Northwestern University Feinberg School of Medicine

Jacob Sznajder Lab

Lab Members

Meet the Lab team members. We welcome requests for information about our work and collaboration opportunities.

Principal Investigator

JacobSznajder

Jacob Sznajder, MD
Professor, Division of Medicine-Pulmonary
312-908-7737
MD: Israel Institute of Technology (1978); Internship: Rambam Medical Center, Israel (1980); Residency: Rambam Medical Center, Israel (1982); Fellowship: University of Chicago Hospitals (1986)
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Research Interests: Lung Biology, Hypercapnia, Influenza, Aging, Chronic obstructive pulmonary disease (COPD), Interstitial lung disease

Research Professors

Laura ADada

Laura A Dada, PhD
lauradada( at )northwestern.edu
Research Associate Professor
312-503-5397
Undergrad: School of Sciences, University of Buenos Aires, Buenos Aires, Argentina; PhD: School of Sciences, University of Buenos Aires, Buenos Aires, Argentina
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MasahikoShigemura

Masahiko Shigemura, PhD
Masahiko.shigemura( at )northwestern.edu
Research Assistant Professor
312-503-1685
Undergrad: Hokkaido University; PhD: Hokkaido University School of Medicine Post-Doctoral Fellowship: Northwestern University, Feinberg School of Medicine
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Carbon dioxide (CO2), a primary product of oxidative metabolism, can be sensed by eukaryotic cells eliciting specific responses via specific signaling pathways. The physiological and pathophysiological effects of high CO2 conditions (hypercapnia) on the lungs and specific lung cells, which are the primary site of CO2 elimination, are incompletely understood. Dr Shigemura has recently reported using combined unbiased molecular approaches with studies in mice and cell culture systems on the mechanisms by which hypercapnia increased airway smooth muscle contractility. The group described that high CO2 levels cause non-apoptotic caspase-7 activation via the calcium-calpain signal, which cleaves the transcription factor myocyte-specific enhancer factor 2D and in turn downregulates miR-133a that increases RhoA protein abundance and myosin light chain phosphorylation, and thus leads to airway smooth muscle contraction. In demonstration of the clinical relevance of this signaling, the group determined that patients with severe chronic obstructive pulmonary disease (COPD) and hypercapnia had elevated airway resistance, which improved after correction of hypercapnia. These data suggest that hypercapnia is not only a manifestation of severe COPD, but it can also worsen the airflow obstruction. Our studies will provide a pathophysiological and mechanistic perspective on the effects of hypercapnia on the lung airways and discuss the recent understanding of high CO2 modulation of the airway function.

Graduate Students

PatriciaBrazee

Patricia Brazee
pbrazee( at )u.northwestern.edu
DGP Graduate Student
312-503-1685
Undergrad: Smith College

Project Summary: Seasonal influenza virus A (IAV) infection can cause severe pneumonitis and have negative effects on patients’ health. As the primary target for IAV replication, alveolar epithelial cells (AEC) are important in releasing innate immune mediators that contribute to recruitment of monocytes and macrophages to the site of infection to orchestrate the host response. We are assessing the role of linear ubiquitination assembly complex (LUBAC) in modulating the inflammatory response of IAV-infection in the lungs.

Lab Manager

Lynn C.Welch

Lynn C. Welch
L-welch2( at )northwestern.edu
Research Laboratory Manager
312-503-4847
Undergrad: University of Evansville

Research Staff

Constance Runyan
c-runyan( at )northwestern.edu
Research Staff
312-503-1685