Project Grant R03HL171347
- This federal Project Grant award from the National Heart, Lung, and Blood Institute (NHLBI), under the Cardiovascular Diseases Research program (CFDA 93.837), provides $166,395 to Columbia University to conduct a 5-year research project on the impact of hyperoxia (excess oxygen) on the function of respiratory progenitor cells in neonates. The project aims to develop a better understanding of the mechanisms by which post-natal lung development occurs in the face of injurious agents like oxygen...
- This $480,990 Project Grant awarded by the National Heart, Lung, and Blood Institute under the Cardiovascular Diseases Research program (CFDA 93.837) aims to establish the central role of a recently identified lung cell type, "aerocytes," in regulating alveolar regeneration following lung injury. The research proposal has two key objectives: Investigate the role of aerocyte-derived R-spondin3 in lung growth and recovery using animal studies within disease-related lung injury models....
- This Project Grant award from the National Heart, Lung, and Blood Institute (CFDA 93.837 Cardiovascular Diseases Research) provides $773,868 to Baylor College of Medicine to elucidate the mechanisms regulating inflammation and the role of regulatory T cells (Tregs) in the development of bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH). The award aims to use well-established murine models and human biosamples to examine the mechanistic and therapeutic potential of Tregs in...
- This $136,050 Project Grant was awarded on June 30, 2025 by the National Heart, Lung, and Blood Institute (NHLBI), under the Cardiovascular Diseases Research (CFDA 93.837) program, to Tufts University School of Medicine. The grant supports research to characterize lung resident B1 cells and their impact on lung homeostasis during development. The research aims to investigate the functional role of B1 cells in developing lungs and their contribution to maintaining lung homeostasis, which...
- This Project Grant award from the National Heart, Lung, and Blood Institute (NHLBI) under CFDA 93.837 - Cardiovascular Diseases Research provides $750,162 to The Children's Hospital of Philadelphia (CHOP) to conduct research aimed at understanding the role of lymphatic dysfunction in the development of post-lung transplant bronchiolitis obliterans syndrome (BOS), a serious complication. The research project will use murine models to investigate the mechanisms of lymphatic vascular function after...
- This Project Grant award of $497,628.00 from the National Heart Lung and Blood Institute, under the Cardiovascular Diseases Research program (CFDA 93.837), supports research into pulmonary vagal sensory neurons and their role in breathing abnormalities associated with bronchopulmonary dysplasia (BPD) in preterm infants. The research aims to elucidate the dose- and duration-dependent effects of neonatal hyperoxia exposure on breathing control and the functional roles of distinct populations of...
- This Project Grant award from the National Heart, Lung, and Blood Institute (NHLBI) under the Cardiovascular Diseases Research program (CFDA 93.837) provides $684,814 to The Regents of the University of California, San Francisco (UCSF) to conduct research on the suppression of alveolar stem cells by tissue-resident lymphocytes in emphysema. The research aims to investigate how tissue factors in the lung alter the inflammatory response to viral infections, leading to the loss of alveolar type 2...
- This federal Project Grant award from the National Heart, Lung, and Blood Institute (NHLBI), under the Cardiovascular Diseases Research program (CFDA 93.837), provides $656,988 to the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University to enable new therapies for bacterial pneumonia. The objective of this 5-year project is to develop a therapeutic strategy that can replace a failed component of the macrophage lung injury response and allow healing in patients with...
- This Project Grant award from the National Heart, Lung, and Blood Institute (CFDA 93.837 - Cardiovascular Diseases Research) provides $167,705 to support Dr. Amit Bery's 5-year research and career development plan at Washington University. The project aims to investigate how interleukin-1B (IL-1B) promotes the differentiation, release, and trafficking of immunosuppressive neutrophils that can downregulate alloimmune responses after lung transplantation. The research will utilize techniques...
- This Project Grant award from the National Heart, Lung, and Blood Institute (CFDA 93.837 Cardiovascular Diseases Research) supports a 2-year $189,000 research project led by an Assistant Professor at the University of Colorado to investigate the role of aldehyde dehydrogenase 2 (ALDH2) in the pathogenesis and resolution of fibroproliferative acute respiratory distress syndrome (FP-ARDS). The research aims to improve understanding of the mechanisms underlying pathologic pulmonary fibrogenesis...
PROTECTIVE ROLE OF B CELLS IN HYPEROXIC LUNG INJURY - HIGH CONCENTRATIONS OF INSPIRED OXYGEN ARE NECESSARY DURING TREATMENT OF CRITICALLY ILL PATIENTS WITH IMPAIRED LUNG FUNCTION, SUCH AS THOSE WITH ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS). HOWEVER, STUDIES IN ANIMAL MODELS SHOW THAT HYPEROXIA MAY FURTHER EXACERBATE PULMONARY INFLAMMATION AND COMPOUND LUNG INJURY. FOUR-DAY EXPOSURE OF C57BL/6 MICE TO FIO2>90% LEADS TO DIFFUSE ALVEOLAR DAMAGE AND IMMUNE CELL INFILTRATION OF THE LUNGS, INCLUSIVE OF NKT CELLS AND NEUTROPHILS. WE RECENTLY DISCOVERED THAT EXPERIMENTAL HYPEROXIA IS ASSOCIATED WITH PROFOUND LOSS OF PULMONARY B CELLS. SUCH B CELL DEPLETION HAS ALSO BEEN REPORTED IN PATIENTS WITH ARDS. WE NOW SHOW THAT ADOPTIVE TRANSFER OF NAIVE B CELLS DURING HYPEROXIC EXPOSURE NOT ONLY ADDRESSES THE B CELL DEPLETION BUT ALSO LIMITS NEUTROPHIL INFILTRATION AND DECREASES THE SEVERITY OF LUNG INJURY. OUR CENTRAL HYPOTHESIS FOR THIS NOVEL LINE OF INVESTIGATION IS THAT HYPEROXIA IMPACTS PULMONARY B CELL NUMBERS AND/OR REGULATORY FUNCTIONS PROVOKING INFLAMMATION. THE COROLLARY IS THAT THIS PROCESS CAN BE REVERSED, AND LUNG INJURY MITIGATED BY ADMINISTRATION OF NAIVE B CELLS. WE PROPOSE THAT STRATEGIES PRESERVING OR AUGMENTING B CELL NUMBERS IN THE LUNGS COULD PROMOTE IMMUNE REGULATION AND MITIGATE INFILTRATION WITH INFLAMMATORY CELL SUBSETS (E.G., NKT CELLS, NEUTROPHILS) DURING HYPEROXIA. IN AIM 1, WE WILL CHARACTERIZE THE DYNAMICS OF B CELL RESPONSES DURING HYPEROXIA AND EXAMINE THE PROTECTIVE IMPACTS OF B CELL SUPPLEMENTATION. WE WILL ALSO TEST WHETHER PROTECTIVE EFFECTS OF EXOGENOUS B CELLS ARE MEDIATED BY IL-10 OR OTHER FACTORS. IN AIM 2, WE WILL STUDY MECHANISTIC INTERACTIONS BETWEEN PROTECTIVE B CELLS AND PATHOGENIC NKT CELLS DURING HYPEROXIA AS MEDIATED VIA THE AUTOTAXIN- LYSOPHOSPHATIDIC ACID PATHWAY. WE WILL TEST WHETHER DELETION OF NKT CELLS OR INHIBITION OF AUTOTAXIN FUNCTIONS IMPROVE B CELL NUMBERS IN THE LUNGS AND/OR OTHERWISE ENHANCE PROTECTIVE EFFECTS OF ADOPTIVE B CELL IMMUNOTHERAPY. THIS R03 AWARD WILL PROVIDE NEW DATA ON THE REGULATORY ROLE OF B CELLS IN HYPEROXIC LUNG INJURY AND ENSURE ESSENTIAL SUPPORT TO PI DR. HANIDZIAR ON HIS PATH TO BECOME AN INDEPENDENT, R01 FUNDED INVESTIGATOR.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $124.5k | 7/21/25 | ||
| Not listed | $124.5k | 7/17/24 |