Vineet Bhandari MBChB, MD, DM.

Associate Professor of Pediatrics (Neonatology) and of Obstetrics, Gynecology, and Reproductive Sciences; Director, Program in Perinatal Research, Yale University School of Medicine

Research Interests

Bronchopulmonary Dysplasia; Cytokines; Lung development; Hyperoxia-Induced Lung Injury; Nitric Oxide

Current Projects

1. Role of Angiogenic Agents in Alveolar Maturation and Injury.
2. Role of Angiopoietin 2 in Hyperoxia-induced Lung Injury in the Newborn.
3. Nasal Ventilation in Preterms (NIP) Trial
4. Screening for Genetic Causes of Neonatal Respiratory Distress
5. The temporal kinetics of circulating angiopoietin levels in children with sepsis.

Research Summary

Babies born prematurely have immature lungs and are at high risk to develop the commonest chronic lung disease of infancy known as bronchopulmonary dyplasia or BPD. My research aims to understand the cause, early diagnosis and identify substances that can potentially be used for treatment of BPD. To achieve these goals, my research laboratory uses mouse models that mimic the human condition. Using genetic approaches, our laboratory targets specific substances in the lungs of newborn mice and modifies them and then evaluates the impact on the condition of the lungs. In addition, we look for the same targets identified in our mouse experiments in the lung secretions of the human premature babies to evaluate their clinical relevance.

Extensive Research Description

The overall focus of my research is to improve understanding of the etiopathogenesis of Bronchopulmonary Dysplasia (BPD) and find innovative methods to prevent and manage this disease. To achieve this, I have been doing bench, translational and clinical research covering the myriad aspects of this complex disorder. The focus of my laboratory research has been in understanding hyperoxia-induced lung injury in the developing lung, a major factor in causing BPD. I use genetic gain- and loss-of-function strategies in vitro and in vivo in developmentally-appropriate modeling systems to identify agents and dissect out their signal transduction pathways to understand the mechanisms of hyperoxia-induced injury. Towards the translational aspect, we measure specific agents identified in our in vivo murine experiments in tracheal aspirates obtained from premature neonates to assess their clinical relevance. In addition, I also study neonatal outcomes in relation to infection/inflammation-induced preterm birth. I have identified and quantified the genetic contribution in common neonatal disorders. I am also interested in early diagnosis of neonatal sepsis, a major factor in the pathogenesis of BPD. Since ventilation-induced lung injury is also a major contributor to BPD, I have focused on techniques to decrease the time spent on endotracheal intubation by neonates i.e. by using non-invasive ventilation. I have pioneered (and coined the term) the use of a novel technique of non-invasive ventilation that I developed, Synchronized Nasal Intermittent Positive Pressure Ventilation (SNIPPV).


Selected Publications

  • Streimish, I., Bizzarro, M., Northrup, V., Wang, C., Renna, S., Koval, N., Li, F.Y., Ehrenkranz, R., Rinder, H.M., and Bhandari, V. (2012). Neutrophil CD64 as a diagnostic marker in neonatal sepsis. The Pediatric infectious disease journal 31, 777-781. 3375383
  • Meller, S., and Bhandari, V. (2011). VEGF levels in humans and animal models with RDS and BPD: temporal relationships. Experimental lung research 38, 192-203.
  • Bhandari, V. (2012). Noninvasive respiratory support in the preterm infant. Clinics in perinatology 39, 497-511.
  • Meneses, J., Bhandari, V., and Alves, J.G. (2012). Nasal intermittent positive-pressure ventilation vs nasal continuous positive airway pressure for preterm infants with respiratory distress syndrome: a systematic review and meta-analysis. Archives of pediatrics & adolescent medicine 166, 372-376.
  • Li A, Choo-Wing R, Sun H, Angara S, Sakurai R, Rehan VR, Bhandari V. A potential role of the JNK pathway in hyperoxia-induced cell death, myofibroblast transdifferentiation and TGF-beta 1-mediated injury in the developing murine lung. BMC Cell Biology 2011; 12:54
  • Bhandari V, Choo-Wing R, Harijith A, Sun H, Syed MA, Homer RJ, Elias JA. Increased hyperoxia-induced lung injury in nitric oxide synthase 2 null mice is mediated via angiopoietin2. Am J Resp Cell Mol Biol 2012 [Epub Jan 6]
  • Aghai, Z.H., Camacho, J., Saslow, J.G., Mody, K., Eydelman, R., Bhat, V., Stahl, G., Pyon, K., and Bhandari, V. (2012). Impact of histological chorioamnionitis on tracheal aspirate cytokines in premature infants. American journal of perinatology 29, 567-572.
  • Aghai ZH, Mody K, Saslow J, Eydelman R, Bhat V, Stahl G, Pyon K, Bhandari V. IFN-y and IP-10 in tracheal aspirates from premature infants: relationship with bronchopulmonary dysplasia. Pediatr Pulmonol 2012 (in Press)

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