Browsing by Author "Hartert, Tina V."

Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    Bronchopulmonary Dysplasia: Executive Summary of a Workshop
    (Elsevier, 2018-06) Higgins, Rosemary D.; Jobe, Alan H.; Koso-Thomas, Marion; Bancalari, Eduardo; Viscardi, Rose M.; Hartert, Tina V.; Ryan, Rita M.; Kallapur, Suhas G.; Steinhorn, Robin H.; Konduri, Girija G.; Davis, Stephanie D.; Thebaud, Bernard; Clyman, Ronald I.; Collaco, Joseph M.; Martin, Camilia R.; Woods, Jason C.; Finer, Neil N.; Raju, Tonse N. K.; Pediatrics, School of Medicine
    Comment in Bronchopulmonary Dysplasia: The Ongoing Search for One Definition to Rule Them All. [J Pediatr. 2018] Midlife crisis? In its 50th year, BPD redefines itself. [J Pediatr. 2018]
  • Thumbnail Image
    Item
    Respiratory syncytial virus infection activates IL-13–producing group 2 innate lymphoid cells through thymic stromal lymphopoietin
    (Elsevier, 2016-09) Stier, Matthew T.; Bloodworth, Melissa H.; Toki, Shinji; Newcomb, Dawn C.; Goleniewska, Kasia; Boyd, Kelli L.; Quitalig, Marc; Hotard, Anne L.; Moore, Martin L.; Hartert, Tina V.; Zhou, Baohua; McKenzie, Andrew N.; Peebles Jr., R. Stokes; Department of Pediatrics, IU School of Medicine
    BACKGROUND: Respiratory syncytial virus (RSV) is a major health care burden with a particularly high worldwide morbidity and mortality rate among infants. Data suggest that severe RSV-associated illness is in part caused by immunopathology associated with a robust type 2 response. OBJECTIVE: We sought to determine the capacity of RSV infection to stimulate group 2 innate lymphoid cells (ILC2s) and the associated mechanism in a murine model. METHODS: Wild-type (WT) BALB/c, thymic stromal lymphopoietin receptor (TSLPR) knockout (KO), or WT mice receiving an anti-TSLP neutralizing antibody were infected with the RSV strain 01/2-20. During the first 4 to 6 days of infection, lungs were collected for evaluation of viral load, protein concentration, airway mucus, airway reactivity, or ILC2 numbers. Results were confirmed with 2 additional RSV clinical isolates, 12/11-19 and 12/12-6, with known human pathogenic potential. RESULTS: RSV induced a 3-fold increase in the number of IL-13-producing ILC2s at day 4 after infection, with a concurrent increase in total lung IL-13 levels. Both thymic stromal lymphopoietin (TSLP) and IL-33 levels were increased 12 hours after infection. TSLPR KO mice did not mount an IL-13-producing ILC2 response to RSV infection. Additionally, neutralization of TSLP significantly attenuated the RSV-induced IL-13-producing ILC2 response. TSLPR KO mice displayed reduced lung IL-13 protein levels, decreased airway mucus and reactivity, attenuated weight loss, and similar viral loads as WT mice. Both 12/11-19 and 12/12-6 similarly induced IL-13-producing ILC2s through a TSLP-dependent mechanism. CONCLUSION: These data demonstrate that multiple pathogenic strains of RSV induce IL-13-producing ILC2 proliferation and activation through a TSLP-dependent mechanism in a murine model and suggest the potential therapeutic targeting of TSLP during severe RSV infection.