Advanced megaesophagus (Group III) secondary to vector-borne Chagas disease in a 20-month-old infant

Rassi, Anis; Rezende, Joffre Marcondes de

doi:10.1590/s0037-86822012000200026

Cited by 5 publications

(2 citation statements)

References 2 publications

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“…Trypanosoma brucei is an important parasitic protozoan that is the etiological agent of sleeping sickness in sub-Saharan Africa. Related parasites are responsible for Chagas disease and Leishmaniasis in South America and many tropical countries [ 1 , 2 , 3 ]. At the G1 stage of the T .…”

Section: Introductionmentioning

confidence: 99%

BILBO1 Is a Scaffold Protein of the Flagellar Pocket Collar in the Pathogen Trypanosoma brucei

et al. 2015

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The flagellar pocket (FP) of the pathogen Trypanosoma brucei is an important single copy structure that is formed by the invagination of the pellicular membrane. It is the unique site of endo- and exocytosis and is required for parasite pathogenicity. The FP consists of distinct structural sub-domains with the least explored being the annulus/horseshoe shaped flagellar pocket collar (FPC). To date the only known component of the FPC is the protein BILBO1, a cytoskeleton protein that has a N-terminus that contains an ubiquitin-like fold, two EF-hand domains, plus a large C-terminal coiled-coil domain. BILBO1 has been shown to bind calcium, but in this work we demonstrate that mutating either or both calcium-binding domains prevents calcium binding. The expression of deletion or mutated forms of BILBO1 in trypanosomes and mammalian cells demonstrate that the coiled-coil domain is necessary and sufficient for the formation of BILBO1 polymers. This is supported by Yeast two-hybrid analysis. Expression of full-length BILBO1 in mammalian cells induces the formation of linear polymers with comma and globular shaped termini, whereas mutation of the canonical calcium-binding domain resulted in the formation of helical polymers and mutation in both EF-hand domains prevented the formation of linear polymers. We also demonstrate that in T. brucei the coiled-coil domain is able to target BILBO1 to the FPC and to form polymers whilst the EF-hand domains influence polymers shape. This data indicates that BILBO1 has intrinsic polymer forming properties and that binding calcium can modulate the form of these polymers. We discuss whether these properties can influence the formation of the FPC.

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Section: Introductionmentioning

confidence: 99%

BILBO1 Is a Scaffold Protein of the Flagellar Pocket Collar in the Pathogen Trypanosoma brucei

et al. 2015

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“…This could explain the higher frequency of idiopathic megaesophagus (achalasia) compared with idiopathic megacolon. It would also allow more severe denervation of the esophagus compared with the colon, favoring earlier onset of megaesophagus compared with megacolon 6 , 19 , 20 , 21 , despite the need for a higher degree of denervation in megaesophagus than in chagasic megacolon 1 , 2 , 3 , 4 , 14 .…”

Section: Discussionmentioning

confidence: 99%

Blood Vessels in Ganglia in Human Esophagus Might Explain the Higher Frequency of Megaesophagus Compared With Megacolon

Adad

Etchebehere

Jammal

2014

Rev. Inst. Med. trop. S. Paulo

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This study aimed to determine the existence of blood vessels within ganglia of the myenteric plexus of the human esophagus and colon. At necropsy, 15 stillborns, newborns and children up to two years of age, with no gastrointestinal disorders, were examined. Rings of the esophagus and colon were analyzed and then fixed in formalin and processed for paraffin. Histological sections were stained by hematoxylin-eosin, Giemsa and immunohistochemistry for the characterization of endothelial cells, using antibodies for anti-factor VIII and CD31. Blood vessels were identified within the ganglia of the myenteric plexus of the esophagus, and no blood vessels were found in any ganglia of the colon. It was concluded that the ganglia of the myenteric plexus of the esophagus are vascularized, while the ganglia of the colon are avascular. Vascularization within the esophageal ganglia could facilitate the entrance of infectious agents, as well as the development of inflammatory responses (ganglionitis) and denervation, as found in Chagas disease and idiopathic achalasia. This could explain the higher frequency of megaesophagus compared with megacolon.

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Esophageal Achalasia

Plourde

Aspirot²

2022

Pediatric Neurogastroenterology

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Advanced megaesophagus (Group III) secondary to vector-borne Chagas disease in a 20-month-old infant

Cited by 5 publications

References 2 publications

BILBO1 Is a Scaffold Protein of the Flagellar Pocket Collar in the Pathogen Trypanosoma brucei

BILBO1 Is a Scaffold Protein of the Flagellar Pocket Collar in the Pathogen Trypanosoma brucei

Blood Vessels in Ganglia in Human Esophagus Might Explain the Higher Frequency of Megaesophagus Compared With Megacolon

Esophageal Achalasia

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