HHS Recovery Act Recipient Reporting Readiness Tool

Step 4. Review and Copy the Grant Awards Data

TAGGS provides some – but not all – of the data needed for the Recipient Report. Recipients are responsible for directly collecting and reporting all required data to FederalReporting.gov. Data that HHS does not currently collect are highlighted in yellow. Do not copy this highlighted information. Please enter the appropriate data for your organization in these required fields. For assistance with entering these data please contact FederalReporting.gov.

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Prime Recipient Report

Award Detail for: ROLE OF DPPI & SERINE PROTEASES IN INFLAMMATORY DISEASES
Recipient Name:WASHINGTON UNIVERSITY
DUNS Number: 068552207
CAMPUS BOX 1034
SAINT LOUIS, MO 63112

Reporting Information

Award Type*: Grant

Award Number*: 3R01AI049261-08S1

Final Report*: Recipient responsible for this data

Award Recipient Information

Recipient DUNS Number*: 068552207

Recipient Account Number: Recipient responsible for this data

Recipient Congressional District*: 1

Award Information

Funding Agency Code*: 7529

Awarding Agency Code*:7529

Award Date*: 05-24-2010

Amount of Award*: $ 10,263

Program Source (TAS)*: 750900

CFDA Number*: 93.701

Sub Account Number for Program Source (TAS)*: Recipient responsible for this data

Total Number of Sub Awards to Individuals*: Recipient responsible for this data

Total Amount of Sub Awards to Individuals*: Recipient responsible for this data

Total Number of Payments to Vendors less than $25,000/award*: Recipient responsible for this data

Total Amount of Payments to Vendors less than $25,000/award*: Recipient responsible for this data

Total Number of Sub Awards less than $25,000/award*: Recipient responsible for this data

Total Amount of Sub Awards less than $25,000/award*: Recipient responsible for this data

Award Description* DESCRIPTION (provided by applicant): The long-term goal of this project is to fully characterize the mechanisms by which neutrophil serine proteases regulate the inflammatory response. We hope that information gained from these studies can be used to develop strategies to inhibit the activity of these proteases in inflammatory diseases while preserving their ability to kill invading pathogens. Over the past several years, we have learned that, more than being degradative enzymes, neutrophil serine proteases can act as specific regulators of inflammation by modulating the release of cytokines and chemokines as well as activating specific receptors. Yet, the exact mechanisms by which these proteases exert these regulatory effects are still unknown. To further characterize these regulatory mechanisms in vitro and in vivo, we propose the following aims: 1. We will define the mechanisms by which cell-surface-bound cathepsin G (CG) modulates neutrophil effector functions. Our data indicate that extracellular CG cleaves a yet-unidentified molecule (or molecules) and this proteolytic modification leads to cytoskeleton reorganization, cell spreading, and effector functions. We have identified two candidate proteins as potential substrates for CG, syndecan-4 and CD43. In this aim, we will determine whether CG directly proteolyses syndecan-4 and CD43 and whether this enzymatic modification is critical for CG-dependent neutrophil effector functions. 2. We will generate a loss-of-function mutation model for proteinase 3 (PR3) to define its role in cytokine production and its contribution to inflammation in vivo. Our preliminary data suggest that in several inflammatory models, PR3 plays an important role in the local production or processing of pro- inflammatory cytokines and chemokines. To definitively study the role of PR3 in inflammation in vivo, we propose to generate a loss-of-function mutation in PR3. We will fully characterize the PR3-deficient mice and use these mutant mice for in vitro assays and in vivo models to define the physiologic role of PR3. 3. We will generate a murine model of anti-neutrophil cytoplasmic antibody (ANCA)-mediated inflammation and determine the factors that dictate disease development. ANCAs are associated with several small vessel vasculitides, including Wegener's granulomatosis. In 90% of Wegener's, ANCAs are directed against PR3, although ANCAs specific for other serine proteases are also found. We propose to determine whether all ANCAs are potentially pathogenic. We also hypothesize that decreased expression of complement regulators in the kidney may be a determinant that influences disease severity in target organ.

Project Information

Project Name or Project/Program Title*: ROLE OF DPPI & SERINE PROTEASES IN INFLAMMATORY DISEASES

Project Status*: Recipient responsible for this data

Total Federal Amount of ARRA Funds Received/Invoiced*: Recipient responsible for this data

Number of Jobs*: Recipient responsible for this data

Description of Jobs Created*: Recipient responsible for this data

Quarterly Activities/Project Description*: Recipient responsible for this data

Activity Code (NAICS or NTEE-NPC)*: Recipient responsible for this data

Total Federal Amount of ARRA Expenditure* (Enter the cumulative total amount of Recovery Funds received that were expended to projects or activities. Refer to the Data Model for details on how to calculate this amount.): Recipient responsible for this data

Total Federal ARRA Infrastructure Expenditure Recipient responsible for this data

Infrastructure Contact Name: Recipient responsible for this data

Infrastructure Contact Email: Recipient responsible for this data

Infrastructure Contact Phone: Recipient responsible for this data

Infrastructure Contact Phone Ext: Recipient responsible for this data

Infrastructure Contact Street Address 1: CAMPUS BOX 1034

Infrastructure Contact Street Address 2: Not Available

Infrastructure Contact Street Address 3: Recipient responsible for this data

Infrastructure City: SAINT LOUIS

Infrastructure State: MO

Infrastructure ZIP Code+4: 63112

Infrastructure Purpose and Rationale (If applicable, enter an explanation about how the infrastructure investment will contribute to one or more purposes of the Recovery Act. Refer to the Data Model for details on what to report. 4000 characters or less.): Recipient responsible for this data

Primary Place of Performance

Street Address 1: CAMPUS BOX 1054

Street Address 2: SAINT LOUIS

City*: SAINT LOUIS

State*: MO

ZIP Code+4*: 631304899

Congressional District*: 1

Country*: US

Recipient Highly Compensated Officers

Prime Recipient Indication of Reporting Applicability*: Recipient responsible for this data

1. Officer Name and Compensation: Recipient responsible for this data
2. Officer Name and Compensation: Recipient responsible for this data
3. Officer Name and Compensation: Recipient responsible for this data
4. Officer Name and Compensation: Recipient responsible for this data
5. Officer Name and Compensation: Recipient responsible for this data

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