Comorbidity associated to Ascaris suum infection during pulmonary fibrosis exacerbates chronic lung and liver inflammation and dysfunction but not affect the parasite cycle in mice.

Ascariasis is considered the most neglected tropical disease, and is a major problem for the public health system. However, idiopathic pulmonary fibrosis (IPF) is a result of chronic extracellular deposition of matrix in the pulmonary parenchyma, and thickening of the alveolar septa, which reduces a...

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Bibliographic Details
Published in:PLOS Neglected Tropical Diseases
Main Authors: Fabrício Marcus Silva Oliveira, Pablo Hemanoel da Paixão Matias, Lucas Kraemer, Ana Clara Gazzinelli-Guimarães, Flaviane Vieira Santos, Chiara Cássia Oliveira Amorim, Denise Silva Nogueira, Camila Simões Freitas, Marcelo Vidigal Caliari, Daniella Castanheira Bartholomeu, Lilian Lacerda Bueno, Remo Castro Russo, Ricardo Toshio Fujiwara
Format: Article in Journal/Newspaper
Language:English
Published: Public Library of Science (PLoS) 2019
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Online Access:https://doi.org/10.1371/journal.pntd.0007896
https://doaj.org/article/9664bc25e0044c75938c481793ac9bed
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Summary:Ascariasis is considered the most neglected tropical disease, and is a major problem for the public health system. However, idiopathic pulmonary fibrosis (IPF) is a result of chronic extracellular deposition of matrix in the pulmonary parenchyma, and thickening of the alveolar septa, which reduces alveolar gas exchange. Considering the high rates of ascariasis and pulmonary fibrosis, we believe that these two diseases may co-exist and possibly lead to comorbidities. We therefore investigated the mechanisms involved in comorbidity of Ascaris suum (A. suum) infection, which could interfere with the progression of pulmonary fibrosis. In addition, we evaluated whether a previous lung fibrosis could interfere with the pulmonary cycle of A. suum in mice. The most important findings related to comorbidity in which A. suum infection exacerbated pulmonary and liver injury, inflammation and dysfunction, but did not promote excessive fibrosis in mice during the investigated comorbidity period. Interestingly, we found that pulmonary fibrosis did not alter the parasite cycle that transmigrated preferentially through preserved but not fibrotic areas of the lungs. Collectively, our results demonstrate that A. suum infection leads to comorbidity, and contributes to the aggravation of pulmonary dysfunction during pulmonary fibrosis, which also leads to significant liver injury and inflammation, without changing the A. suum cycle in the lungs.