35 results about "M2 phenotype" patented technology

A therapeutic effect of Nurr1 and Foxa2 in inflammatory neurologic disorders by M1-to-M2 polarization of glial cells is provided. Specifically, a method of converting glial cells from an M1 phenotype to an M2 phenotype, wherein Nurr1 and Foxa2 are introduced into the glial cells to be overexpressed in the glial cells and a method of preventing or treating an inflammatory neurologic disorder, which includes glial cells into which Nurr1 and Foxa2 are introduced, or a viral vector loaded with Nurr1 and Foxa2, are provided.

Disclosed are methods of polarizing macrophages to exhibit M2 phenotype, including introducing an effective amount of gingiva-derived mesenchymal stem cells to an environment comprising a population of macrophages such that the macrophages are in fluid communication with the gingiva-derived mesenchymal stem cells. Also disclosed are methods of promoting cutaneous wound healing including administering to a patient an effective amount of human gingiva-derived mesenchymal stem cells, thereby resulting in at least one of accelerated wound closure, rapid re-epithelialization, improved angiogenesis and improved tissue remodeling relative to untreated controls. Also disclosed are methods for attenuating contact hypersensitivity in a patient, the methods including administering to a patient an effective amount of human gingiva-derived mesenchymal stem cells at a time at least timeframe selected from the group consisting of before sensitization, after sensitization and before challenge and after challenge, thereby attenuating contact hypersensitity.

The invention provides a bone induction and immunization double-effect coating, a preparation method and application in osseointegration. According to the method provided by the invention, by virtue of a mussel molecule mediated metal-phenol coordination chemical and biological orthogonal reaction strategy, a bone implant with a double-effect coating with immunomodulatory activity and bone induction is designed. Zn <2+> with immunocompetence and BMP-2 peptide with bone induction performance are jointly modified on the surface of the bone implant through mussel molecule surface adhesion chemistry, ion coordination and biological orthogonal reaction, and it is found that the Zn/BMP-2 double-effect coating can better improve the biocompatibility of the bone implant, promote polarization of macrophages to an anti-inflammatory M2 phenotype, and synergistically improve the immune microenvironment of the bone-implant interface to induce the optimal osteogenesis performance and osseointegration effect of the bone-implant interface, so that the in-vivo mechanical stability is improved.

The invention belongs to the technical field of medicines, and in particular discloses application of fructose 1,6-diphosphate (FDP) in preparation of a fetus protection medicine for spontaneous abortion. In vitro and in vivo animal experiments show that the concentration of the FDP in peripheral blood and decidual tissues of patients with recurrent spontaneous abortion is decreased compared withnormal pregnancy. Compared with control pregnant mice, the model plasma and uterus FDP levels of pregnant mice with spontaneous abortion are reduced, the uterus macrophage M2 phenotype molecule expression of the pregnant mice with spontaneous abortion is decreased, the proportions of helper cells T(Th)2 and regulatory T cells are reduced, and the phenomena of poor endometrium decidualization and decreased embryonic trophoblast infiltration degree occur in an accompanied way. The results indicate that the supplement of the FDP can significantly improve the uterine immune tolerance pattern, decidualization and embryonic trophoblast infiltration in the pregnant mice with spontaneous abortion, and obviously reduces embryonic loss in the pregnant mice. Therefore, the FDP is expected to be an early-warning and diagnostic indicator for the patients with spontaneous abortion, and can be used for preparing the fetus protection medicine for the spontaneous abortion.

The inhibition of miRNA miR-33 is shown to promote the polarization of macrophages from an M1 to an M2 phenotype. MiR-33 inhibitors are therefore useful for treating inflammation in subjects. Endogenous microRNAs can be silenced using antagomirs. The miR-33 inhibitor is preferably an antagomir having a single-stranded nucleic acid sequence that is complementary to at least 12 contiguous nucleotides in miR-33 and therefore forms a duplex with miR-33 under physiological conditions.

The invention discloses application of carnosol in preparation of medicines for preventing and treating experimental autoimmune encephalomyelitis. Whole animal model experiments verifies that the carnosol not only can effectively delay the occurrence and development of the experimental autoimmune encephalomyelitis, significantly reduces the infiltration of peripheral inflammatory cells into the central nervous system and relieves the degree of demyelination, but also can promote the transformation of infiltrating macrophages and intrinsic microglial proinflammatory phenotypes to an M2 phenotype with an immunoregulatory function. Furthermore, the carnosol can inhibite Th17 cell differentiation and STAT3 phosphorylation and block NF-kappa B nuclear translocation of a transcription factor. Therefore, the carnosol has a great potential in the preparation of the medicines for preventing and treating the autoimmune diseases such as multiple sclerosis.

The invention belongs to the technical field of medicaments, and relates to application of RANK<+> macrophages, in particular to the application of the RANK<+> macrophages in preparation of a medicament for treating spontaneous abortion and preventing miscarriage. According to the application of the RANK<+> macrophages in the preparation of the medicament for treating the spontaneous abortion andpreventing the miscarriage, in-vitro experiments and in-vivo animal experiments show that an RANKL/RANK signal in an early pregnant mother-fetal interface can obviously induce differentiation from decidual macrophages to an M2 phenotype so as to induce Th2 immune deviation of the early pregnant mother-fetal interface, which is beneficial to establishment and maintenance of normal pregnancy; adoptively transferred RANK<+> macrophages can remarkably reverse fetal resorption of a pregnant mice caused by dysfunction of the macrophages, and can be further used for the preparation of the medicamentfor treating the spontaneous abortion and preventing the miscarriage.

The invention discloses new application of a carboxylated multiwalled carbon nanotube to preparation of anti-tumor metastasis medicine. The application is characterized in that the carboxylated multiwalled carbon nanotube can restrain proliferation of tumor cells by targeting tumor microenviroment and reprogramming tumor-associated macrophages (mainly in an M2 phenotype) to be in an M1 phenotype, and is safe and low in toxin for normal cells of a human body. In this way, the carboxylated multiwalled carbon nanotube has the application prospect in preparation of the anti-tumor metastasis medicine.

The invention provides a polar conversion accelerator to anti-inflammatory M2 phenotype microglia. The polar conversion accelerator comprises a cyclic peptide derivative represented by formula (1). Inthe formula, m is 0 to 3, n>=1, R1 to R6 are hydrogen atoms or hydrocarbon groups, R7 and R8 are carboxyl or salts thereof or alkoxycarbonyl, R9 is a hydrocarbon group, hydroxyl, alkoxy or alkylcarbonyloxy, R10 and R11 are hydrogen atoms, hydrocarbon groups or alkylcarbonyloxy, and R12 to R16 are hydrogen atoms or hydrocarbon groups. The Chemical formula 1 is shown in the specification.

The invention belongs to the field of genetic engineering and medicines, and particularly relates to a method for performing Hemopexin protein specific induction and maintaining selective polarization of microglial cells, and applications thereof in treatment of spinal cord injury repair. According to the main technical scheme, the method comprises the following steps: (I) transplanting microglial cells into Hemopexin-knockout mice spinal cord to hinder the microglial cells to be selectively polarized; and (II) co-incubating the Hemopexin protein and microglial cells to be capable of inducing and maintaining the selective polarization of the microglial cells. The Hemopexin-induced microglial cells show an M2 phenotype, so that the repair of the spinal cord nerve injury can be effectively promoted.

The invention relates to the field of biomedicines and discloses a high-throughput drug screening system for inhibiting the survival of breast cancer cells stimulated by macrophages. The high-throughput drug screening system comprises 1) preliminary screening: performing mixed culture on the macrophages and the breast cancer cells and analyzing the inhibitory effect of drugs on the activities of the breast cancer cells stimulated by the macrophages to obtain primary screening positive drugs; 2) secondary screening: adding the primary screening positive drugs in the individually-cultured macrophages and breast cancer cells, and analyzing and judging to screen a drug capable of reshaping TAM from an M2 phenotype to an M1 phenotype or interfering/blocking a signal loop between the breast cancer cells and the macrophages. The screening system disclosed by the invention can screen the drug capable of reshaping the macrophages to the M1 phenotype or interfering/blocking the signal loop between the breast cancer cells and the macrophages through individual culture and common culture of the mouse macrophages RAW264.7 and the mouse three-negative breast cancer cells 4T1.

The invention provides an in vitro method for inducing macrophage polarization to an M2 phenotype useful for tissue repair. The method described in the present invention comprises the in vitro exposure of macrophages to repeated series of hypoxia-reoxygenation. Activated M2 macrophages obtained by this method overexpress molecules important for tissue remodeling and amelioration of inflammation, such as NGAL and anti-inflammatory cytokines (IL-10). Thus, M2 macrophages obtained by this method are useful as cell therapy for tissue regeneration. The invention also provides pharmaceutical compositions and kits comprising the M2 macrophages obtained by the described method. The invention further refers to a device for inducing hypoxia and re-oxygenation conditions on isolated macrophages according to the described method.

The invention belongs to the field of gene engineering and medicine and particularly relates to a method of specifically inducing microglial cells selective polarization with MSX3 gene and an application of the method in preparation of a drug for treating multiple sclerosis. The method includes following steps: (1) according to the structure of the MSX3 gene, preparing an MSX3 cDNA sequence, constructing an MSX3-over-expressed eukaryotic expression vector and constructing MSX3-over-expressed (MSX3-GFP) lentivirus; and (2) transfecting the MSX3-over-expressed lentivirus to mice and human microglial cells. A research result proves that the MSX3-over-expressed microglial cells have same M2 phenotype, so that diseases progress of EAE can be effectively alleviated.

The invention discloses an ROS (reactive oxygen species) response type nano-carrier based on microglia phenotype regulation and intracerebral iron removal as well as a preparation method and application thereof, and belongs to the technical field of medicines, under the dual effects of Alzheimer's disease (AD) pathology intracerebral ROS and a slightly acidic environment, the micro aperture between chain proteins on the surface of the nano-particle carrier is enlarged, and a medicine entrapped in the carrier is released, so that the drug release effect is improved. The hollow carrier acts on microglial cells in the brain, the effect of adjusting the pro-inflammatory M1 phenotype of the microglial cells to the anti-inflammatory M2 phenotype is achieved, due to the affinity of the hollow carrier with iron, excessive iron accumulated in the brain can be adsorbed after the hollow carrier releases the medicine, and the reaction which enables inflammation in the brain to be aggravated and forms high-reactivity and destructive active oxygen and the like under catalysis in the presence of excessive active iron is reduced; and aggregation and oligomerization of A beta protein caused by iron are reduced. Aiming at the pathophysiological characteristics of AD, the invention constructs a multifunctional nano delivery carrier for targeting microglial cell phenotypic regulation and accumulated iron removal for AD treatment.

The invention discloses application of naringenin in preparation of an accelerant for promoting polarization of M1 microglial cells to M2. Researches show that the naringenin promotes polarization of A beta-induced M1 microglial cells to M2, and the addition of the naringenin activates the number of M2 microglial cells, so that A beta degrading enzyme is highly expressed; and further researches show that the naringenin participates in the transformation of M2 microglial cell subtypes induced by the naringenin by up-regulating the expression of PPAR gamma. The naringenin has the effect of promoting the microglial cells to be transformed from M1 phenotype to M2 phenotype, and has a relatively great application prospect in the aspects of inhibiting inflammatory response, removing toxic substances, repairing injured nerves and the like.

Provided herein are polymeric particles and compositions (i.e., "backpacks") that can adhere to cells and provide delivery of payload immunomodulatory agents to those cells. For examples, the particles can adhere to macrophages and/or monocytes and release cytokines that promote an M1 or M2 phenotype to improve therapeutic efficacy of the cells.

The invention discloses a preparation method of a breast milk-based wound dressing and an application thereof. The invention provides the breast milk-based wound dressing preparation method, which comprises the following steps: S1, freeze-drying breast milk, and dissolving in a biocompatible solvent to obtain a breast milk solution; wherein the concentration of the breast milk solution in the stepS1 is greater than or equal to 1 [mu] g/mL; S2, filtering and sterilizing the breast milk solution obtained in the step S1 to obtain the wound dressing. The wound dressing has relatively low immunogenicity, and does not cause additional inflammatory reaction of an organism; hydroxyl free radicals and intracellular active oxygen can be removed, the proliferation rate of cells is increased, migration of fibroblasts and endothelial cells is promoted, and the angiogenesis capacity of the endothelial cells is enhanced; M2 phenotype of macrophages is regulated and controlled, hair follicle regeneration is promoted, and healing wounds are normalized. Besides, the wound dressing is prepared from food breast milk, is green and safe, is simple and convenient in preparation process, and has a wide popularization and application prospect.

Aspects of the present disclosure include methods for modulating macrophage activity. Methods according to certain embodiments include contacting a macrophage with a mannose receptor (CD206) binding agent in a manner sufficient to modulate activity of the macrophage. Methods for converting a phenotype of a macrophage from an M2 phenotype to an M1 phenotype are also provided. Methods for inhibiting growth of a CD206-expressing cell as well as methods for treating a subject for a neoplastic condition (e.g., cancer) or a condition associated with chronic inflammation are described. Immuno-modulating peptides suitable for use in the subject methods are also presented.