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2-Arachidonoylglycerol signaling in nitrogen mustard-induced lung injury

Award Number: R21ES037516
ORGANIZATION: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 06/23/2026
PERIOD OF PERFORMANCE END DATE: 06/22/2028

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2-Arachidonoylglycerol signaling in nitrogen mustard-induced lung injury - Summary: Nitrogen mustard (NM), a potent cytotoxic vesicant, can cause acute lung injury and potentially lead to chronic conditions like fibrosis, emphysema, and bronchiolitis obliterans. NM remains a significant chemical threat due to its ease of synthesis and weaponization. Currently, there are no effective medical countermeasures to mitigate NM-induced lung damage, therefore, the search for an effective therapeutic or prophylactic treatment persists. The endocannabinoids and their lipid-related mediators contribute to the modulation of oxidative stress and lipid peroxidation and 2- Arachidonoylglycerol (2-AG), is the most abundant endocannabinoid. 2-AG is produced ‘on demand’ and rapidly degraded, and monoacylglycerol lipase (MAGL or MgII) is the main enzyme responsible for 2-AG catabolism. The hydrolysis of 2-AG by MAGL terminates the activation of CB receptors, releasing free AA that serves as a precursor for the synthesis of pro-inflammatory eicosanoids. Enhancing the 2-AG signaling displays an anti-inflammatory response to proinflammatory and mechanical insults. Our preliminary findings indicated that acute exposure to NM resulted in a significant increase in MAGL in mouse lung tissues, immune cells, and human alveolar macrophages. Furthermore, our pilot study showed that the administration of JZL184, a potent inhibitor of MAGL resulted in a significant reduction in NM-induced acute lung injury and immune cell infiltration in mice. Given these promising indications, this project aims to further investigate how augmenting the 2-AG signaling by inactivation of MAGL could confer protection against NM-induced lung injury. Aim 1: To assess the efficacy of MAGL inhibition/inactivation in protection against NM-induced acute lung injury, inflammatory response, and oxidative stress. Aim 2: To delineate the mechanism of protection by MAGL inhibition/inactivation in NM-induced acute lung injury, inflammatory response, and oxidative stress. These efforts would assist in translational strategies for the development of therapeutic agents against NM-induced lung damage.


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: 2026 ( Subtotal = $458,144 )
2026	2026	OLD DOMINION UNIVERSITY	HAMPTON BLVD	NORFOLK	VA	23529	NORFOLK CITY	USA	Environmental Health	000	1	6/23/2026	NEW	$458,144
														Subtotal = $458,144

Grand Total All Awards = $458,144

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2-Arachidonoylglycerol signaling in nitrogen mustard-induced lung injury

Award Number: R21ES037516

ORGANIZATION: NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 06/23/2026

PERIOD OF PERFORMANCE END DATE: 06/22/2028

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