Chronic polyposis rhinosinusitis (CPRS) is an inflammatory disease of the nose and paranasal sinuses, accompanied by the formation and recurrent growth of polyps. PDRS is an urgent medical problem, because it is difficult to treat and is accompanied by constant exacerbations. The important role of neutrophil granulocytes in the pathogenesis of CPRS has been proved, as they are the first line of defense in response to tissue damage and active participants in the pathological process. There is evidence of successful use of immunocorrectors in the treatment of patients with CPPS, but they are often prescribed without regard to possible pathogenetic mechanisms of the disease. One of the promising immunomodulators of local use is a preparation of human recombinant interferon gamma. It is known that interferon gamma is able to activate neutrophils due to the receptors to this cytokine, which are located on their surface. The aim of the study was to investigate the functional activity of neutrophils in patients with CPPS and the effect of human recombinant interferon gamma on these indicators. Thirty-five patients with CHRS were examined before and after therapy with intranasal interferon gamma. The control group included 30 healthy subjects. Functional activity of neutrophils was studied in whole blood by chemiluminescent method using double stimulation. Patients with CPRS before treatment revealed increased indexes of neutrophils stimulated activity, maximal intensity of cells luminescence, activation coefficient and decreased time of neutrophils output at maximal luminescence. After treatment with intranasal preparation of interferon gamma there was significant decrease of spontaneous and stimulated activity of neutrophils and maximum intensity of cell luminescence. As a result, after the treatment, in patients with CHRS the values of stimulated production of neutrophils and maximum intensity of cell luminescence were reduced to the level of the control group, and the spontaneous activity of neutrophils was even lower than in healthy subjects, while the neutrophils activation factor remained elevated as in patients before therapy. The results obtained testify to normalization of the main indexes of neutrophil functional activity in CHPS patients after treatment with human recombinant interferon gamma.
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http://dx.doi.org/10.51620/0869-2084-2022-67-6-339-344 | DOI Listing |
J Immunother Cancer
January 2025
Division of Infection, Immunity and Respiratory Medicine, The University of Manchester, Manchester, UK
Background: Programmed cell death 1 (PD-1) signaling blockade by immune checkpoint inhibitors (ICI) effectively restores immune surveillance to treat melanoma. However, chronic interferon-gamma (IFNγ)-induced immune homeostatic responses in melanoma cells contribute to immune evasion and acquired resistance to ICI. Poly ADP ribosyl polymerase 14 (PARP14), an IFNγ-responsive gene product, partially mediates IFNγ-driven resistance.
View Article and Find Full Text PDFInt J Pharm
January 2025
Department of Chemical Sciences, Bernal Institute, University of Limerick, Ireland; SSPC Science Foundation Ireland Research Centre for Pharmaceuticals, University of Limerick, Ireland. Electronic address:
The potent pro-inflammatory cytokine, interferon gamma (IFN-γ), is an enticing therapeutic target because of its accelerator role in several acute and chronic inflammatory processes. In this work, poloxamer 407 is developed as an in-situ gelling polymer for a long-acting formulation to deliver a serine protease, C5a peptidase (ScpA) from Streptococcus pyogenes. ScpA is well known for its activity against the complement factor C5a but has also recently been shown to cleave IFN-γ in vitro into inactive fragments.
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January 2025
Department of Gastroenterology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Electronic address:
Tuberculosis (TB), caused by Mycobacterium TB, is the most significant infectious cause of mortality across the globe. While TB disease can prey on immunocompetent individuals, it is more likely to occur in immunocompromised individuals. Immune-mediated inflammatory diseases (IMIDs) are a group of diseases (rheumatoid arthritis, inflammatory bowel disease, ankylosing spondylitis, psoriasis, hidradenitis suppurative, autoimmune blistering diseases, and others) where there may be a need for systemic immunosuppression to control the disease manifestations, treat symptoms and improve long term outcomes.
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January 2025
Chinese Medicine Research and Development Center, China Medical University Hospital, Taichung, Taiwan; Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan; Master Program of Pharmaceutical Manufacture, College of Pharmacy, China Medical University, Taichung, Taiwan; Department of Medical Laboratory Science and Biotechnology, College of Medical and Health Science, Asia University, Taichung, Taiwan. Electronic address:
The immunoglobulin E (IgE) receptor FcεRI (Fc epsilon RI) plays a crucial role in allergic reactions. Recent studies have indicated that the interaction between FcεRIβ and the downstream protein phospholipase C beta 3 (PLCβ3) leads to the production of inflammatory cytokines. The aim of this study was to develop small molecules that inhibit the protein-protein interactions between FcεRIβ and PLCβ3 to treat allergic inflammation.
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January 2025
Guangdong Provincial Key Laboratory of Tumor Interventional Diagnosis and Treatment, Zhuhai Institute of Translational Medicine, Zhuhai People's Hospital (The Affiliated Hospital of Beijing Institute of Technology, Zhuhai Clinical Medical College of Jinan University), Jinan University, Zhuhai 519000, China; State Key Laboratory of Bioactive Molecules and Druggability Assessment, The Biomedical Translational Research Institute, Health Science Center (School of Medicine), Jinan University, Guangzhou 510632, China; Key Laboratory of Viral Pathogenesis & Infection Prevention and Control (Jinan University), Ministry of Education, Guangzhou 510632, China. Electronic address:
Previous studies have established that γδ T cells play a significant role in liver fibrosis. However, their specific functions and mechanisms in fibrotic liver tissue remain unclear. Using online microarray expression profiles, we observed that USF3 was upregulated in patients with liver fibrosis and was associated with immune cells.
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