Leishmaniose visceral experimental: dinâmica das alterações intestinais na infecção por leishmania (l.) chagasi
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Data
2018-07-31
Autores
Oliveira, Karine Soares de
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Universidade Estadual Paulista (Unesp)
Resumo
A leishmaniose visceral é considerada a forma clínica mais grave das leishmanioses. É causada pelo parasita da espécie Leishmania chagasi que pode ser transmitida para animais silvestres, animais domésticos e também para o homem e que vem expandindo seu território. A infecção atinge principalmente o baço, o fígado e a medula óssea, porém, a infecção também atinge outros sistemas do organismo, como o trato gastrointestinal (TGI). O TGI é controlado pelo sistema nervoso entérico (SNE) que tem como função controlar o fluxo sanguíneo, relaxamento e contração da musculatura lisa local, agindo de maneira independente do sistema nervoso central, mas mantendo contato através do eixo cérebro-intestinal. Além disso, tem relação com o sistema imunológico, visto que o intestino é considerado o maior órgão imune do corpo. Os neurônios mioentéricos do SNE são responsáveis por toda motilidade do TGI sofrendo alterações sempre que sofrem algum tipo de estresse, como por envelhecimento, dietas e até mesmo doenças. Essas alterações mostram a plasticidade neuronal para que seja mantida sempre a homeostase do intestino. Portanto, visto a importância do SNE para o funcionamento adequado do organismo, o objeivo desse trabalho foi observar como o parasitismo causado por L. chagasi atinge o intestino delgado de hamsters em diferentes períodos, avaliando a plasticidade neuronal ao decorrer da infecção parasitária. Para isso foram utilizados hamsters dourados que foram divididos em grupo controle e experimental. Os animais foram eutanasiados após 30, 60 e 90 dias de infecção e foram coletados fragmentos do baço, fígado e intestino delgado para realizar análises de carga parasitária através de LDU (Unidades de Leishman-Donovan) e imunoistoquímica. Também foram coletadas porções do duodeno, jejuno e íleo que foram submetidas as técnicas de marcação neuronal NADPH-dp e NADH-dp e após realizadas as análises morfoquantitativas dos neurônios mioentéricos. Através das análises de carga parasitária foi possível observar que as formas amastigotas do parasita chegam ao intestino desde o primeiro período estudado. Os neurônios mioentéricos NADPH-dp e NADH-dp apresentaram alterações morfoquantitativas durante todos os períodos de infecção estudados, indicando que essas alterações foram decorrentes das ações imunológicas do organismo. A relação entre o sistema imune e o SNE são fundamentais para o equilíbrio da homeostase intestinal. Portanto, concluímos que a infecção parasitária causada por L. (L.) chagasi provocam alterações na plasticidade dos neurônios mioentéricos do intestino delgado.
Visceral leishmaniasis is considered the most severe clinical form of leishmaniasis. It is caused by the parasite of the species Leishmania chagasi that can be transmitted to wild animals, domestic animals and also to the human and, it has been expanding its territory. The infection mainly affects the spleen, liver and bone marrow, but the infection can also affect other systems of the body, such as the gastrointestinal (GI) tract. GI tract is controlled by the enteric nervous system (ENS), whose function is to control blood flow, relaxation and contraction of the local smooth muscle, acting independently of the central nervous system, but maintaining contact through the cerebellar-intestinal axis. In addition, it is related to the immune system, since the intestine is considered the largest immune organ in the body. The myenteric neurons of the ENS are responsible for all the motility of the GI tract undergoing changes whenever they suffer some type of stress, such as by aging, diets and even illnesses. These changes show the neuronal plasticity so that intestinal homeostasis is always maintained. The objective of this work was to observe how the parasitism caused by L. chagasi reaches the small intestine of hamsters in different periods, evaluating the neuronal plasticity during the parasitic infection. For this purpose, golden hamsters were used, which were divided into control and experimental groups. The animals were euthanized after 30, 60 and 90 days of infection and fragments of spleen, liver and small intestine were collected to perform parasite load analysis through LDU (Leishman-Donovan Units) and immunohistochemistry. Portions of the duodenum, jejunum and ileum were also collected, which were submitted to NADPH-dp and NADH-dp neuronal marking techniques and after morph-quantitative analysis of the myenteric neurons. Through the analysis of parasite load it was possible to observe how the amastigote forms of the parasite reach the intestine from the first period studied. The myenteric neurons NADPH-dp and NADH-dp plus morpho-quantitative changes during all years of infection, given that the occurrences were the body's immune actions. The relationship between the immune system and the ENS is fundamental for the balance of intestinal homeostasis. Therefore, we conclude that parasitic infection by L. (L.) chagasi causes changes in the plasticity of myenteric neurons of the small intestine.
Visceral leishmaniasis is considered the most severe clinical form of leishmaniasis. It is caused by the parasite of the species Leishmania chagasi that can be transmitted to wild animals, domestic animals and also to the human and, it has been expanding its territory. The infection mainly affects the spleen, liver and bone marrow, but the infection can also affect other systems of the body, such as the gastrointestinal (GI) tract. GI tract is controlled by the enteric nervous system (ENS), whose function is to control blood flow, relaxation and contraction of the local smooth muscle, acting independently of the central nervous system, but maintaining contact through the cerebellar-intestinal axis. In addition, it is related to the immune system, since the intestine is considered the largest immune organ in the body. The myenteric neurons of the ENS are responsible for all the motility of the GI tract undergoing changes whenever they suffer some type of stress, such as by aging, diets and even illnesses. These changes show the neuronal plasticity so that intestinal homeostasis is always maintained. The objective of this work was to observe how the parasitism caused by L. chagasi reaches the small intestine of hamsters in different periods, evaluating the neuronal plasticity during the parasitic infection. For this purpose, golden hamsters were used, which were divided into control and experimental groups. The animals were euthanized after 30, 60 and 90 days of infection and fragments of spleen, liver and small intestine were collected to perform parasite load analysis through LDU (Leishman-Donovan Units) and immunohistochemistry. Portions of the duodenum, jejunum and ileum were also collected, which were submitted to NADPH-dp and NADH-dp neuronal marking techniques and after morph-quantitative analysis of the myenteric neurons. Through the analysis of parasite load it was possible to observe how the amastigote forms of the parasite reach the intestine from the first period studied. The myenteric neurons NADPH-dp and NADH-dp plus morpho-quantitative changes during all years of infection, given that the occurrences were the body's immune actions. The relationship between the immune system and the ENS is fundamental for the balance of intestinal homeostasis. Therefore, we conclude that parasitic infection by L. (L.) chagasi causes changes in the plasticity of myenteric neurons of the small intestine.
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Palavras-chave
Parasitologia, Leishmaniose visceral, Leishmania chagasi, Intestino delgado, Sistema Nervoso Entérico, Parasitology, Visceral leishmaniasis, Small intestine, Enteric Nervous System, Leishmania chagasi