Treatment of Type 1 Diabetes and Other Conditions Using the Gut Microbiome

• US 20190328839A1
• Filed: 03/04/2019
• Published: 10/31/2019
• Est. Priority Date: 11/16/2017
• Status: Abandoned Application

• Current Assignee: Claresa Levetan
• Original Assignee: Claresa Levetan
• Inventors: Levetan, Claresa
• Application Number:
  US16/291,207
• Publication Number:
  US 20190328839A1
• Time in Patent Office: Days
• CPC Class Codes: A61K 38/212 IFN-alpha
• CPC Class Codes: A61K 9/0053 Mouth and digestive tract, i.e. intraoral and peroral administration rectal administration A61K9/0031
• CPC Class Codes: A61P 3/10 for hyperglycaemia, e.g. antidiabetics

Abstract

The disclosure provides new methods for treatment of inflammatory and autoimmune diseases including diseases of impaired glucose homeostasis and includes the usage oral usage immunotherapies that are T lymphocyte helper cell 17 (Th17)-inhibitors and usage is based on the patient'"'"'s gut microbiome to determine if they are at risk for targeted organ(s) attack by Th17. The delivery of Th17-inhibitors is delivered preferably orally because Th17 lines the mucosa of the gastrointestinal tract. With the treatment of Type 1 diabetes, both a Th17-inhibitor is used with existing or new islet neogenesis agents presented within.

Claims

1. A method of treating or preventing impaired glucose homeostasis in a subject comprising the steps of:

mapping the subject'"'"'s gut microbiome;

comparing the subject'"'"'s gut microbiome results with known mapped gut microbiomes of individuals suffering from particular forms of impaired glucose homeostasis;

determining the particular type of glucose impairment of the subject based on the subject'"'"'s mapped gut microbiome, matching a known mapped gut microbiome of an individual suffering from a particular form of impaired glucose homeostasis;

using one or more islet or beta cell regeneration or replacement therapies; and

administering a T helper lymphocyte 17 (Th17)-inhibitor in an amount that is effective for protection of beta cells from immune-mediated destruction in the subject.

2. The method of claim 1, wherein the Th17-inhibitor is Interferon alfa-2a, PEGylated Interferon alfa-2a, or an optimized version of either.

3. The method of claim 2, wherein the Interferon alfa-2a or the PEGylated Interferon alfa-2a is administered orally to the subject.

4. The method of claim 3, wherein the Interferon alfa-2a or the PEGylated Interferon alfa-2a is administered to the subject at a dosage in the range of 100 to 50,000 IU.

5. The method of claim 1, wherein the one or more islet or beta cell regeneration or replacement therapies comprise one or more islet neogenesis or beta cell regeneration agents.

6. The method of claim 5, wherein the islet neogenesis or beta cell regeneration agent binding to the 20-amino acid binding region [SEQ ID:

3] of the 920-amino acid Reg receptor [SEQ;

ID 4].

7. The method of claim 6, wherein islet neogenesis or beta cell regeneration agent is a binding site analog, a stimulatory antibody to the binding site, or a small molecule capable of binding to the Reg receptor binding region [SEQ ID:

3].

8. The method of claim 5, wherein the islet neogenesis or beta cell regeneration agent has been modified to increase its stability in plasma, increase its solubility, increase its protease resistance, reduce its immunogenicity, increase Tmax, and/or increase its bioavailability.

9. The method of claim 1, wherein the one or more islet or beta cell regeneration or replacement therapies comprise one or more of an islet transplant, beta cell transplant, or stem cell transplant.

10. The method of claim 1, wherein the one or more islet or beta cell regeneration or replacement therapies comprise one or more devices or modalities that house or encapsulate one or more of islets, stem cells or beta cells.

11. The method of claim 1, wherein conditions frequently seen in family members who have Type 1 diabetes who have progressive diseases which may have an autoimmune basis for which there may be no treatment available and methods above may stop the progression of such autoimmune diseases or conditions that is one or more of Amyotrophic Lateral Sclerosis (ALS), forms of Parkinson'"'"'s disease, pulmonary fibrosis, pediatric autoimmune neurobiological disorders, Myasthenia gravis, Chronic inflammatory demyelinating polyneuropathy (CIDP), Multifocal motor neuropathy (MMN), POEMS syndrome (osteosclerotic myeloma:

polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, skin changes), anti-myelin associated glycoprotein (MAG)-related neuropathies, Combined Sensorimotor Neuropathy in Rheumatoid Arthritis, Juvenile Rheumatoid Arthritis, Frontotemporal Lobar Dementia and progressive neurologic conditions.

12. A method of treating or preventing one or more autoimmune diseases or conditions in a subject comprising:

mapping the subject'"'"'s gut microbiome;

comparing the subject'"'"'s gut microbiome results with known mapped gut microbiomes of other individuals suffering from a particular forms autoimmune disease or condition;

determining the particular type of autoimmune disease or condition of the subject based on the subject'"'"'s mapped gut microbiome matching a known mapped gut microbiome of an individual suffering from a particular form of autoimmune disease or condition; and

administering a Th17-inhibitor at an amount that is effective for alleviating or preventing symptoms of the autoimmune disease or condition in the subject.

13. The method of claim 12, wherein the Th17-inhibitor is Interferon alfa-2a or PEGylated Interferon alfa-2a.

14. The method of claim 13, wherein the Interferon alfa-2a or the PEGylated Interferon alfa-2a is administered orally to the subject.

15. The method of claim 14, wherein the Interferon alfa-2a or the PEGylated Interferon alfa-2a is administered to the subject at a dosage in the range of 100 to 50,000 IU.

16. A method of diagnosing and treating one or more diseases that is based on a Th17-initiated inflammatory or autoimmune attack in a subject comprising:

mapping the subject'"'"'s gut microbiome;

comparing the subject'"'"'s gut microbiome results with known mapped gut microbiomes relating to aberrant gut microbiomes of individual'"'"'s suffering symptoms of Th17-initiated inflammatory or autoimmune attacks; and

diagnosing the subject'"'"'s particular type disease based on the subject'"'"'s mapped gut microbiome matching a known mapped gut microbiome of an individual suffering from a particular form of Th17-initiated inflammatory or autoimmune attack.

17. The method of claim 16, further comprising the step of administering a Th17-inhibitor at an amount that is effective for alleviating or preventing symptoms of the Th17-initiated inflammatory or autoimmune attack in the subject.

18. The method of claim 17, wherein the Th17-inhibitor is Interferon alfa-2a or PEGylated Interferon alfa-2a.

19. The method of claim 18, wherein the Interferon alfa 2-a or the PEGylated Interferon alfa-2a is administered orally to the subject.

20. The method of claim 19, wherein the Interferon alfa 2-a or the PEGylated Interferon alfa-2a is administered to the subject at a dosage in the range of 100 to 50,000 IU.