387 results about "Neutrophil granulocyte" patented technology

The present invention comprises a method to identify granulocytic cell genes that are differentially expressed upon exposure to a pathogen or in a sterile inflammatory disease by preparing a gene expression profile of a granulocytic cell population exposed to a pathogen or isolated from a subject having a sterile inflammatory disease and comparing that profile to a profile prepared from quiescent granulocytic cells. The present invention is particularly useful for identifying cytokine genes, genes encoding cell surface receptors and genes encoding intermediary signaling molecules. The invention also includes methods to identify a therapeutic agent that modulates the expression of at least one gene in a granulocytic population. Genes which are differentially expressed during neutrophil contact with a pathogen, such as a virulent bacteria, or that are differentially expressed in a subject having a sterile inflammatory disease are of particular importance.

A tissue cell growth-promoting solution produced by this invention comprising water containing at least 1 to 500 ppm of active oxygen, when applied to a wound, supplies active oxygen originating from outside the biobody to supplement the active oxygen produced by the biobody's own protective system cells such as neutrophils and macrophages which gather at the wound site, thus increasing the concentration of active oxygen at the site of the wound, mimicking a state in which a large quantity of such bio-signals is secreted by the biobody itself, to promote the reconstruction of tissues, the action corresponding to the last of the four main steps involved in wound healing biochemical processes of "blood vessel reaction", "blood vessel coagulation", "inflammation", "reconstruction of tissues" and which would otherwise have to rely on the natural healing power of the biobody itself.

Methods for treating chronic wounds in a human are described by topically administering a dermatological composition comprising a TNF antagonist, a TACE inhibitor, a neutrophil antagonist, or a combination of a TNF antagonist and/or TACE inhibitor and a neutrophil antagonist. The TNF antagonist administered includes alefacept, efalizumab, etanercept, adalimumab, and onercept, while the neutrophil antagonist administered includes dapsone, colchicine, its analogs and prodrugs. The combination of TNF-antagonist and neutrophil antagonist administered includes sulfapyridine, sulfasalazine, mesalamine, and derivatives and prodrugs thereof. The topical compositions can be formulated to include the one or more of the antagonists in dissolved, semi-dissolved, and micro-particulate states.

α-MSH and other amino acid sequences derived from α-MSH were determined to have antimicrobial influences, including against two major and representative cutaneous and mucosal pathogens; Staphylococcus aureus and Candida albicans, Pharmaceutical compositions useful as antimicrobial agents, including for use in reducing the viability of microbes, reducing the germination of yeasts, killing microbes without reducing the killing of microbes by human neutrophils, for treating inflammation in which there is microbial infection without reducing microbial killing, and for increasing the accumulation of cAMP in microbes are disclosed. The antimicrobial agent is selected from the group consisting of one or more peptides including the amino acid sequence KPV, one or more peptides including the amino acid sequence MEHFRWG, or a biologically functional equivalent of any of the foregoing. The most effective of the peprides were those bearing the C-terminal amino acid sequence of α-MSH. i.e., α-MSH (1-13), (6-13), and (11-13).

A method of inhibiting the adverse effects of alternative complement pathway activation products in a subject comprising administering to the subject an amount of anti-factor Ba antibody effective to selectively inhibit formation of an alternative complement pathway activation products C3a, C5a, and C5b-9, and activation of neutrophils, monocytes, and platelets.

A method of inhibiting complement activation mediated by C3b inhibitors in a subject includes administering a C3B inhibitor to the subject to inhibit at least one of C3b binding to factors B and properdin, inhibit C3 cleavage, inhibit the activation of neutrophils, monocytes, platelets, and endothelium; or inhibit the formation of C3a, C5a, and MAC.

Described herein are methods, devices and systems for inhibition of granulocyte activation by appropriate stimulation of the vagus nerve. Methods of treating granulocyte-mediated disorders (including inflammatory disorders) by stimulating the vagus nerve to inhibit granulocyte activation (particularly neutrophil activation) are also described. Appropriate stimulation may be very low levels of stimulation, including stimulation that does not result in desensitization. The level of granulocyte activation may be detected and used to at least partially control stimulation.

Methods of assessing the ongoing kidney status in a subject afflicted with chronic renal failure (CRF) by detecting the quantity of Neutrophil Gelatinase-Associated Lipocalin (NGAL) in fluid samples over time is disclosed. NGAL is a small secreted polypeptide that is protease resistant and consequently readily detected in the urine and serum as a result of chronic renal tubule cell injury. Incremental increases in NGAL levels in CRF patients over a prolonged period of time are diagnostic of worsening kidney disease. This increase in NGAL precedes and correlates with other indicators of worsening CRF, such as increased serum creatinine, increased urine protein secretion, and lower glomerular filtration rate (GFR). Proper detection of worsening (or improving, if treatment has been instituted) renal status over time, confirmed by pre- and post-treatment NGAL levels in the patient, can aid the clinical practitioner in designing and/or maintaining a proper treatment regimen to slow or stop the progression of CRF.

A particle/cell separation device is described which is particularly adapted for neutrophil depletion from a preparation of whole blood or platelet-rich plasma. Also described are blood and platelet rich plasma compositions produced using the device which are neutrophil-depleted.

An object of the present invention is to provide a method for suppressing surgical site infections (SSI) that have occurred at extremely high incidence rates at the time of surgical operations and particularly surgical operations on digestive system organs, and to provide a column to be used for the method. According to the present invention, a method is provided for suppressing surgical site infections, which comprises the steps of: (a) administering a chemotherapeutic drug for treating and/or preventing a surgical site infection; and (b) collecting blood from a surgical subject and removing leukocytes that comprise neutrophils from the blood during or within 24 hours after surgical operation, and then returning the blood from which the leukocytes have been removed to the surgical subject. The present invention also provides a column for blood circulation which is filled with a carrier having affinity for leukocytes comprising neutrophils, which is used for suppressing a surgical site infection during or within 24 hours after surgical operation on a digestive system organ.

A method for enhancing the overall beneficial immune system response in a host that works in conjunction with the host's natural immune system response to simultaneously enhance the host's ability to eliminate infectious microbes while suppressing the toxicity of the immune system response to the host. The method utilizes the non-enzymatic formation of allicin in response to the localized generation of H2O2 by immune system cells (such as neutrophils) to simultaneously increase the antimicrobial effect while reducing the cytotoxicity to the host. It is shown that enzymes can be reversibly inhibited that would not normally be sensitive to deactivation by a thiol-disulfide exchange reaction. This results in part from the recognition that deactivation of SH dependant enzymes by allicin does not take place by the previously attributed mechanism of thiol-disulfide exchange reactions. Allicin, cysteine, and related organosulfur compounds have a variety of antimicrobial and immunomodulatory properties that work together with the host's immune system in the prevention and treatment of disease. Prophylactic and therapeutic treatment is provided by administering an allium-related organosulfur compound such that a localized thiosulfinate is caused to be non-enzymatically formed in response to localized generation of H2O2 by the activated immune system cells. Allicin, cysteine and related organosulfur compounds may be simultaneously delivered in an efficient manner through the use of protein-bound S-AllylMercaptoCysteine (SAMC) or similar prodrugs.

The present invention relates generally to the use of recombinant human CC10 (rhCC10), also known as recombinant human uteroglobin, for use as a therapeutic in the treatment of Respiratory Distress Syndrome (RDS), Bronchopulmonary dysplasia (BPD), chronic lung disease and/or pulmonary fibrosis, Asthma and Chronic Obstructive Pulmonary Disease (COPD). More particularly, the invention provides methods, including broadly the critical dosage ranges of rhCC10, which may be administered to safely and effectively treat the aforementioned conditions. The invention further provides a composition useful in administering rhCC10 to humans.

The invention belongs to the field of pharmaceutical preparations, and relates to activated neutrophil membrane coated neutrophil like nanoparticles and a preparation method. According to the activated neutrophil membrane coated like nanoparticles and the preparation method disclosed by the invention, a polymer, namely a poly(lactic-co-glycolic acid) copolymer PLGA, or a poly(lactic acid) copolymer PLA, or a polycaprolactone copolymer PCL is used as a material for preparing nanoparticles, the nanoparticles are used as kernels and are used for coating and loading model medicines, natural activated neutrophil membranes as a shell are used for coating the surfaces of the nanoparticles, and an activated neutrophil membrane coated biodegradable neutrophil like particle nanometer carrier system is prepared. Experiments in vivo and vitro indicate that the like particle nanometer carrier system can have the characteristics of being high in targetability and high in efficiency in accordance with a like treatment system for circulating tumor cells and micrometastases, provides new thought for individual and precision treatment and has higher clinical practice significance.

The invention discloses a compound probiotic agent for improving immunity of dogs and reducing incidence of diarrhea as well as a preparation method and application thereof, and belongs to the field of the compound probiotic agent. The compound probiotic agent is prepared by mixing and compounding a lactobacillus plantarum KT-Lp9 microbial agent, a lactobacillus casei zhang microbial agent, a lactobacillus plantarum P-8 microbial agent, a bifidobacterium animalis subsp. lactis V9 microbial agent and a dilution carrier, wherein the quantity of viable bacteria of the four kinds of microbial agents is more than or equal to 2*10<11>CFU/g. The compound probiotic agent with different contents of viable bacteria only can be applied to 96 dogs at different ages for 60 days, so that the immunity of the test dogs can be improved, and the incidence of diarrhea and the sickness degree are reduced. Main representations are that the feed intake and growth rate of the dogs are increased, leukocyte counts, lymphocytes counts and neutrophil counts in blood are controlled, and the contents of four immunologic factors including immune globulin G, interleukin 6, interferon alpha and tumor necrosis factor alpha in the blood can be increased; and meanwhile, the content of secretory immunoglobulin A (SigA) in excrement is increased.

The present invention relates to pharmaceutical kits and methods to treat lung inflammation and redox imbalance in human cystic fibrosis patients using pharmaceutical compositions containing N-acetylcysteine (NAC), pharmaceutically acceptable salts of N-acetylcysteine, or N-acetylcysteine derivatives. In phase I studies, treatment with oral NAC at a dose of from about 1800 mg/day to about 3000 mg/day for a period of 4 weeks produced significant positive effects, namely, it decreased absolute numbers of white blood cells and neutrophils in the sputum and produced concomitant decreases in sputum neutrophil elastase specific activity and sputum interleukin-8 levels, suggesting an amelioration of lung inflammation in the patients. These effects were associated with an increased total GSH level in whole blood as well increased staining for reduced GSH in blood neutrophils, both of which reflect an amelioration of the redox imbalance in the patients. In ongoing phase II studies, oral NAC at a dose of about 2700 mg/day administered in double-blind manner for 12 weeks showed excellent safety and significantly decreased white blood cells in sputum as compared to placebo.

The present invention relates to a method and composition for inducing lymphocyte proliferation and migration, and for reducing the risks of microbial infections in patients immuno-supressed. The present invention particularly relates to the use of S100 protein, such as MRP, to induce the proliferation, differentiation and release of immune cells from bone marrow. More particularly, S100A8, S100A9, S100A12 and S100A8/A9 are administered to patients with lowered neutrophil blood concentrations.

A method for efficient generation of neutrophils, eosinophils, macrophages, osteoclasts, dendritic cells an Langerhans cells from human embryonic stem cells is disclosed.

Disclosed herein are compounds that selectively activate the FPRL1 receptor. Further disclosed are methods of alleviating inflammatory responses by regulating key steps in leukocyte trafficking and preventing neutrophil-mediated tissue damage by administering to a subject a therapeutically effective amount of the compounds disclosed herein. In addition, methods of modulating, or specifically agonizing, the FPRL1 receptor by administering an effective amount of the compounds disclosed herein are provided.

A composition and method for promoting neutrophil survival and activation such as the treatment of neutropenia arising as an undesirable side effect of chemotherapy and radiation therapy. A composition containing medium-chain fatty acids, such as Capri acid or caprylic acid, or salts or triglycerides thereof, or mono- or diglycerides or other analogues thereof or medium-chain triglycerides (MCT) is administered to a human or animal needing treatment in an amount sufficient to reduce or eliminate neutropenia. The composition is administered in an amount effective to treat the disorder. The methods are also useful in the management of bone narrow transplantation and in the treatment of various neutropenic diseases.

The present invention includes a method of measuring cytolytic activity including providing a device capable of monitoring cell-substrate impedance operably connected to an impedance analyzer, adding target cells to at least one well of the device, adding effector cells to the at least one well, monitoring impedance of the at least one well and optionally determining a cell index from the impedance, wherein monitoring impedance includes measuring impedance during at least one time point before and at least one time point after adding effector cells, and determining viability of said target cells after adding effector cells by comparing the impedance or optionally the cell index at the at least one time point after adding effector cells to the impedance or optionally the cell index at the at least one time point before adding effector cells

The invention relates to polypeptide conjugates comprising a polypeptide exhibiting G-CSF activity and having an amino acid sequence that differs from the amino acid sequence of human G-CSF in at least one specified introduced and/or removed amino acid residue comprising an attachment group for a non-polypeptide moiety, and having at least one non-polypeptide moiety attached to an attachment group of the polypeptide. The attachment group may e.g. be a lysine, cysteine, aspartic acid or glutamic acid residue or a glycosylation site, and the non-polypeptide moiety may e.g. be a polymer such as polyethylene glycol or an oligosaccharide. The conjugate, which has a reduced in vitro bioactivity compared to hG-CSF, has one or more improved properties such as increased biological half-life and increased stimulation of neutrophils.