Research

W Bi/J Alcorn: Basal, stress-induced and lipopolysaccharide (LPS)-induced proinflammatory cytokine expression, as well as toll-like receptor 4 (TLR4) expression, in epithelial cells and intestinal damage resembling NEC is greater in SP-A-deficient mouse pups compared to wildtype pups. Gavage with purified SP-A reduces cytokine expression, TLR4 expression and intestinal damage. The goal is to define the mechanisms by SP-A reduces inflammation in epithelial cells by regulating expression of TLR4.

C Meyer: The presence of SP-A in mouse and human breast milk has been demonstrated by Dr. Meyer for the first time. When reared by wild type dams, SP-A-deficient newborn pups have reduced expression of cytokines and TLR4 compared to pups reared by SP-A-deficient dams. The goal is to define to impact of SP-A on the immunomodulatory properties of breast milk.

T Tran: Acute hyperoxia increases inflammation and damage in neonatal lung. Vitamin D has been reported to alleviate inflammation in adult lung. The goal is to investigate the impact of high and low doses of vitamin D on pulmonary inflammation and damage in neonatal mice exposed to hyperoxia using SP-A-deficient pups as a model of premature birth.

C Crocker. SP-A has been reported in brain in the intraventricular region. Our goal is to investigate the potential role of SP-A in modulating experimentally-induced inflammation in the neonatal brain using wild type and SP-A deficient pups.

Current interests include:

  1. The Role of Surfactant Protein-A (SP-A) on Gastrointestinal Inflammation in Neonates
  2. Impact of Surfactant Protein-A (SP-A) on Breast Milk
  3. Impact of Vitamin D on Pulmonary Inflammation in Neonatal Mice Exposed to Acute Hyperoxia at Birth
  4. The Role of Surfactant Protein-A (SP-A) in Neuroinflammation Using a Murine Model