Immunohistochemical characterization of inflammatory changes in the pituitary gland of dogs with visceral leishmaniasis.

Abstract

Canine Visceral Leishmaniasis (CanL) is caused by the amastigote forms of the protozoan Leishmania infantum, found inside the cells of the phagocytic mononuclear system and disseminated in the host organism, which can develop a variety of clinical signs due to the diversity of tropism of the protozoan. Clinical neurological signs, inflammatory lesions and vascular complications are occasionally observed in the central nervous system (CNS) of infected dogs, whose pathogenesis is not fully understood. The circumventricular organs (CVOs) are vascularized compartments of the CNS devoid of effective barriers, enabling communication between blood and cerebrospinal fluid, making them susceptible to exposure to components present in the blood. The pituitary is composed of the neurohypophysis and adenohypophysis, involved by the cerebral arterial circle, and classified as an endocrine organ responsible for controlling the physiological metabolic, reproductive and growth functions, helping to maintain homeostasis. It is suggested that the immune response in the CNS, during CVL, occurs through specific pathways, unlike in other tissues, since CD3+ T lymphocytes are the main inflammatory cells found in this system after peripheral immune activation. Because CVOs facilitate communication between the CNS, peripheral blood and the peripheral immune response, the possible involvement of pituitary regions in CVL, through the direct action of the parasite or the local production of inflammatory mediators, may contribute to the triggering mechanisms of the lesions observed in the brain of the animals. This project aims to investigate the histological changes in the pars nervosa, pars distalis and pars intermedia of the pituitary, using hematoxylin and eosin (HE) staining, and to characterize inflammatory cells by immunohistochemistry through the detection of CD3+ and CD79+ T lymphocytes. in dogs with CVL.