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Defining the impact of membrane vesicle deficiency on M. tuberculosis-macrophage interactions

Award Number: R03AI153560
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 06/04/2020
PERIOD OF PERFORMANCE END DATE: 05/31/2023

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Defining the impact of membrane vesicle deficiency on M. tuberculosis-macrophage interactions - Summary Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB) in humans, releases extracellular vesicles in vitro and in vivo. Like extracellular vesicles released by Gram-positive bacteria mycobacterial extracellular vesicles originate at the plasma membrane and are therefore, refer to as membrane vesicles (MV). Mycobacterial MVs contain a broad range of immunologically active proteins and glycolipids. When added to cells in culture, isolated MVs can regulate the immune response of uninfected macrophages, T-cells and dendritic cells. However, the influence of MVs on the interaction(s) between Mtb and the infected macrophage and the overall relevance of MVs production during infection is unclear, mainly because MV-deficient Mtb mutants have not yet been described. It has been recognized that MV biogenesis in M. tuberculosis is an active and regulated process, but the molecular mechanisms and factors involved remain largely unknown. Our previous work demonstrated that iron limitation, a condition encountered in the host, induces the production of MVs in Mtb. Preliminary studies based on this finding identified a pair of iron-responsive, mycobacterial dynamin-like protein (DLP)-encoding genes, isoniazid‐inducible gene A and C (iniAC) that are necessary for MV production. Our preliminary data indicate that a DLP null mutant grows normally in low-iron conditions and in macrophages. However, it exhibits a substantial defect in MV biogenesis. We postulate that this mutant will help define the role of MVs in immunomodulation and pathogenic interactions with the host. The proposed research will test our central hypothesis that MV production during macrophage infection requires the DLPs IniAC and that comparison of the immune response associated with macrophages infected with WT Mtb or the MV-deficient iniAC mutant will reveal substantial differences. The outcome of this project will increase understanding of MV biogenesis in Mtb and its relevance during macrophage infection, and provide the foundation for in vivo studies that evaluate the relevance of MVs at the Mtb-host interface.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2024 ( Subtotal = $0 )
2024	2021	RUTGERS, THE STATE UNIVERSITY	185 S ORANGE AVE	NEWARK	NJ	07103	ESSEX	USA	Allergy and Infectious Diseases Research	000	2	3/11/2024	NON-COMPETING CONTINUATION	$0
														Subtotal = $0

Issue Date FY: 2021 ( Subtotal = $78,459 )
2021	2021	RUTGERS, THE STATE UNIVERSITY OF NEW JERSEY	185 S ORANGE AVE	NEWARK	NJ	07103	ESSEX	USA	Allergy and Infectious Diseases Research	000	2	5/14/2021	NON-COMPETING CONTINUATION	$78,459
														Subtotal = $78,459

Issue Date FY: 2020 ( Subtotal = $78,000 )
2020	2020	RUTGERS, THE STATE UNIVERSITY OF NEW JERSEY	185 S ORANGE AVE	NEWARK	NJ	07103	ESSEX	USA	Allergy and Infectious Diseases Research	000	1	6/1/2020	NEW	$78,000
														Subtotal = $78,000

Grand Total All Awards = $156,459

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Defining the impact of membrane vesicle deficiency on M. tuberculosis-macrophage interactions

Award Number: R03AI153560

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 06/04/2020

PERIOD OF PERFORMANCE END DATE: 05/31/2023

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