Serum uric acid levels in Chagas' disease

Abreu, Menandro Cardoso; Guimarães, Romeu Cardoso; Krieger, Henrique

doi:10.1590/s0074-02761989000200002

Cited by 2 publications

(2 citation statements)

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“…These changes were correlated with indicators of disease severity in mice [73]. Conflicting results have been found in human studies: In one study, higher serum uric acid was found in patients with more severe disease [79], whereas no difference was observed between infected versus uninfected, asymptomatic versus symptomatic, or patients with or without cardiomyopathy in an older study [80]. Beyond CD, higher uric acid is associated with proportionally higher risk of cardiovascular disease mortality [81].…”

Section: Host Metabolic Changes: Protective or Maladaptive?mentioning

confidence: 91%

Small molecule mediators of host-T. cruzi-environment interactions in Chagas disease

Kwakye-Nuako,

Middleton,

McCall

2024

PLoS Pathog

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Small molecules (less than 1,500 Da) include major biological signals that mediate host-pathogen-microbiome communication. They also include key intermediates of metabolism and critical cellular building blocks. Pathogens present with unique nutritional needs that restrict pathogen colonization or promote tissue damage. In parallel, parts of host metabolism are responsive to immune signaling and regulated by immune cascades. These interactions can trigger both adaptive and maladaptive metabolic changes in the host, with microbiome-derived signals also contributing to disease progression. In turn, targeting pathogen metabolic needs or maladaptive host metabolic changes is an important strategy to develop new treatments for infectious diseases. Trypanosoma cruzi is a single-celled eukaryotic pathogen and the causative agent of Chagas disease, a neglected tropical disease associated with cardiac and intestinal dysfunction. Here, we discuss the role of small molecules during T. cruzi infection in its vector and in the mammalian host. We integrate these findings to build a theoretical interpretation of how maladaptive metabolic changes drive Chagas disease and extrapolate on how these findings can guide drug development.

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Section: Host Metabolic Changes: Protective or Maladaptive?mentioning

confidence: 91%

Small molecule mediators of host-T. cruzi-environment interactions in Chagas disease

Kwakye-Nuako,

Middleton,

McCall

2024

PLoS Pathog

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“…The sample consisted of 350 individuals from 180 families living in Bambui (State of Minas Gerais) in southeastern Brazil, an area endemic for Chagas' disease (for more details see Dias et al, 1983;Abreu et al, 1989;Krieger et al, 1992;Moro-Furlani and Krieger, 1992).…”

Section: Samplementioning

confidence: 99%

Evidence for biological inheritance of the eosinophil response to internal parasites in southeastern Brazil

et al. 1999

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One hundred and seventy-seven individuals belonging to 120 complete or incomplete nuclear families from Bambui, in the State of Minas Gerais, southeastern Brazil, were studied in order to examine causes of variation in the eosinophil rate among subjects infested by intestinal worms with an extra-digestive cycle. Segregation analysis without correction for skewness showed that the hypothesis of the presence of an additive major gene was consistent with the data, although a dominant, recessive, or a multifactorial hypothesis could not account properly for the observed significant familial aggregation. The most parsimonious correction for skewness showed similar results, but could not distinguish between dominant and recessive models, although co-dominance was rejected. Since these models assume that skewness was attributable to the commingling of two distributions, these results seem to agree with those for uncorrected data. These findings suggest that several genetically independent factors determine the resistance/susceptibility to helminth infestation mainly through their ability to influence the eosinophil response.
Uma amostra de 177 indivíduos pertencentes a 120 famílias nucleares, completas ou incompletas, de Bambui, Estado de Minas Gerais, sudeste do Brasil, foi estudada com o objetivo de apurar algumas das causas da variabilidade da taxa de eosinófilos em pessoas parasitadas por vermes intestinais com ciclo de vida extra-digestivo. A análise de segregação, aplicada aos dados sem correção para a assimetria, mostrou que a hipótese de um gene principal aditivo é consistente com os dados, enquanto que as hipóteses que supõem a ação de um gene dominante, de um gene recessivo ou ainda herança multifatorial não explicam, adequadamente, a significante agregação familial observada. A correção mais parcimoniosa para assimetria mostrou resultados semelhantes, mas não permitiu a distinção entre os modelos dominante e recessivo, embora permitisse a rejeição do modelo codominante. Considerando que esse modelo supõe ser a assimetria devida ao entrelaçamento de duas distribuições, esses resultados parecem concordar com aqueles obtidos quando os dados não foram corrigidos. Pode-se sugerir que o papel desempenhado por vários fatores genéticos independentes na resistência/suscetibilidade à infestação por helmintos seja determinado, principalmente, por suas capacidades de agir no estabelecimento de uma resposta eosinofílica

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Serum uric acid levels in Chagas' disease

Cited by 2 publications

References 0 publications

Small molecule mediators of host-T. cruzi-environment interactions in Chagas disease

Small molecule mediators of host-T. cruzi-environment interactions in Chagas disease

Evidence for biological inheritance of the eosinophil response to internal parasites in southeastern Brazil

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