A unifying theme of the Program Project is the focus on cellular and molecular studies of the evolving microenvironment of airway inflammation. All three projects take advantage of genetic mouse models. Mycoplasma pulmonis infected mice as a model of chronic airway inflammation, and cutting-edge 2-photon and confocal imaging of cells and tissues in the ainways and lung. To this end, the mouse tools core, jointly administered by the co-directors, will serve the common needs of the projects by providing three main functions: (i) to standardize M. pulmonis preparation, infection procedures, and handling of infected mice;(ii) to develop, optimize and implement genotyping procedures for identifying mutant mice;and (iii) to develop and provide access to cutting edge methods for the real-time analysis of cells involved in the development of inflammation in the ainways and lung. First, the core staff will produce stocks of virulent M. pulmonis organisms, which will be tested for use in all experiments to ensure a consistent supply with minimal variability. Second, the core will use standardized flow cytometric, DNA preparation and polymerase chain reaction procedures to genotype mice from the mutant colonies that will be used in the three projects. Third, the core will provide access to and assist in novel and newly developed techniques for real-time viewing of living cells in the ainways and lung through a collaboration with the UCSF Biological Imaging Development Center (www.ucsf edu/bidc/). Centralizing and coordinating infection, genotyping procedures, and imaging approaches will avoid duplication of resources, ensure that standardized procedures are used by all groups, facilitate the exchange of information, and foster collaborative interactions.

Public Health Relevance

The three core functions are essential to all three projects. They serve to provide standardized reagents, services and protocols to all investigators as well as a repository for the community at large. They are all highly specialized for the studies of lung inflammation and the relevance of each specific scientific aim is established for each project.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL024136-34
Application #
8451353
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2013-04-01
Budget End
2014-03-31
Support Year
34
Fiscal Year
2013
Total Cost
$312,644
Indirect Cost
$109,533
Name
University of California San Francisco
Department
Type
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94143
Caughey, George H (2016) Mast cell proteases as pharmacological targets. Eur J Pharmacol 778:44-55
Korhonen, Emilia A; Lampinen, Anita; Giri, Hemant et al. (2016) Tie1 controls angiopoietin function in vascular remodeling and inflammation. J Clin Invest 126:3495-510
Kim, Minah; Allen, Breanna; Korhonen, Emilia A et al. (2016) Opposing actions of angiopoietin-2 on Tie2 signaling and FOXO1 activation. J Clin Invest 126:3511-25
Huang, Jennifer L; Woolf, Adrian S; Kolatsi-Joannou, Maria et al. (2016) Vascular Endothelial Growth Factor C for Polycystic Kidney Diseases. J Am Soc Nephrol 27:69-77
Sen, Debasish; Jones, Stephen M; Oswald, Erin M et al. (2016) Tracking the Spatial and Functional Gradient of Monocyte-To-Macrophage Differentiation in Inflamed Lung. PLoS One 11:e0165064
Greenland, John R; Wong, Charissa M; Ahuja, Rahul et al. (2016) Donor-Reactive Regulatory T Cell Frequency Increases During Acute Cellular Rejection of Lung Allografts. Transplantation 100:2090-8
Headley, Mark B; Bins, Adriaan; Nip, Alyssa et al. (2016) Visualization of immediate immune responses to pioneer metastatic cells in the lung. Nature 531:513-7
Lindsay, Robin S; Corbin, Kaitlin; Mahne, Ashley et al. (2015) Antigen recognition in the islets changes with progression of autoimmune islet infiltration. J Immunol 194:522-30
Le, Catherine T K; Laidlaw, Grace; Morehouse, Christopher A et al. (2015) Synergistic actions of blocking angiopoietin-2 and tumor necrosis factor-α in suppressing remodeling of blood vessels and lymphatics in airway inflammation. Am J Pathol 185:2949-68
Bose, Oishee; Baluk, Peter; Looney, Mark R et al. (2015) Mast cells present protrusions into blood vessels upon tracheal allergen challenge in mice. PLoS One 10:e0118513

Showing the most recent 10 out of 584 publications