In addition, lysophosphatidylcholine increases intracellular calcium concentrations in macrophages, ultimately enhancing parasite invasion. Finally, lysophosphatidylcholine inhibits nitric oxide production in macrophages stimulated by T. cruzi and thus interferes with the immune system of the vertebrate host. Because the chemical profile of metabolites in the triatomine intestine may affect parasite development, it is important to understand how a certain species of triatomine may tune the ecological niche of T. cruzi. Indeed, many metabolic classes found in our 
study, such as prenol lipids, amino acids, glycerolipids, steroids, phenols, fatty acids and derivatives, benzoic acid and derivatives, flavonoids, glycerophospholipids, benzopyrans, and quinolones were enriched in the triatomine species studied. These data show that in addition to factors previously shown to affect the interaction of T. cruzi and its vector, there are many chemical determinants of the intestinal environment that may be specifically tuned based on the species of triatomine involved, and this may also affect the vectorparasite interaction. The concept of metabolic niche in parasitic protozoa has been extensively discussed. Given the availability of an assortment of metabolites within the host, it is not surprising that some pathways were abandoned in obligate Homatropine Bromide parasites such as trypanosomatids as opposed to opportunistic parasites. The gut is an environment with reduced oxygen availability, which implies anaerobic fermentation of glucose and amino acid carbon sources. T. cruzi exhibits a specific optimization to allow the metabolism of histidine to glutamate. Glutamate can then be converted to a-ketoglutarate, a precursor of the citric acid cycle, which correlates with the occurrence of histidine as the predominant free amino acid in R. prolixus feces. An important group of fatty acid derivatives that may be involved in vector specificity is the eicosanoids, which are oxygenated metabolites of polyunsaturated fatty acids. PUFAs cannot be synthesized de novo by most animals or protists and must be obtained from dietary plant products. Estradiol Benzoate eicosanoids are a family of lipid mediators that participate in a wide range of biological activities in animals. In insects, eicosanoids are mainly synthesized from arachidonic acid released from cell membrane phospholipids via phospholipase A2 activation. Arachidonic acid is subsequently metabolized via the following three pathways: the cyclooxygenase pathway, forming prostaglandins, thromboxanes or prostacyclins; the various lipoxygenase pathways, forming leukotrienes, lipoxins, hepoxilins, hydroxy and hydroxy fatty acids; and the cytochrome P-450 pathways, forming epoxy derivatives. In insects, including R. prolixus, eicosanoids mediate specific cell actions, including phagocytosis, microaggregation, nodulation, hemocyte migration, hemocyte spreading and the release of prophenoloxidase in reaction to bacterial and protozoan challenges. According to insect models, the chemical components of infecting microorganisms, such as lipopolysaccharide, stimulate a number of intracellular transduction systems, including those responsible for upregulation of eicosanoid biosynthesis by phospholipase A2 activation. Arachidonic acid released from the plasma membrane is subsequently converted into prostaglandin E2 or other eicosanoids. Prostaglandins are exported from the cell by specific transporter proteins. The prostaglandins can interact with receptors on the exporting cell or on neighboring cells. Moreover, it has been demonstrated that T. cruzi has access to the arachidonic acid pathway through the Old Yellow Enzyme. T. cruzi also synthesizes eicosanoids, preferentially thromboxane A2.