Dana Garcia
Research Mentor(s): Wendy Fonseca Aguilar
Mentor Department: Pathology Department
Authors: Dana Garcia, Grace Lombardo, Wendy Fonseca
Session: Session 6 (3:00pm – 3:50pm)
Presentation Type: Poster 90
Abstract
Respiratory syncytial virus (RSV) infects nearly all children by age 2, and infants hospitalized with severe RSV infection are at higher risk of developing asthma. In our lab we investigate the immunopathology mechanism activated during RSV infection to understand the mechanisms involving RSV-related disease. Our research will help to identify new therapeutic targets to control the severity of RSV infection and possible the development of asthma later in life. Pediatric infectious diseases are one of the most important causes of mortality in infants. Despite recent advances in the knowledge of RSV immunopathology, the mechanisms involved in asthma predisposition after severe RSV infection remain unknown. We are investigating the molecular and cellular mechanism related to this long term disease. To study the effects of RSV infection during early life, we have established a murine neonatal infection model that resembles the immature lung and immune environment of the human infants. We used this animal model to ask questions by blocking different pathways activated during RSV infection, we followed the animal until adulthood to study asthma predisposition. We use several molecular and cellular biology techniques, such as qPCR, immunoblots, primary cell culture, among others. In this work, we investigated the alter phenotype of hematopoietic derived macrophages after 4 weeks of early life RSV infection and their role in asthma predisposition, as well as their cross-talk to structural cells using primary cultures of lung fibroblast. We observed that bone marrow macrophages harvested from early life RSV infected mice presented long term alteration in their phenotype, this changes affected the phenotype of the lung fibroblast of naive mice when co-culture in vitro, suggesting that early life RSV infection generated long term alteration in the mielod cell population that impact the immunemicroenviroment of the lung, specifically the lung fibroblast.
