Indian Journal of Inflammation Research
http://old.chanrejournals.com/index.php/indiainflammation
<p>Indian Journal of Inflammation Research, a publication of Indian Society of Inflammation, is a peer-reviewed, biannual, open access online journal that publishes articles on all aspects of research on inflammation.</p>ChanRe Journalsen-USIndian Journal of Inflammation Research2581-7914<p class="western" style="margin-bottom: 0cm;" lang="en-US">Copyright for articles published in this journal is retained by the authors, with first publication rights granted to the ‘Indian journal of Inflammation Research’. All the published content, except where otherwise noted, is licensed under Creative Commons license (<a href="http://creativecommons.org/licenses/by/3.0/" target="_blank">CC-BY</a>).</p><p class="western" style="margin-bottom: 0cm;" lang="en-US">Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) after the publication of the manuscript in IJIR, as it can lead to productive exchanges, as well as earlier and greater citation of published work.</p>Exploring cell-free mitochondria as a potential non-invasive biomarker of lupus nephritis
http://old.chanrejournals.com/index.php/indiainflammation/article/view/388
<p>Systemic lupus erythematosus (SLE) is a systemic chronic autoimmune disease. Lupus nephritis (LN) is one of the major manifestations of SLE affecting up to ~60% SLE patients. According to European League Against Rheumatism (EULAR) and American College of Rheumatology (ACR), a positive renal biopsy along with a positive antinuclear antibody (ANA) and/or anti-double-stranded DNA (anti-dsDNA) antibody is required for confirmation and classification of LN. Renal biopsy is the gold standard to diagnose and classify LN, but it is invasive and costly. Therefore, there is a need for less invasive, risk-free systemic biomarkers to predict disease activity and treatment outcomes. Cells under oxidative stress can release various mitochondrial Danger Associated Molecular Patterns (DAMPs) including naked or vesicle-enclosed forms of mitochondria itself known as cell-free mitochondria (cf-mitochondria), mitochondrial DNA etc. Stressful conditions are also well known to cause mitochondrial extrusion by damaged organs. The cf-mitochondria can act as auto-antigen, thus triggering immune response leading to production of anti-mitochondrial DNA autoantibodies. </p>Khushboo RanaSharath GowdaAnkit KumarPradip PrajapatiNamisha PatelSapan PandyaRatika Srivastava
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-11-172023-11-177110.15305/ijir.v7i1.388Understanding the role of scavenger receptor CD36 in modulation of dendritic cell responses
http://old.chanrejournals.com/index.php/indiainflammation/article/view/389
<p>Dendritic cells (DCs) are professional antigen-presenting cells (APCs) that play a central role in immunity. DCs, like other innate immune cells, usually rely on various germ-line encoded pattern recognition receptors (PRRs) to recognize some of the conserved patterns, called pathogen-associated molecular patterns (PAMPs), on microbes. Recent studies from various groups highlight the emergence of scavenger receptors (SRs) as non-classical PRRs.</p>Dwipjyoti SarmaVinica DharArunika Mukhopadhaya
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-11-252023-11-257110.15305/ijir.v7i1.389Angiopoietin-like protein 2 mediates vasculopathy-driven fibrogenesis in a mouse model of skin fibrosis
http://old.chanrejournals.com/index.php/indiainflammation/article/view/386
<p>Fibrosis is a pathological condition wherein excessive deposition of extracellular matrix components leads to tissue hardening and loss of function. Though fibrosis contributes to ~40% of deaths worldwide, the lack of effective treatments highlights the need for a molecular understanding of fibrogenesis. Vasculature abnormalities are a foundational cause of fibrotic disorders such as the skin fibrotic disease scleroderma, however the underlying mechanisms are largely unknown.</p>Dyuti SahaSujaya ThannimangalathNeha PinchaRavikiran AnnadoraiSunny KatariaBinita DamAnkita HiwalePraveen VemulaColin Jamora
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-11-152023-11-157110.15305/ijir.v7i1.386The matricellular protein mindin induces a pro-inflammatory response in fibroblasts to manifest dermal fibrosis in scleroderma
http://old.chanrejournals.com/index.php/indiainflammation/article/view/385
<p>Scleroderma, or systemic sclerosis (SSc), is a rare autoimmune and genetic disease. It is characterized by chronic inflammation and fibrosis, primarily in the skin, and progresses to internal organs, including the heart, lungs, and kidneys. While the root cause of scleroderma remains elusive, a major driver of the pathology is chronically activated fibroblasts (myofibroblasts) that excessively secret extracellular matrix (ECM) proteins. The lack of an effective treatment for scleroderma underlies the need to elucidate the molecular mechanisms of scleroderma pathogenesis that will shed new insights into potential new routes of therapeutic intervention. </p>Gaurav KansagaraSunny KatariaIsha RanaKrithika BadarinathRania ZaarourRakesh DeyAkash GulyaniYou-Wen He Colin Jamora
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-11-142023-11-147110.15305/ijir.v7i1.385High throughput screening identifies novel pharmacological inhibitors of interferon-gamma-induced nitric oxide production, alleviating ulcerative colitis and bacterial sepsis in mice
http://old.chanrejournals.com/index.php/indiainflammation/article/view/384
<p>Interferon-gamma (IFN-γ) is a type II interferon primarily produced by T cells and natural killer cells. One of the key markers in IFN-γ signaling is the expression of NOS2 catalyzing the production of Nitric Oxide (NO). IFN-γ signaling and NO production combat infectious diseases like Mycobacterium tuberculosis and Salmonella Typhimurium infections. However, excessive IFN-γ-activated NO production is implicated in several inflammatory diseases, including ulcerative colitis, multiple sclerosis, systemic lupus erythematosus, and sepsis. Disease exacerbation in chronic inflammatory diseases is managed with steroidal medications; however, long-term use of corticosteroids often leads to unavoidable adverse effects. These problems necessitate identifying alternative non-steroidal anti-inflammatory drugs, potentially targeting IFN-γ-induced NO hyperproduction.</p>Avik ChattopadhyayJoel JosephSirisha JagdishSomak ChaudhuriNikita RamtekeAagosh KarhaleUchenna WaturuochaDeepak SainiDipankar Nandi
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-11-092023-11-097110.15305/ijir.v7i1.384Nuclear Receptor Co-repressor NCoR1 governs immune tolerance in conventional dendritic cells by fine-tuning glycolysis and fatty acid oxidation
http://old.chanrejournals.com/index.php/indiainflammation/article/view/372
<p>Dendritic cells (DCs) undergo rapid metabolic reprogramming events to induce signal-specific immune responses. The transcriptional control of energy metabolism in tolerogenic-DCs remains elusive. We have recently reported that NCoR1 ablation in DCs leads to immune tolerance by altering the balance of naive T helper cells towards T-regs. Here, comprehensive metabolic profiling of these tolerogenic DCs identified that they meet their anabolic requirements through enhanced glycolysis and OxPhos, supported by FAO-driven oxygen consumption.</p>Kaushik SenRashmirekha PatiAtimukta JhaGyan Prakash Mishra Prakash MishraSubhasish PrustyShweta ChaudharySwati SwetalikaSreeparna PodderAishwarya SenMamuni SwainRanjan NandaSunil K. Raghav
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-01-312023-01-317110.15305/ijir.v7i1.372Analysis of complete blood count parameters throughout disease severity in COVID-19 survivors
http://old.chanrejournals.com/index.php/indiainflammation/article/view/373
<p><strong> The pandemic of Coronavirus disease 2019 (COVID-19) represented a scientific and social crisis. Among the most pressing unmet needs for coronavirus disease in 2019 was its unpredictable clinical course, which resulted in an irreversible outcome. The presence of post-acute COVID-19 syndrome in survivors, as well as the exploration of different blood cell counts in Covid 19 survivors, seems to be unclear, and scientific data is still being summarized. Patients can be divided into three categories: mild, moderate, and severe in terms of infection severity. Platelets, white blood cell total count, lymphocytes, neutrophils and hemoglobin levels have all been linked to COVID-19 infection and severity. In this regard, evaluation of hematological abnormalities at the beginning, during and after COVID-19 infection and during COVID-19 that can be indicative of prognosis in the recovery phase. The purpose of this study was to analyze the complete blood picture among COVID-19 survivors & co-relate it with disease severity which can be implemented as a prognostic biomarker of the disease. </strong></p>Tanusha PathakRachna ParasharPragati RaghuwanshiDeepti JoshiAnkur JoshiRajnish JoshiRagini Shrivastava
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-01-312023-01-317110.15305/ijir.v7i1.373Inflammation status in COVID-19 survivors in the recovery phase
http://old.chanrejournals.com/index.php/indiainflammation/article/view/374
<p>The pathogenesis of the post-COVID syndrome is multifactorial, and multiple mechanisms may be involved in various clinical manifestations. Post-acute COVID-19 syndrome persists among survivors but the association of residual inflammation in COVID-19 survivors is still unknown. The literature illustrating the role of inflammatory markers such (S. Ferritin, IL-6, and CRP) remain unconsolidated. The purpose of this study was to evaluate the association of inflammatory markers and their role in disease severity among COVID-19 survivors. The current study aimed to estimate the concentrations of serum Interleukin-6 (IL-6), C reactive protein, and serum ferritin levels in COVID-19 survivors & correlating the different inflammatory markers with disease severity to find out the best-correlated marker.</p>Pragati RaghuwanshiRachna ParasharSukhes MukherjeeAnkur JoshiRajnish JoshiHimadri Singh
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-02-022023-02-0271SIRCON 2023: A brief overview
http://old.chanrejournals.com/index.php/indiainflammation/article/view/383
<p><em>A report on the conference of the Society of Inflammation Research-SIRCON-2023 held at Indian Institute of Science, Bengaluru on 17th September 2023. </em></p>Chandrashekara S
Copyright (c) 2023 Indian Journal of Inflammation Research
2023-11-082023-11-087110.15305/ijir.v7i1.383