Participation of Central Muscarinic Receptors on the Nervous Form of Chagas Disease in Mice Infected via Intracerebroventricular with Colombian Trypanosoma cruzi Strain

Abstract

Acute chagasic encephalitis is a clinically severe central nervous system (CNS) manifestation. However, the knowledge of the nervous form of Chagas disease is incomplete. The role of the muscarinic acetylcholine receptor (mAChR) on mice behavior and brain lesions induced by Trypanosoma cruzi (Colombian strain) was herein investigated in mice treated with the mAChR agonist and antagonist (carbachol and atropine), respectively. Immunosuppressed or non-immunosuppressed mice were intracerebroventricularly (icv) or intraperitoneally (ip) infected. All groups were evaluated 15 d.p.i. (days post infection). Intraperitoneally infected animals had subpatent parasitemia. Patent parasitemia occurred only in icv infected mice. The blockade of mAChR increased the parasitemia, parasitism and lesions compared to its activation. Infected not treated (INT ip) mice did not present meningitis and encephalitis, regardless of immunosuppression. INT icv brains presented higher cellularity, discrete signs of cellular degeneration, frequent presence of parasites and focal meningitis. The immunosuppressed atropine + icv mice presented increased intracellular parasitism associated with degenerative parenchymal changes, while carbachol + icv mice presented discrete meningitis, preservation of the cortex and absence of relevant parasitism. Cholinergic receptor blockage increased impairment of coordination vs. receptor activation. Muscarinic cholinergic pathway seems to be involved in immune mediated cell invasion events while its blockade favored infection evolution, brain lesions, and behavioral alterations.

Respiratory Infections by virus: a review properties

“…The viruses are capable of provoke beta-adrenergic block, but it seems not be an important event. The principal abnormality would be the intense parasympathetic predominance, perhaps due of the receptor M2-Muscarinic destruction or disfunction [36,37]. Some virus destroys the receptors calico acid resides and, thus take along to this alteration.…”

Host–Pathogen Interaction Involved in Trypanosoma cruzi Infection

“…This Special Issue includes several original articles. A study about the role of the muscarinic acetylcholine receptor on mice behavior and brain lesions induced by T. cruzi is included [ 3 ]. Thus, the muscarinic cholinergic pathway seems to be involved in immune-mediated cell invasion events, while its blockade favors infection, brain lesions, and behavioral alterations.…”