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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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Award Detail for: NON-OXIDATIVE RESISTANCE TO A. FUMIGATUS BY ALVEOLAR MACROPHAGES
UNIVERSITY OF WISCONSIN - STOUT
DUNS Number: 802853403
POST OFFICE BOX 790
MENOMONIE, WI 54751
Recipient Report: Grant or Loan
Prime Recipient

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Reporting Information
Award Type Award Number Final Report
Grant R21AI078151-2-003 Recipient responsible for this data

Award Recipient Information
Recipient DUNS Number Recipient Account Number Recipient Congressional District
802853403 Recipient responsible for this data 3

Award Information
Funding Agency Code Awarding Agency Code Award Date
7529 7529 06-23-2010
Amount of Award Sub Account Number for Program Source (TAS)  
$ 186,340 Recipient responsible for this data
Program Source (TAS)* CFDA Number 
750900 93.701
Total Number of Sub Awards to Individuals Total Amount of Sub Awards to Individuals
Recipient responsible for this data Recipient responsible for this data
Total Number of Payments to Vendors less than $25,000/award Total Amount of Payments to Vendors less than $25,000/award
Recipient responsible for this data Recipient responsible for this data
Total Number of Sub Awards less than $25,000/award Total Amount of Sub Awards less than $25,000/award
Recipient responsible for this data Recipient responsible for this data
Award Description
DESCRIPTION (provided by applicant): Infections caused by Aspergillus fumigatus are a leading cause of death in immune compromised individuals. A. fumigatus is also a threat to those lacking a functional NADPH oxidase system, a defensive oxidant-generating system of phagocytic immune cells. Alveolar macrophages (AM) are phagocytes known to be important in the early innate defense against A. fumigatus conidia, and have been reported to produce oxidants to kill engaged pathogens. However, many details about the molecular mechanisms by which AM kill A. fumigatus are not well understood. With conflicting data about the antifungal mechanisms of AM, and the role of NADPH oxidase in this process, we proposed to better define the microbicidal mechanism of AM that protects from infections by A. fumigatus. The overall hypothesis being investigated is that the AM-derived resistance to A. fumigatus conidia is mediated by NADPH oxidase-independent microbicidal mechanisms that involve nutrient sequestration, leading to conidial killing. Three aims proposed to address this goal are: 1) to compare the conidiacidal activity of AM from normal and gp91phox-/- mice that lack a functional phagocyte oxidase, using both in vitro and in vivo analyses. Reports on the role of NADPH oxidase of AM in protecting humans from IPA are conflicting, and our data do not indicate the respiratory burst in AM is necessary for a resistance to aspergillosis, as we have shown it is in neutrophils. This information will provide a better understanding of how the NADPH oxidase is applied in aspergillosis immunity. 2) to compare NADPH oxidase-dependent superoxide liberation by AM from normal C57Bl/6 and gp91phox-/- mice to describe the capabilities of oxidant production of AM in these mouse strains. Our preliminary data suggest that oxidant production in AM from normal and gp91phox-/- mice is not significantly different when triggered by oxidant-triggering stimulants, or by phagocytosis of fungal particles. This information will provide a better understanding of the capacity of oxidant generation by AM, and 3) to compare transcriptional responses of conidia exposed to AM from normal C57Bl/6 mice, to those in conidia subjected to low nutrient conditions. This aim will test whether nutrient sequestration is a conidiacidal mechanism of AM. If oxidative killing of conidia is not utilized by AM, then the use of A. fumigatus conidia as a bioprobe of the conidiacidal environment of the AM should be suggested by transcriptional responses of internalized conidia. This information will provide a better understanding of the antifungal mechanism of AM that kills A. fumigatus conidia. The long-term goal of these approaches is to identify potential therapeutic targets to augment the natural immunity that protects from infections by A. fumigatus. PUBLIC HEALTH RELEVANCE: Aspergillus fumigatus is an inhaled fungus that can infect human patients with various types if immune suppression. At this time, most individuals that become infected by this organism do not survive, despite aggressive medical management. The long- term goal of this work is to identify molecular mechanisms that enable alveolar macrophages to kill the spore-like conidial form of A. fumigatus, so that natural immunity can be augmented in those at risk.

Project Information
Project Name or
Project/Program Title
Project Status Total Federal Amount ARRA Funds
Received/Invoiced
NON-OXIDATIVE RESISTANCE TO A. FUMIGATUS BY ALVEOLAR MACROPHAGES Recipient responsible for this data Recipient responsible for this data
Number of Jobs Description of Jobs Created
Recipient responsible for this data Recipient responsible for this data
Quarterly Activities/Project Description
Recipient responsible for this data
 
Activity Code (NAICS or NTEE-NPC)
1Recipient responsible for this data2Recipient responsible for this data
3Recipient responsible for this data4Recipient responsible for this data
5Recipient responsible for this data6Recipient responsible for this data
7Recipient responsible for this data8Recipient responsible for this data
9Recipient responsible for this data10Recipient responsible for this data
Total Federal Amount of ARRA
Expenditure
Total Federal ARRA
Infrastructure Expenditure
Infrastructure Contact Name
Recipient responsible for this data Recipient responsible for this data Recipient responsible for this data
Infrastructure Contact Email Infrastructure Contact Phone Infrastructure Contact Phone Ext.
Recipient responsible for this data Recipient responsible for this data Recipient responsible for this data
Infrastructure Contact Street Address 1 Infrastructure Contact Street Address 2 Infrastructure Contact Street Address 3
POST OFFICE BOX 790 Not Available Recipient responsible for this data
Infrastructure City Infrastructure State Infrastructure ZIP Code+4
MENOMONIE WI 54751
Infrastructure Purpose and Rationale
Recipient responsible for this data

Primary Place of Performance
Street Address 1 Street Address 2 City
DEPARTMENT OF BIOLOGY 184 MICHEELS HALL Recipient responsible for this data MENOMONIE
State Zip Code+4 Congressional District
WI 54751 Not Available
Country  
US

Recipient Highly Compensated Officers
Prime Recipient Indication of Reporting Applicability # Officer Name Officer Compensation
Recipient responsible for this data 1 Recipient responsible for this data Recipient responsible for this data
2 Recipient responsible for this data Recipient responsible for this data
3 Recipient responsible for this data Recipient responsible for this data
4 Recipient responsible for this data Recipient responsible for this data
5 Recipient responsible for this data Recipient responsible for this data

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USE IN THE RECIPIENT REPORT

The information provided by this tool is baseline data that the Recipient should include in the Recipient Report that must be submitted to FederalReporting.gov beginning October 1, 2009. The data from this tool can be cut and pasted directly into the Recipient Report.