Showing 6 results for Inflammation
Omolbanin Amjadi, Alireza Rafiei, Abolghasem Ajami, Vahid Hosseini, Hossein Asgarian-Omran,
Volume 2, Issue 2 (5-2014)
Abstract
Inflammatory condition is the consequence of defensive mechanism of immune system against viral and bacterial infection, tissue injury, UV radiation, stress and etc. Persistently acute inflammation leads to chronic phase which is characterized by production of pro-inflammatory mediators from T cells. These molecules (e.g. IL-6, TNF-&alpha, IL-1&beta and IL-17) are mostly pleiotropic cytokines involved in multiple signaling cascades. NF-&kappaB, STAT3, and HIF-1&alpha are the major engaged pathways directing to several downstream targets associating with tumorigenesis and inflammation. Carcinogenesis processes such as DNA mutation/damage, proliferation, angiogenesis, apoptosis, and invasion are implicated to inflammation. Clearly there is a closely association between cancer and inflammation reported as “Seven Hallmark of Cancer”. The elucidation of relationship between inflammation and cancer and their interaction may result in effective therapy and prevention. Gastric cancer is one of the main cancer involved in complex correlation of inflammation and cancer. Inflammation in gastric epithelium could trigger cellular transformation and promote invasion by inducing immune responses and utilizing signaling cascades. Gastric tumor microenvironment has inverse association by providing cytokines and inflammatory mediators. This closely relationship facilitates gastric tumor development and the induction of chronic inflammation in tumor microenvironment. The current review will focus on describing the possible and critical ways in which inflammation and cancer are linked together with specific view to gastric cancer and inflammation. Finally, it introduces some putative treatment generally used in this way in order to direct more attention for further exploration.
Narges Karimi, Nasim Tabrizi, Mahmoud Abedini,
Volume 3, Issue 3 (8-2015)
Abstract
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system that inflammation, demyelination, oligodendrocyte loss, gliosis, axonal injury and neurodegeneration are the main histopathological hallmarks of the disease. Although MS was classically thought as a demyelinating disease, but axonal injury occurs commonly in acute inflammatory lesions. In MS microglial activation is not only responsible for inflammatory cascade but also creates degenerative cascade. The evidence has shown mitochondrial dysfunction plays an important role in axonal degeneration in all stages of MS due to neuronal cell loss and activation pro-inflammatory cytokines. Neuronal loss occurs as a result of apoptosis and necrosis and mitochondrial pathway is the main important system for apoptosis and this way was involved in neurodegenerative disorders such as MS. Hence in multiple sclerosis, mitochondrial dysfunction causes energy failure and then increases inflammation and demyelination in neurons.
Leila Pirdel, Manijeh Pirdel,
Volume 9, Issue 1 (2-2021)
Abstract
Background: Vitamin D plays a key role in the modulation of numerous immune functions against infectious agents. We aimed to explore the association between serum 25‑hydroxyvitamin D (25[OH] D) levels and cytokine responses, along with hematological changes, in patients with urinary tract infection (UTI).
Materials and Methods: Vitamin D level, cytokines (interferon [IFN]−γ, interleukin [IL]−4, IL−6, IL–10, IL−17A, tumor necrosis factor [TNF]−α, and transforming growth factor [TGF]−β), hematological indices (neutrophil-to-lymphocyte ratio [NLR], monocyte-to-lymphocyte ratio [MLR], neutrophil-to-monocyte ratio [NMR], platelet-to-lymphocyte ratio [PLR], and mean platelet volume [MPV]), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were evaluated in a case-control human study included 65 patients and 45 controls.
Results: Among the enhanced cytokine levels in patients, the cytokines IFN-γ, IL-17A, and IL-10 had a significant association with 25(OH)D, but not IL-6, TNF-α, and TGF-β. The IL-4 levels remained unchanged. By comparing hematological indices, we found the association of increased NLR and MLR with 25(OH)D and the cytokines IFN-γ and IL-17A, along with a decrease in the PLR without showing such an association. The NMR did not show any significant difference. The platelet count showed an association with IL-6, IL-17A, and TGF-β, but the association of MPV with 25(OH)D was significant. The ESR results exhibited statistically non-significant differences. CRP elevation was directly associated with IL-6 and IL-17A, but not with 25(OH)D.
Conclusion: 25(OH)D-mediated inflammatory cytokine milieu might alter the proportion and function of peripheral blood cells in a regulated manner to support bacterial clearance which needs further studies to be validated.
Samira Jahangiri, Ramin Lotfi, Seyed Hamidreza Mortazavi, Ali Gorgin Karaji, Alireza Rezaiemanesh, Hatam Rashidpour, Farhad Salari,
Volume 9, Issue 3 (8-2021)
Abstract
Background: Rhinitis is a prevalent chronic inflammatory illness of the nasal mucosa. Arachidonic acid-derived lipoxin A4 (LXA4) has long been recognized to exert crucial antiinflammatory and pro-resolving effects on inflammatory responses through a specific receptor named LXA4 receptor/formyl peptide receptor-2 (ALX/FPR2). This study aimed to determine the serum level of LXA4 and the relative mRNA expression level of FPR2 in peripheral blood cells of patients with rhinitis (allergic and nonallergic) compared to healthy individuals.
Materials And Methods: The study groups consisted of 37 patients with Allergic Rhinitis (AR), 16 patients with Nonallergic Rhinitis (NAR), and 20 sex- and age-matched healthy individuals. The measurement of LXA4 serum level was performed by the Enzyme-Linked Immunosorbent Assay (ELISA) technique, and the analysis of FPR2 mRNA expression level was performed by quantitative real-time PCR method.
Results: The serum concentrations of LXA4 decreased in AR and NAR patients compared to healthy controls; however, this difference was not statistically significant (P>0.05). Besides, the mRNA expression level of FPR2 in peripheral blood cells of patients with nonallergic rhinitis was significantly lower than that in allergic rhinitis (P<0.05).
Conclusion: Our results suggest that reduced gene expression of FPR2 may contribute to developing persistent and chronic nasal mucosa inflammation seen in NAR patients. Therefore, stable analogs of LXA4 and its receptor agonist may help develop new therapeutic approaches for rhinitis.
Leila Pirdel, Manijeh Pirdel,
Volume 10, Issue 3 (8-2022)
Abstract
Background: Low vitamin D has been linked to enhance inflammatory markers in various pathological conditions. We aimed to evaluate the urinary tract infection (UTI)-associated hematological and inflammatory markers mediated by low serum levels of 25-hydroxyvitamin D [25(OH)D].
Methods: Vitamin D level, hematological indices (Neutrophil-to-lymphocyte ratio [NLR], Monocyte-to-lymphocyte ratio [MLR], Neutrophil-to-monocyte ratio [NMR], Platelet-to-lymphocyte ratio [PLR], and Mean platelet volume [MPV]), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), interleukin-6, and tumor necrosis factor-a were evaluated in 115 UTI patients and 57 controls.
Results: The findings showed an inverse association between elevated hematological (NLR, MLR, and MPV) and serum markers of inflammation (CRP, IL-6, and TNF-a) with serum 25(OH)D levels in UTI patients. Among the several markers evaluated, the MLR had the ability to suggest the associated inflammation with low serum levels of 25(OH)D.
Conclusion: The involvement of vitamin D deficiency might be characterized by an increase in the inflammatory markers in the patients which have an ability to establish the relationship between vitamin D deficiency and UTI; however, further investigations are needed to validate this finding.
Tamer A. Addissouky,
Volume 11, Issue 3 (11-2023)
Abstract
Background: Cholecystitis, inflammation of the gallbladder, has created a significant burden globally. The prevailing paradigm of awaiting irreversible damage before surgically removing the gallbladder is not only traumatic and risky but also fails to address the underlying causes. However, exponential growth in scientific insights now promises a shift towards precision prevention and cure.
Materials and Methods: Pathophysiological mechanisms involved in cystic duct obstruction by gallstones cause gallbladder stasis, direct mucosal injury, vascular compromise, leukocyte infiltration, and secondary infection. Advanced imaging, multiomics profiling, and machine learning unpack early molecular events in lithogenesis and inflammation missed by traditional techniques. Revolutionary endoluminal interventions, anti-inflammatory pharmaceuticals, antibiotic-eluting stents and medications targeting root lithogenic pathways offer alternatives to surgery for drainage restoration and stone prevention. Lifestyle optimization guided by nutrigenomics and pharmacogenomics increasingly personalizes risk factor modification. Ongoing exponential technological gains in nanomedicine, artificial intelligence integration, and minimally invasive techniques promise further preemptive, curative, non-surgical paradigms addressing pathogenesis at the molecular source.
Results: Analysis revealed previously unidentified molecular signatures in early-stage cholecystitis, enabling intervention before irreversible damage occurs. Personalized risk factor modification guided by nutrigenomic and pharmacogenomic profiling demonstrated significant preventive potential. Integration of artificial intelligence with nanomedicine technologies showed promising results in predicting and preventing stone formation. Novel non-surgical interventions achieved 73% success in restoring drainage and preventing stone formation, with significantly lower complication rates compared to traditional cholecystectomy.
Conclusion: Synergizing breakthroughs across domains now position cholecystitis management for a monumental shift from reactive treatment on macroscopic changes towards proactive precision prevention, cure, and health maintenance by comprehending and controlling the underlying molecular cascades. This transformation promises dramatic improvements in patient safety, quality of life, mortality and healthcare economics.
