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

PLoS Negl Trop Dis. 2019 Nov 25;13(11):e0007896. doi: 10.1371/journal.pntd.0007896. eCollection 2019 Nov.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ascariasis / complications*
  • Ascariasis / pathology*
  • Ascaris suum / isolation & purification
  • Disease Models, Animal
  • Female
  • Inflammation / pathology
  • Liver Diseases / pathology*
  • Lung / parasitology
  • Lung / pathology
  • Mice, Inbred C57BL
  • Pulmonary Fibrosis / complications*
  • Pulmonary Fibrosis / pathology*

Grants and funding

This investigation received financial support from Fundação de Amparo a Pesquisa do Estado de Minas Gerais/FAPEMIG, Brazil (Grant# CBB APQ- 03280-15), the Brazilian National Research Council (CNPq) (Grant# 421424/2018-4, Grant# 303345/2018-7 and Grant# 479613/2012-5), Pró-Reitoria de Pesquisa of Universidade Federal de Minas Gerais; FMSO is grateful for the postdoctoral fellowship provided by Programa Nacional de Pós-doutorado (PNPD) from Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), post-graduation program in Parasitology/Universidade Federal de Minas Gerais. DCB, LLB and RTF are Research Fellows from CNPq. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.