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Regulation of the Microglial Neuroimmune Response by Long Non-Coding RNAs

Award Number: R15AI156879
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: 07/14/2022
PERIOD OF PERFORMANCE END DATE: 03/31/2029

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Regulation of the Microglial Neuroimmune Response by Long Non-Coding RNAs - PROJECT SUMMARY Dysregulated neuroimmune responses following infection are linked to neurodegenerative pathologies such as multiple sclerosis (MS). The long-term goal of this work is to identify neuroinflammatory mechanisms underlying microglial-induced neurotoxicity and contribute to the development of new therapies for neurodegenerative disease. Microglia demonstrate functional plasticity and when activated contribute to both neuroprotection and neurotoxicity. Proper microglial function supports neurogenesis and synapse development, regulates homeostatic neuronal and glial activity, and provides host defense against pathogens. Dysregulated microglial function contributes to demyelination, synaptic restructuring and loss, and neurotoxic inflammation. Mechanisms governing microglial neuroprotective or neurotoxic states are not well understood. Long non- coding RNAs (lncRNAs) are prime candidates for regulating microglial functional plasticity because many lncRNAs are early-primary response genes whose expression is stimulated by environmental signals that trigger immune activation. Differential lncRNA expression is associated with human neuroinflammatory disease pathologies such as MS. Our collaborative work using whole transcriptome analyses has identified novel lncRNAs that regulate proinflammatory gene expression by directing chromatin remodeling in epithelial cells, macrophages, and microglia. Further, silencing neuroinflammatory lncRNAs in microglial cell lines can reduce neurotoxicity. This innovative proposal using multidisciplinary in vivo and in vitro methodologies is designed to address the hypothesis that lncRNAs, like Nostrill, act as primary regulators of NFκB mediated gene transcription in proinflammatory microglia. Aim 1 will determine whether Nostrill, and other lncRNAs, are differentially expressed in microglia of mouse model systems that are susceptible or resistant to pathogen-induced demyelinating neurogenerative disease that is like progressive MS in humans. Aim 2 will elucidate the biological function and molecular mechanisms of Nostrill in TMEV-infected primary cells and in the BV2 microglial cell line. Together, these Aims will evaluate a causal relationship between Nostrill, proinflammatory gene expression and microglial neurotoxicity. This proposal will be impactful since expected outcomes will reveal mechanisms of lncRNA-regulated proinflammatory gene expression in microglia that may be targets for novel neurodegenerative disease therapeutics.


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 = $549,931 )
2026	2026	CREIGHTON UNIVERSITY	2500 CALIFORNIA PLAZA	OMAHA	NE	68178	DOUGLAS	USA	Allergy and Infectious Diseases Research	001	2	4/8/2026	COMPETING CONTINUATION	$549,932
2026	2022	CREIGHTON UNIVERSITY	2500 CALIFORNIA PLAZA	OMAHA	NE	68178	DOUGLAS	USA	Allergy and Infectious Diseases Research	000	1	12/17/2025	NEW	-$1
														Subtotal = $549,931

Issue Date FY: 2022 ( Subtotal = $436,468 )
2022	2022	CREIGHTON UNIVERSITY	2500 CALIFORNIA PLAZA	OMAHA	NE	68178	DOUGLAS	USA	Allergy and Infectious Diseases Research	000	1	7/14/2022	NEW	$436,468
														Subtotal = $436,468

Grand Total All Awards = $986,399

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Regulation of the Microglial Neuroimmune Response by Long Non-Coding RNAs

Award Number: R15AI156879

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: 07/14/2022

PERIOD OF PERFORMANCE END DATE: 03/31/2029

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