After completing a National Institutes of Health Post-baccalaureate Intramural Research Training Award (IRTA) fellowship with the Laboratory of Immunology, National Eye Institute, Dr. Bojanowski received her medical school training at George Washington University School of Medicine. She then completed a dual residency program in Internal Medicine and Pediatrics at Louisiana State University Health Sciences Center – New Orleans (LSUHSC-NO), followed by Adult Pulmonary and Critical Care Fellowship at the University of California, San Diego (UCSD). She is board certified in Pediatrics, Internal Medicine, Adult Pulmonary Disease and Adult Critical Care Medicine.
Since her research fellowship at the National Institutes of Health, Dr. Bojanowski has co-authored over 50 abstracts and papers and was appointed to the T-32 training grant at UCSD during her Pulmonary and Critical Care fellowship. Her primary research interests are in lung immunology and innate host response. Her clinical interests in addition to critical care include chronic transitional pediatric to adult lung disease including cystic fibrosis, non-cystic fibrosis bronchiectasis, and rare lung disease. She joined Tulane faculty as an Assistant Professor of Medicine in 2018 and is particularly excited to join the Tulane Adult Cystic Fibrosis Center as Associate Director.
Dr. Bojanowski is also committed to medical education, training and career development. She is a member of the American Thoracic Society and American College of Chest Physicians. She is currently serving on the national American Thoracic Society Training Committee.
Areas of Expertise (5)
Adult Cystic Fibrosis
Critical Care Medicine
Louisiana Clinical and Translational Science (LA CaTS) Roadmap Scholar Award (professional)
University of California, San Diego: Fellowship, Chief Fellow, Pulmonary and Critical Care Medicine Clinical and Research Fellowship
Louisiana State University Health Sciences Center: Internship and Residency, Internal Medicine and Pediatrics Internship and Residency
George Washington University: Doctor of Medicine, School of Medicine and Health Sciences
Vanderbilt University: B.S., Neuroscience
- American Thoracic Society
- American College of Chest Physicians
- ATS Assembly of Allergy, Immunology and Inflammation Program Committee
- ATS Training Committee
Media Appearances (2)
Vaping wrecks immune cell function, increases infection risk
A new study published in the Journal Cell Physiology shows that e-cigarettes have toxic effects on neutrophils function, making them a threat to human health by increasing the likelihood of infection with Gram-negative bacteria.
Tulane expert available to talk about the exposure, negative effects of vaping
Vaping has become America’s latest epidemic, and the number of vaping-related illnesses continues to increase daily.
Corriden R, Moshensky A, Bojanowski CM, Meier A, Chien J, Nelson RK, Crotty Alexander LE.
2019 E-cigarettes are portrayed as safer relative to conventional tobacco. However, burgeoning evidence suggests that E-cigarettes may adversely affect host defenses. However, the precise mechanisms by which E-cigarette vapor alters innate immune cell function have not been fully elucidated. We determined the effects of E-cigarette exposure on the function and responses to infectious challenge of the most abundant innate immune cell, the neutrophil, using isolated human neutrophils and a mouse model of Gram-negative infection. Our results revealed that human neutrophils exposed to E-cigarette vapor had 4.2-fold reductions in chemotaxis towards the bacterial cell-well component f-Met-Leu-Phe (p < 0.001). F-actin polarization and membrane fluidity were also adversely affected by E-cigarette vapor exposure. E-cigarette exposed human neutrophils exhibited a 48% reduction in production of reactive oxygen species (ROS; p < 0.001). Given the central role of ROS in neutrophil extracellular trap (NET) production, NET production was quantified and E-cigarette vapor exposure was found to reduce NETosis by 3.5-fold (p < 0.01); formulations with and without nicotine containing propylene glycol exhibiting significant suppressive effects. However, non-canonical NETosis was unaffected. In addition, exposure to E-cigarette vapor lowered the rate of bacterial bioparticle phagocytosis by 47% (p < 0.05). In our physiologic mouse model of chronic E-cigarette exposure and sepsis, E-cigarette vapor inhalation led to reduced neutrophil migration into infected spaces and a higher burden of Pseudomonas. These findings provide evidence that E-cigarette use adversely impacts the innate immune system and may place E-cigarette users at higher risk for dysregulated inflammatory responses and invasive bacterial infections.
Alasmari F, Crotty Alexander LE, Hammad AM, Bojanowski CM, Moshensky A, Sari Y.
2019 Electronic (E)-cigarettes are the latest form of nicotine delivery device and are highly popular in the general population. It is currently unknown whether vaping E-cigarettes (E-CIGs) leads to nicotine addiction. Alterations in the levels of the neurotransmitters in the mesocorticolimbic areas have been reported to mediate the initiation and development of nicotine addiction. Therefore, to determine whether E-CIGs activate the same addiction pathways as conventional cigarettes, we investigated for the effects of daily inhalation of nicotine (24 mg/ml)-containing E-CIG vapor for 6 months on the concentrations of these neurotransmitters in the frontal cortex (FC) and striatum (STR) of male C57BL/6 mice as compared to control group that was exposed to air only. We reported here that 6-month E-CIG vapor containing nicotine inhalation decreased dopamine concentration only in the STR. There were no changes in serotonin concentrations in the FC or STR. Chronic E-CIG exposure also increased glutamate concentration in the STR alone, while glutamine concentrations were increased in both the FC and STR. We found that E-CIG exposure also decreased GABA concentration only in the FC. These data suggest that chronic E-CIG use alters homeostasis of several neurotransmitters in the mesocorticolimbic areas, which may result in the development of nicotine dependence in E-CIG users.
Boddu SA, Bojanowski CM, Lam MT, Advani IN, Scholten EL, Sun X, Montgrain P, Malhotra A, Jain S, Alexander LEC.
Hepokoski ML, Bellinghausen AL, Bojanowski CM, Malhotra A.
Tuo J, Ross RJ, Reed GF, Yan Q, Wang JJ, Bojanowski CM, Chew EY, Feng X, Olsen TW, Ferris FL 3rd, Mitchell P, Chan CC.
2008 To assess the association and combined effect on the risk of age-related macular degeneration (AMD) by the HtrA1 and complement factor H (CFH) polymorphisms, smoking, and serum cholesterol.