in vitro, the trypanocidal and immunomodulatory effects of the green microalgae Chlorella vulgaris and Tetradesmus obliquus extracts in peripheral blood mononuclear cells (PBMCs), infected or not with T. cruzi, for a possible alternative therapeutical target for CD.