113 results about "Abnormal macrophage" patented technology

The present invention provides methods for detecting, diagnosing or prognosticating prostate cancer by measuring the levels of macrophage migration inhibitory factor (MIF) in the serum of an individual. The assay for MIF can be an immunoassay, such as ELISA, or a nucleic assay, such as Nouthern blot. Genetic changes within MIF gene can predict patients that express high levels of MIF.

Inhibitors of MIF are provided which have utility in the treatment of a variety of disorders, including the treatment of pathological conditions associated with MIF activity. The inhibitors of MIF have the following structures:including stereoisomers, prodrugs and pharmaceutically acceptable salts thereof, wherein n, R1, R2, R3, R4, X, and Z are as defined herein. Compositions containing an inhibitor of MIF in combination with a pharmaceutically acceptable carrier are also provided, as well as methods for use of the same.

The present invention provides compounds of structural formula (I), which are agonists of formyl peptide receptor (FPR), particularly formyl peptide receptor like 1 (FPRL1). The present invention also provides the therapeutic use of the compounds of formula (I).

The invention belongs to the field of traditional Chinese medicine pharmacy, and relates to the novel medical usage of icaritin, in particular to the usage of icaritin in preparation of medicine for preventing and treating endotoxemia. Lipopolysaccharide (LPS) is used for stimulating the macrophage system RAW264.7 of a mouse and establishing an extraneous endotoxic inflammation model, LPS is used for stimulating the C57BL / 6J mouse and establishing the endotoxemia animal model, icaritin is adopted for intervention, and dexamethasone is used as reference. The experiment result shows that the icaritin can reduce the death rate, the level of the inflammatory factor, the inflammatory mediator and the adhesion molecules and infiltration of inflammatory cells of the tissue after the mouse is attacked by endotoxin, and proves that the icaritin can effectively prevent and treat endotoxemia and can be used for further preparing effective drug for preventing and treating endotoxemia, including dosage forms such as oral and enteric capsules or intravenous injections.

The present invention is directed to compositions and methods for the treatment of diseases comprising the administration of compositions comprising one or more peptide(s) having a stimulatory effect on the afflicted host's immune system. Specifically, the invention relates to methods comprising the use of cationic amphipathic peptides having an alpha-helical structure and effecting activation of macrophages when administered in a therapeutically sufficient amount. The methods of the present invention are useful for the treatment of, for example, infectious diseases or cancer.

A method of treating cachexia is disclosed involving the removal or inactivation of macrophage inhibitory cytokine-1 (MIC-1) present in the blood, plasma or serum of a cachexia subject. In one embodiment, the method comprises the steps of providing a suitable substrate for binding MIC-1 (e.g. a substrate provided with a MIC-1 binding molecule), treating blood, plasma or serum removed from a subject by contacting the blood, plasma or serum ex vivo with the substrate such that MIC-1 present in the blood, plasma or serum is bound to the substrate, separating the treated blood, plasma or serum from the substrate, and thereafter returning the treated blood, plasma or serum to the subject. Also disclosed, is a method of diagnosing or prognosing cachexia in a subject, said method comprising determining the amount of MIC-1 present in the subject.

A method of predicting or diagnosing clinical infection of a wound comprising measuring the concentration of a marker associated with an inflammatory response in wound fluid, wherein the marker is a fibronectin fragment, a neutrophil protease or a macrophage protease. Also provided is a use of a wound dressing or biosensor comprising components of an assay system for measuring the concentration of a marker associated with an inflammatory response, wherein the marker is a fibronectin fragment, a neutrophil protease or a macrophage protease, for use in the manufacture of a medicament for predicting the likelihood of clinical infection of the wound or for diagnosing clinical infection of a wound.

A harmless cancer vaccine is made from cancer cells with extracellular proteins including self-recognition molecular patterns being digested by a proteinase. The cancer vaccine is used to vaccinate an individual to induce immune responses against cancer cells systemically. Cancer cells become harmless when they are digested by Tumorase™. Some proteinases including trypsin cannot kill cancer cells completely and treated cancer cells need to be further processed in order to be harmless and effective. Cancer cells may be from tissue-cultured human or animal cancer cell lines or cancer patients directly. Cancer vaccine vaccinated individuals produce cancer vaccine specific immune responses against cancer cells. Immune response components may be isolated and used to fight against cancer for a cancer patient with a suppressed immune system. Cancer vaccine specific immune components may include cancer vaccine specific polyclonal antibodies, B-cells, T-cells, natural killer cells, monocytes, macrophages and other lymphocytes.

Atherosclerosis is an inflammatory disease of the arterial walls and represents a significant health problem in developed nations. Described is a targeted Magnetic Resonance Imaging (MRI) contrast agent for in vivo imaging of early stage atherosclerosis. Early plaque development is characterized by the influx of macrophages, which express a class of surface receptors known collectively as the scavenger receptors (SR). The macrophage scavenger receptor class A (SRA) is highly expressed during early atherosclerosis. The macrophage SRA therefore presents itself as an ideal target for labeling of lesion formation. By coupling a known ligand for the scavenger receptor, dextran sulfate, to a MRI contrast agent, early plaque formation can be detected in vivo. Targeted MR contrast agents offer a unique opportunity to visualize early plaque development in vivo with high sensitivity and resolution, allowing or early diagnosis and treatment of atherosclerosis.

The disclosure relates to immunoglobulin single variable domains directed against human macrophage mannose receptor (MMR) and their uses in the field of oncology. More specifically, it concerns immunoglobulin single variable domains, including single-domain antibodies (sdAbs), against human MMR and their use in targeting and in vivo imaging of tumor-associated macrophages, with applications in the field of cancer diagnostics and therapeutics and monitoring of the disease.

The invention relates to application of classically activated macrophages in treatment of liver fibrosis. The invention is characterized by application of the classically activated macrophages in treatment of liver fibrosis and preparation of drugs used for treating liver fibrosis. According to the invention, matrix metalloproteinase (MMPs) molecules highly expressed in M1 macrophages and a great number of MMPs secreted by the M1 macrophages and autologous macrophages entering the liver cooperate with each other to accelerate degradation of collagen fibers and mitigate liver fibrosis, wherein autologous macrophages are raised after reinfusion of the M1 macrophages. The M1 macrophages have a good therapeutic effect on liver fibrosis, so a novel effective method is provided for clinical treatment of liver fibrosis and cirrhosis.

In certain embodiments, the invention includes therapeutic methods of using a BTK inhibitor to treat solid tumor cancers by modulation of the tumor microenvironment, including macrophages, monocytes, mast cells, helper T cells, cytotoxic T cells, regulatory T cells, natural killer cells, myeloid-derived suppressor cells, regulatory B cells, neutrophils, dendritic cells, and fibroblasts.

Treatment of microglial cells with nicotine and THC synergistically attenuate the microglial activation. Using microglial activation, the combination of THC and nicotine interact synergistically reduced LPS induced TNF-α release, showing that the combination of THC and nicotine clinically have greater efficacy in reducing neuroinflammation with less side effects than either drug given alone. CD40 signaling was found critically involved in pathological activation of microglial cells. This invention is also relevant to peripheral inflammation as well thru macrophages. In addition, other cannabinoids and other nicotinic-like medications currently in development are also covered under this discovery.

Macrophage migration inhibitory factor (MIF) is a clinically useful biochemical marker of cardiovascular risk. Risk assessment includes the step of detecting in the blood of a person MIF concentration as a marker of cardiovascular risk for the person. The method may further comprise the step of assigning to the person a cardiovascular risk metric proportional to the MIF concentration, and / or prescribing for the person a cardiovascular treatment modality in accordance with the MIF concentration. The method is useful as a primary screen, and may be used in conjunction with or as a substitute for additional tests, such as a stress test, CRP assay, LDL assay, etc. The detecting step may be repeated over time intervals and / or treatment to monitor change in cardiovascular risk for the person over time and / or treatment.

The invention discloses application of long-chain non-coding RNA in regulating polarization of macrophages in viral myocarditis. The applicant found that the differential expression of lncRNA AK085865in M1 / M2 macrophages is the most significant, and that the expression level of AK085865 in M2 macrophages is higher than the expression level of AK085865 in M2 macrophages. The down-regulation of AK085865 gene reduces the phenotypic expression of M2 and promotes the polarization of M1 phenotype. Meanwhile, the susceptibility of AK085865- / - gene knockout mice to CVB3-induced VM increases. In the AK085865- / - gene knockout VM model mice, M1 macrophages increase significantly while the number of M2 cells decreases. The AK085865 specifically interacts with an interleukin enhancer binding factor 2,and plays a negative regulation role in the ILF2 / ILF3 complex-mediated microRNA processing pathway and promotes the polarization of M2 macrophages.

The present invention provides a separating and purifying method and an application of codonopsis pilosula oligosaccharides. Inventors find that the codonopsis pilosula oligosaccharides (CPO) can regulate immune activity through a MAPK signaling pathway in vivo and can also regulate macrophage immune activity through the MAPK signaling pathway in vitro.

Described is a unique class of antiviral molecule that can be applied to control and eliminate HIV infection in patients using myeloablation therapies and replenishment with transformed bone marrow stem cells programmed to express the antiviral molecule. These anti-viral molecules target the HIV genome in a highly conserved domain, and when expressed in cells prior to infection will cause the cell to die upon infection with HIV. Cell death insures no proliferation of new virus. Reconstituting the immune system with cells expressing these antivirals prevents re-establishment of HIV infection from reservoirs in the re-established lymphocyte and macrophage populations. Over time, reservoirs will be depleted entirely, effectively eliminating the virus. In effect, this new type of antiviral can be used to cure HIV infections.

The miRNA miR-33 is shown to inhibit the expression of carnitine O-octaniltransferase (CROT), Carnitine palmitoyltransferase 1A (CPT1a) and hydroxyacyl-CoA-dehydrogenase (HADHB), reduce fatty acid oxidation in hepatic cells, and target the insulin receptor substrate 2 (IRS-2) independent of its ability to elevating plasma high density lipoprotein (HDL) levels. MiR-33 inhibitors are also shown to increase cholesterol efflux from peripheral cells, such as cholesterol-laden macrophages present in atherosclerotic plaques. Compositions and methods are therefore provided for treating or preventing metabolic syndrome and atherosclerosis using miR-33 inhibitors. The miR-33 inhibitors are preferably antagomirs 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 relates to a kit used for diagnosing the acute exacerbation period of chronic obstructive pulmonary disease. The kit comprises a cell factor and an enzyme labeled antibody thereof and is characterized in that the cell factor is interleukin 9, interleukin 18 binding protein A, C-C sequence ligand 28, a human skin T cell capture chemokine, a Beta cytokine, a monocyte chemoattractant protein-3, a monocyte chemoattractant protein-4, a lymphotoxin induced protein entering the T cell, a macrophage-derived chemokine, a human bone marrow suppression factor 1, a human macrophage stimulating protein, an osteopontin and a human thymus expressed chemokine. The invention firstly proposes that the cell factor can be used as a leading indicator for diagnosis of the acute exacerbation period of the chronic obstructive pulmonary disease.

The invention provides a drug delivering miRNA for suppressing tumor growth by targeting tumor-associated macrophages and application. The drug comprises a drug carrier targeting the tumor-associatedmacrophages, miRNA wrapped in the drug carrier and cationized polysaccharide with mannose residues. The sequences of the miRNA are as shown in SEQ. ID. NO. 1 or SEQ. ID. NO. 2. Through an in vitro experiment, miR-99b-5p which can promote M1 type activation of the macrophages and can inhibit M2 type activation of the macrophages is discovered, nano-material targeting tumor-associated macrophages (TAMs) is used for wrapping the miRNA, and the wrapped miRNA is directly transported to a mouse model of liver cancer through a tail vein, it is found that delivery of the miRNA to the targeted TAMs cansignificantly inhibit tumor growth, and delivery of the miR-99b-5p to the targeted TAMs has a better effect of inhibitory action on tumor growth than delivery of other miRNAs, such as miR-125a.

The invention relates to the technical field of medicine, and provides new application of macrophage beta-profilin-1, namely application of macrophage beta-profilin-1 to preparation of a drug for preventing or treating atherosclerosis. It is proved through experiments that in comparison with wild type mice, the serum total cholesterol content of macrophage beta-arrestin-1 specificity myelogenous knockout mice is remarkably increased, and it is found through oil red O dyeing that the aorta overall plaque area and the plaque area of aorta roots are obviously increased compared with those of the wild type mice. By changing the macrophage beta-arrestin-1 gene expression level through virus transfection, and it is found that macrophage phagocytosis lipid is increased by interfering beta-arrestin-1 expression and is decreased by overexpressing beta-arrestin-1. The results show that the beta-arrestin-1 gene has a protective effect on the severity degree and prognosis of atherosclerosis.

The invention is generally directed to treatment of neuronal injury. In particular, the invention is directed to reducing axonal retraction (“dieback”) that occurs as a result of the interaction of activated macrophages with dystrophic axons that are produced during nervous system acute or chronic injury. The invention is also directed to promoting axonal growth / regeneration. The invention is specifically directed to using stem cells or their secreted cellular factors, such as would be produced in conditioned cell culture medium, to ameliorate or prevent axonal dieback and / or promote growth / regeneration of axons.

The present invention relates to methods and compositions for monitoring, diagnosis, prognosis, and determination of treatment regimens in subjects suffering from or suspected of having a renal injury. In particular, the invention relates to using a one or more assays configured to detect a kidney injury marker selected from the group consisting of Interleukin-5, Interleukin-6 receptor subunit beta, Tissue factor, Sex hormone-binding globulin, Alpha-2-macroglobulin, Apolipoprotein A-I, Calcitonin, Thrombopoietin, C-reactive protein, Intercellular adhesion molecule 3, Macrophage metalloelastase, Apolipoprotein B-100, and Fibrinogen as diagnostic and prognostic biomarkers in renal injuries.

The invention discloses an application of an Akt inhibitor in preparation of a drug for treating platelet number decrease related diseases. Experiments prove that Akt regulates apoptosis and activation of platelet by activating cyclic adenosine monophosphate dependent phosphodiesterase and phosphodiesterase medicated PKA (protein kinase A), the apoptotic and activated platelet exposes phosphatidylserine, so that the phosphatidylserine is swallowed by macrophages. Inhibition or gene knockout of Akt or Akt medicated platelet activation and apoptosis or blocking of phosphatidylserine ectropion can stop clearance of antibody-bound platelet. Research indicates that the Akt inhibitor can be used for an anti-platelet membrane glycoprotein Ib alpha antibody to induce the treatment process of platelet number change related diseases and inhibit decrease of the number of platelets in peripheral circulation blood, so that the Akt inhibitor has the potential of being developed into novel platelet protection drugs and novel drugs for treating thrombocytopenic diseases and has great scientific research and economic value.

The invention belongs to the fields of gene functions and applications, and specifically discloses an application of an FKBP11 gene in prevention and treatment of aortic dissection. In-vitro cell experiments show that vascular endothelial cell SiRNA-mediated FKBP11 gene silencing can inhibit activation of an NF-kB signal pathway, the expression of a proinflammatory cytokine is decreased, and migration of macrophage to an aortic middle layer is inhibited, so that the degradation of a middle-layer substrate is inhibited, and results show that the FKBP11 inhibitor can prevent and treat occurrenceof aortic dissection, and provides theoretical basis and clinical basis for new targets and new strategies for prevention, relieving and / or treatment of aortic dissection.

Described herein are compositions and methods for enhancing peripheral macrophage Aβ phagocytosis activity. The methods include inhibiting the TGF-β signaling pathway and activating the BMP signaling pathway in peripheral macrophages to promote central nervous system infiltration and enhance macrophage Aβ phagocytosis activity. Inhibition of TGF-β signaling and activation of BMP signaling in peripheral macrophages represents an advantageous anti-amyloid therapeutic approach for Alzheimer's disease.

The invention discloses an application of Lambda interferon in resisting human immunodeficiency virus. IFN-Lambda resisting HIV infection can inhibit the infection and replication of HIV-1 in human macrophage, which is presented by the following processes: (1) IFN-Lambda1 / Lambda2 differentiates mature human macrophage through pretreatment, then HIV-1R5 type strain respectively infects the cells, a DMEM culture medium is used for washing and then a DMEM culture medium containing 10 percent of fetal calf serum is added for culture; and (2) after infection, the formed multinucleate giant cells of IFN-Lambda treatment group are rather less than those of a virus contrast group, and the HIV-1 reverse transcriptase and envelope protein P24 in culture supernatant fluid of the IFN-Lambda treatment group are detected to be rather less than that of the virus contrast group. After infection, the HIV-1RT in the culture supernatant fluid is respectively detected. The effect of inhibiting the HIV-1 is obvious after infection. The IFN-Lambda treatment group has obvious time and dose-effect relationship in inhibiting the activity of HIV-1RT after infection. The function of IFN-Lambda in resisting the HIV-1 is similar to that of other interferons and has the antivirus effect. The IFN-Lambda shows obvious effect of inhibiting the replication of virus as regards to the human macrophage before, in and after the infection of the HIV-1 virus.