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The authors began the study of cytokines or the so-called plasma activators of the acute inflammatory reaction in infections in September 1997. As far back as with the origina report describing the Chagas’ Disease (CD), Carlos Chagas (1911)3,4 , Gaspar Vianna (1911)15 and Okumura (1967)11 interpreted the etiopathogenesis of the Chagas’ Disease as follows. The first event is the invasion of the host cell by the trypomastigote form of the Trypanosoma cruzi (Chagas 1909)2. The flagellum becomes disconnected from the parasite and the trypomastigotes change into the amastigote form. The amastigotes multiply by successive binary fission clustering together to form a compact nest of parasites inside the host cell. The parasites subsequently evolve to the epiand trypomastigote flagellate forms releasing their cellular content into the nest fluid. These flagellate forms move actively in the nest fluid, provoking the rupture of the amastigote nest and consequently host cell injury. Lastly, the epi and trypomastigote forms gain access the interstitial space. These authors3,11,15 stressed the fact that absolutely no inflammatory changes surrounding the unruptured nest were recorded as long as the amastigote nests remained intact or at the time of the nest rupture. Amastigote cell nest rupture releases several chemical factors produced by the distinct evolutionary stages of the parasite, that is, the trypo, epi, and amastigote forms. These chemical factors are metabolic and degradation products, namely, proteins, lipids, carbohydrates, RNA and DNA fractions, cytoplasmic, and cell membrane particles11,12,13. The authors’ objectives in this experiment were to study the formation and the action of these factors in experimental Chagas’ Disease. The description of several factors in the 70’s , namely, lymphocyte activating factor by Gery & Waksman7, the leucocytic endogenous mediator by Merriman et al.9, and the cytokines by Dinarello in 19846 who described “ the activators of immunity in defense of the host”, led us to believe that a familiar substance participates actively in the etiopathogenesis of the experimental Chagas ́Disease. (Figs. 1, 2, 3, 4). Using cytokine markers, we observed that while the mastigote nest remains intact or at the moment of nest rupture, no cytokine markers are detected. However, the interstitial cell space becomes stained brown or chestnut brown immediately after the acute inflammatory reaction is in proRHCFAP/2965

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Cytokine-like substance: origin and fate in chagas'disease a new hypothesis about the local inflammatory reaction etiopathogenesis (experimental study in white mice)