About

Shampa Chatterjee, Ph.D., is a Research Associate Professor of Physiology at the University of Pennsylvania's Perelman School of Medicine, within the Department of Physiology. Her research focuses on understanding endothelial cell responses to mechanical forces and chemical stimuli, particularly how these responses initiate and amplify inflammation. She employs various models, including in vitro, in situ, and in vivo systems, to study inflammation signaling pathways and their role in tissue injury, with the aim of designing strategies to mitigate tissue damage. Her work includes developing specialized models such as pulmonary endothelial cell networks, mouse models of lung inflammation, and clinical studies on e-cigarette smokers, as well as an endotoxin-exposed 3D in vitro gum model for periodontal inflammation.

Research topics

• Medicine
• Internal medicine
• Anesthesia
• Pathology
• Psychology
• Immunology
• Surgery
• Environmental health
• Cardiology
• Intensive care medicine

Selected publications

• Inflammation and the oral and gut microbiota with COVID-19

  Elsevier eBooks · 2025-01-01

  book-chapterSenior author
  PublisherDOI

• What have we learnt from the COVID-19 pandemic?

  Elsevier eBooks · 2025-01-01

  book-chapter1st authorCorresponding
  PublisherDOI

• Population-specific polymorphisms and SARS-CoV-2 infectivity

  Elsevier eBooks · 2025-01-01

  book-chapterSenior author
  PublisherDOI

• Circadian Control of Pulmonary Endothelial Signaling Occurs via the NADPH Oxidase 2-NLRP3 Pathway

  Journal of Biological Rhythms · 2025-09-14

  articleOpen accessSenior authorCorresponding

  Circadian rhythms are endogenous oscillations that occur with a 24-h periodicity and support organismal homeostasis. While the role of the circadian clock in systemic vasculature is well known, its role in pulmonary vasculature, specifically in the pulmonary endothelium, has remained unexplored. We hypothesized that the circadian clock directly regulates pulmonary endothelium to control lung inflammation. Using pulmonary artery segments and endothelial cells isolated from lungs of mPer2luciferase transgenic mice, we monitored circadian rhythms and observed that lipopolysaccharide (LPS) treatment disrupted rhythmicity. This disruption was mediated by reactive oxygen species (ROS) generated via NADPH oxidase 2 (NOX2). Remarkably, the pharmacologic inhibition of NOX2 before LPS exposure restored circadian rhythmicity in the pulmonary endothelium. In wild-type (WT) mice, LPS activated a NOX2-NLRP3 signaling axis that drove inflammation as evidenced by increased polymorphonuclear neutrophil (PMN) accumulation and intercellular adhesion molecule-1 (ICAM-1) expression on the pulmonary endothelium. In contrast, disruption of the clock using two different clock mutants ( Bmal 1 –/– and Cry1/2 –/– ) resulted in a sustained baseline elevation of PMN and ICAM-1, which changed minimally with LPS. This effect was attributed to aberrant activation of the NLRP3 inflammasome at baseline in the clock mutants, as supported by lung transcriptomic data and reversal of the phenotype with an NLRP3 inhibitor. Importantly, these findings also reveal an intriguing bidirectional relationship: while the circadian clock modulates inflammatory responses, inflammatory stimuli in turn alter circadian rhythmicity via the NOX2 pathway. Together, our results identify a novel mechanism by which circadian control of pulmonary endothelial inflammation may be leveraged to mitigate the consequences of clock disruption in lung disease.

  PublisherDOI

• SARS-CoV-1, SARS-CoV-2, and MERS-CoV: Similarities and differences in origin and transmission

  Elsevier eBooks · 2025-01-01 · 1 citations

  book-chapterSenior author
  PublisherDOI

• Implications of inflammation: Bone and joint health with COVID-19

  Elsevier eBooks · 2025-01-01

  book-chapterSenior author
  PublisherDOI

• Contributors

  Elsevier eBooks · 2025-01-01

  book-chapter
  PublisherDOI

• Reactive oxygen species in endothelial signaling in COVID-19: Protective role of the novel peptide PIP-2

  PLoS ONE · 2024-05-21 · 3 citations

  articleOpen accessSenior authorCorresponding

  INTRODUCTION: Recent research suggests that endothelial activation plays a role in coronavirus disease 2019 (COVID-19) pathogenesis by promoting a pro-inflammatory state. However, the mechanism by which the endothelium is activated in COVID-19 remains unclear. OBJECTIVE: To investigate the mechanism by which COVID-19 activates the pulmonary endothelium and drives pro-inflammatory phenotypes. HYPOTHESIS: The "inflammatory load or burden" (cytokine storm) of the systemic circulation activates endothelial NADPH oxidase 2 (NOX2) which leads to the production of reactive oxygen species (ROS) by the pulmonary endothelium. Endothelial ROS subsequently activates pro-inflammatory pathways. METHODS: The inflammatory burden of COVID-19 on the endothelial network, was recreated in vitro, by exposing human pulmonary microvascular endothelial cells (HPMVEC) to media supplemented with serum from COVID-19 affected individuals (sera were acquired from patients with COVID-19 infection that eventually died. Sera was isolated from blood collected at admission to the Intensive Care Unit of the Hospital of the University of Pennsylvania). Endothelial activation, inflammation and cell death were assessed in HPMVEC treated with serum either from patients with COVID-19 or from healthy individuals. Activation was monitored by measuring NOX2 activation (Rac1 translocation) and ROS production; inflammation (or appearance of a pro-inflammatory phenotype) was monitored by measuring the induction of moieties such as intercellular adhesion molecule (ICAM-1), P-selectin and the NLRP3 inflammasome; cell death was measured via SYTOX™ Green assays. RESULTS: Endothelial activation (i.e., NOX2 activation and subsequent ROS production) and cell death were significantly higher in the COVID-19 model than in healthy samples. When HPMVEC were pre-treated with the novel peptide PIP-2, which blocks NOX2 activation (via inhibition of Ca2+-independent phospholipase A2, aiPLA2), significant abrogation of ROS was observed. Endothelial inflammation and cell death were also significantly blunted. CONCLUSIONS: The endothelium is activated during COVID-19 via cytokine storm-driven NOX2-ROS activation, which causes a pro-inflammatory phenotype. The concept of endothelial NOX2-ROS production as a unifying pathophysiological axis in COVID-19 raises the possibility of using PIP-2 to maintain vascular health.

  PublisherOA PDFDOI

• Review 2: "Epigenetic Liquid Biopsies Reveal Elevated Vascular Endothelial Cell Turnover and Erythropoiesis in Asymptomatic COVID-19 Patients"

  2023-09-12

  peer-reviewOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Reviews of "Epigenetic Liquid Biopsies Reveal Elevated Vascular Endothelial Cell Turnover and Erythropoiesis in Asymptomatic COVID-19 Patients"

  2023-09-12

  peer-reviewOpen accessSenior author

  This preprint analyzes cell-free DNA methylation patterns in COVID-19 patients to assess tissue damage and cellular turnover.The two reviewers provided positive feedback on the study's rationale, methods, and findings.They lauded the use of liquid biopsies to non-invasively monitor COVID-19 severity and progression.Both reviewers provided a clear summary of the main claims and key results showing

  PublisherOA PDFDOI

Recent grants

• The NLRP3 inflammasome in regulating injury with lung transplant

  NIH · $405k · 2019–2021

Frequent coauthors

• Aron B. Fisher

  University of Pennsylvania

  139 shared

• Nankang Hong

  University of Pennsylvania

  54 shared

• Sheldon I. Feinstein

  52 shared

• Chandra Dodia

  University of Pennsylvania

  41 shared

• Kevin Yu

  Harvard University

  28 shared

• Kris DeBolt

  Institute for Environmental Management

  24 shared

• Intae Lee

  19 shared

• Jian Tao

  Institute for Environmental Management

  17 shared

Labs

• Shampa Chatterjee LaboratoryPI

Education

• Ph.D., Chemistry

  Indian Institute of Technology, Bombay, India

  1997