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Inflammation Induction and Tissue Repair

Technology Application
The non-coding U1 snRNA potentially can be used to induce tissue necrosis in certain types of cancers and may have therapeutic applications in infectious diseases. Conversely, anti RNAs could be synthesized to block the inflammatory effects of U1 snRNA, or TLR3 antagonists could be used to attenuate inflammation from some forms of tissue necrosis injury such as radiation.
Detailed Technology Description
UCSD researchers have found that non-coding U1 small nuclear RNAs (snRNA) play an important role in the inflammation process. In an irradiated mouse model, endogenous non-coding U1 snRNA becomes altered and is recognized by the Toll-like Receptor 3 (TLR3). Together with TLR3, U1 RNA can then induce the NF-kappa B inflammatory cascade. The induction can be replicated by injecting the mice with radiated U1 RNA. The role of TLR3 is essential since the U1 RNA-mediated induction of inflammation does not occur in mice lacking TLR3 expression. Furthermore, the newly generated fractions from the radiated U1 RNA that are less than 100 nucleotides are potent stimuli of TNF-alpha.
Supplementary Information
Inventor: GALLO, Richard, L. | BERNARD, Jamie
Priority Number: WO2012138846A3
IPC Current: A61K004800 | A61K00317105 | A61K003816 | A61K003817 | A61P002900
Assignee Applicant: The Regents of the University of California
Title: METHOD AND COMPOSITIONS COMPRISING SMALL RNA AGONIST AND ANTAGONISTS TO MODULATE INFLAMMATION | PROCÉDÉ ET COMPOSITIONS COMPRENANT UN AGONISTE ET DES ANTAGONISTES DE PETITS ARN POUR MODULER UNE INFLAMMATION
Usefulness: METHOD AND COMPOSITIONS COMPRISING SMALL RNA AGONIST AND ANTAGONISTS TO MODULATE INFLAMMATION | PROCÉDÉ ET COMPOSITIONS COMPRENANT UN AGONISTE ET DES ANTAGONISTES DE PETITS ARN POUR MODULER UNE INFLAMMATION
Summary: For treating an infection in a subject, where the infection is a skin infection including skin wound; for identifying an agonist or antagonist of inflammation which is used treating an inflammatory disease or disorder selected from acne, rosacea, atopic dermatitis, contact dermatitis, drug eruptions, psoriasis, seborrheic dermatitis, lupus, scleroderma, rheumatoid arthritis, blistering disease, bullous pemphigoid or pemphigus, inflammatory hyperpigmentation, melasma and vitiligo, and urticaria or hives (claimed). Also used in treating pneumonia, meningitis, osteomyelitis, endocarditis, sinusitis, urinary tract infections, tetanus, gangrene, colitis, acute gastroenteritis, and impetigo.
Novelty: Composition used in treating e.g. skin infection, acne, rosacea, dermatitis, psoriasis, seborrheic dermatitis, lupus, scleroderma, rheumatoid arthritis comprises isolated photo fragmented small nuclear ribonucleic acid oligonucleotides
Industry
Biomedical
Sub Category
DNA/Gene Engineering
Application No.
9303258
Others

State Of Development

The ability of radiated U1 snRNA to elicit the inflammatory cascade through its interaction with TLR3 has been demonstrated in mice.


Intellectual Property Info

UCSD seeks commercial partners for development of this invention, and the invention is available for licensing.


Related Materials

Bernard JJ, Cowing-Zitron C, Nakatsuji T, Muehleisen B, Muto J, Borkowski AW, Martinez L, Greidinger EL, Yu BD, Gallo RL. Ultraviolet radiation damages self non-coding RNA and is detected by TLR3. Nat Med. 2012 Jul 8. doi: 10.1038/nm.2861. [Epub ahead of print]
“What Happens When We Sunburn: Red Is RNA Damage to Skin Cells”, ScienceDaily, July 8, 2012.
“Cause of sunburn's painful inflammation discovered by UCSD researchers”, North County Times, July 8, 2012.


Tech ID/UC Case

22814/2011-226-0


Related Cases

2011-226-0

*Abstract
Inflammation is an important response for resisting infection and repairing damage. Under circumstances such as cancer or infectious diseases, stimulation of the inflammatory response is therapeutic. It is unclear why the existing adjuvant therapies tend to be more effective in the treatment of some disease, such as breast and colon cancer, than others. This invention identifies additional ways to stimulate the immune response and induce inflammation in order to accelerate repair of disease-related tissue injury.
*IP Issue Date
Apr 5, 2016
*Principal Investigator

Name: Jamie Bernard

Department:


Name: Richard Gallo

Department:


Name: Richard Gallo

Department:

Country/Region
USA

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