Evasion and immuno-endocrine regulation in parasite infection: Two sides of the same coin in Chagas disease?

MORROT ALEX; VILLAR, SILVINA RAQUEL; GONZALES, FLORENCIA; PEREZ, ANA ROSA

Frontiers in microbiology

Switzerland

Año: 2016 vol. 7 p. 1 - 10

Chagasdisease, also known as American trypanosomiasis, is a serious illness caused bythe protozoan parasite Trypanosoma cruzi(T. cruzi). Seven million people are infected worldwide. Although most ofthose infected are in Latin America, migration flows have spread the disease toother non-endemic continents. Chagas disease present an acute and a chronicphase, and both could be asymptomatic or symptomatic. While oral acute Chagasdisease has emerged nowadays as the principal acute and lethal endemic form of infection,almost 30% of chronically infected people (by vectorial, congenital,oral and otherforms) develop cardiac, digestive or mixed alterations, suggesting a broadrange of host-parasite interactions that finally impact upon chronic diseaseoutcome. The ability of T. cruzi topersist and cause pathology seems to depend on diverse factors likeT. cruzi strains and the infective load,the route of infection, the release of immunomodulatory or virulence factors,the parasite capacity of avoid protective immune response, the strength andtype of host defence mechanisms and the genetic background of the host. In thiscontext, the host-parasite interaction is subject to a constant neuro-endocrineregulation, and as the infection proceeds can lead to a broad range ofoutcomes, from elimination of the pathogen to its continued persistence in thehost with the consequent induction of pathology. In particular, neuro-endocrinebalance, effector and regulatory T cells are key points where the host can takeadvantage to improve their defence mechanisms, or contrarily may be exploitedby parasites to survive and persist. In this context, T. cruzi evasion strategies and hostdefence mechanisms can be envisioned as two sides from the same coin at thecomplex host-parasite relationship influencing parasite persistence and differentoutcomes observed in Chagas disease. Understanding on how T. cruzi evade innate and adaptive immune response and how parasitepersistence might be favoured by immuno-neuro-endocrine regulation will provideimportant clues to better dissect mechanisms underlying the pathophysiology ofChagas disease.