scholarly journals Role of immune mediators in predicting hospitalization of SARS-CoV-2 positive patients

Cytokine ◽  
2021 ◽  
pp. 155790
Author(s):  
S. Ashrafzadeh-Kian ◽  
M.R. Campbell ◽  
J.C. Jara Aguirre ◽  
J. Walsh ◽  
A. Kumanovics ◽  
...  
Keyword(s):  
Immune Mediators

scholarly journals Proteomic Analysis of Synovial Fibroblasts and Articular Chondrocytes Co-Cultures Reveals Valuable VIP-Modulated Inflammatory and Degradative Proteins in Osteoarthritis

2021 ◽  
Vol 22 (12) ◽  
pp. 6441
Author(s):  
Selene Pérez-García ◽  
Valentina Calamia ◽  
Tamara Hermida-Gómez ◽  
Irene Gutiérrez-Cañas ◽  
Mar Carrión ◽  
...  
Keyword(s):  
Isotope Labeling ◽  
Articular Chondrocytes ◽  
Synovial Fibroblasts ◽  
Immune Mediators ◽  
Cartilage Extracellular Matrix ◽  
Fibronectin Fragments ◽  
Ecm Degradation ◽  
Key Events ◽  
First Time

Osteoarthritis (OA) is the most common musculoskeletal disorder causing a great disability and a reduction in the quality of life. In OA, articular chondrocytes (AC) and synovial fibroblasts (SF) release innate-derived immune mediators that initiate and perpetuate inflammation, inducing cartilage extracellular matrix (ECM) degradation. Given the lack of therapies for the treatment of OA, in this study, we explore biomarkers that enable the development of new therapeutical approaches. We analyze the set of secreted proteins in AC and SF co-cultures by stable isotope labeling with amino acids (SILAC). We describe, for the first time, 115 proteins detected in SF-AC co-cultures stimulated by fibronectin fragments (Fn-fs). We also study the role of the vasoactive intestinal peptide (VIP) in this secretome, providing new proteins involved in the main events of OA, confirmed by ELISA and multiplex analyses. VIP decreases proteins involved in the inflammatory process (CHI3L1, PTX3), complement activation (C1r, C3), and cartilage ECM degradation (DCN, CTSB and MMP2), key events in the initiation and progression of OA. Our results support the anti-inflammatory and anti-catabolic properties of VIP in rheumatic diseases and provide potential new targets for OA treatment.

Houttuynia cordatamodulates oral innate immune mediators: potential role of herbal plant on oral health

Oral Diseases ◽  
2015 ◽  
Vol 21 (4) ◽  
pp. 512-518 ◽  
Author(s):  
S Satthakarn ◽  
WO Chung ◽  
A Promsong ◽  
W Nittayananta
Keyword(s):  
Oral Health ◽  
Potential Role ◽  
Innate Immune ◽  
Immune Mediators ◽  
Herbal Plant

scholarly journals Early Defensive Mechanisms against Human Papillomavirus Infection

2015 ◽  
Vol 22 (8) ◽  
pp. 850-857 ◽  
Author(s):  
Andrea Moerman-Herzog ◽  
Mayumi Nakagawa
Keyword(s):  
Human Papillomavirus ◽  
Immune Responses ◽  
Precancerous Lesion ◽  
Hpv Infection ◽  
Immune Mediators ◽  
Common Cancer ◽  
Papillomavirus Infection ◽  
Abnormal Cells ◽  
Defensive Mechanisms

ABSTRACTCervical cancer is the fourth most common cancer in women and is almost exclusively caused by human papillomavirus (HPV) infection. HPV is also frequently associated with other cancers arising from mucosal epithelium, including anal and oropharyngeal cancers, which are becoming more common in both men and women. Viral persistence and progression through precancerous lesion stages are prerequisites for HPV-associated cancer and reflect the inability of cell-mediated immune mechanisms to clear infections and eliminate abnormal cells in some individuals. Cell-mediated immune responses are initiated by innate pathogen sensing and subsequent secretion of soluble immune mediators and amplified by the recruitment and activation of effector T lymphocytes. This review discusses early defensive mechanisms of innate responders to natural HPV infection, their influence on response polarization, and the underappreciated role of keratinocytes in this process.

scholarly journals Immune Mediators in Osteoarthritis: Infrapatellar Fat Pad-Infiltrating CD8+ T Cells Are Increased in Osteoarthritic Patients with Higher Clinical Radiographic Grading

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Jirun Apinun ◽  
Panjana Sengprasert ◽  
Pongsak Yuktanandana ◽  
Srihatach Ngarmukos ◽  
Aree Tanavalee ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Peripheral Blood ◽  
Underlying Mechanism ◽  
Infrapatellar Fat Pad ◽  
Fat Pad ◽  
Immune Mediators ◽  
Adaptive Immune Cells ◽  
Radiographic Grading

Osteoarthritis is a condition of joint failure characterized by many pathologic changes of joint-surrounding tissues. Many evidences suggest the role of both innate and adaptive immunity that interplay, resulting either in initiation or in progression of osteoarthritis. Adaptive immune cells, in particular T cells, have been demonstrated to play a role in the development of OA in animal models. However, the underlying mechanism is yet unclear. Our aim was to correlate the frequency and phenotype of tissue-infiltrating T cells in the synovial tissue and infrapatellar fat pad with radiographic grading. Our results show that CD8+ T cells are increased in osteoarthritic patients with higher radiographic grading. When peripheral blood CD8+ T cells were examined, we show that CD8+ T cells possess a significantly higher level of activation than its CD4+ T cell counterpart (P<0.0001). Our results suggest a role for CD8+ T cells and recruitment of these activated circulating peripheral blood CD8+ T cells to the knee triggering local inflammation within the knee joint.

scholarly journals Pulmonary Biomarkers of Bronchopulmonary Dysplasia

2008 ◽  
Vol 3 ◽  
pp. BMI.S834 ◽  
Author(s):  
Alecia Thompson ◽  
Vineet Bhandari
Keyword(s):  
Bronchopulmonary Dysplasia ◽  
Cell Types ◽  
Premature Neonate ◽  
Respiratory Disorder ◽  
Immune Mediators ◽  
Pulmonary Disorder ◽  
Postmenstrual Age ◽  
Endothelial Integrity ◽  
Physiologic Role

Bronchopulmonary dysplasia, or BPD, is a chronic pulmonary disorder of premature infants, commonly defined as having an oxygen requirement at 36 weeks postmenstrual age. It is an important source of morbidity and mortality in premature neonates. Its’ etiology appears to be multifactorial with the most common associations being prematurity, need for mechanical ventilation, and oxygen exposure. Implied in the pathogenesis of BPD is the role of cytokines which are immune mediators produced by most cell types. This is evidenced by studies in which there exist alterations in the levels of “pro-inflammatory” and “anti-inflammatory” cytokines. The imbalance of these cytokines have either heralded the onset or predicted the presence of BPD, or indicated a decreased propensity to developing this chronic respiratory disorder of preterm infants. Many other pulmonary markers have been shown to be altered in patients with BPD. These include markers indicative of altered lung repair processes, decreased endothelial integrity, oxidative damage and abnormal fibrinolytic activity, all of which are thought to be mechanisms contributing to the development of BPD. In this review, we will discuss the physiologic role of specific biomarkers in the pulmonary tract of the human premature neonate, the perturbations that enable them to be deranged, and their proposed association with BPD.

scholarly journals The Collision of Meta-Inflammation and SARS-CoV-2 Pandemic Infection

Endocrinology ◽  
2020 ◽  
Vol 161 (11) ◽  
Author(s):  
Gabrielle P Huizinga ◽  
Benjamin H Singer ◽  
Kanakadurga Singer
Keyword(s):  
Immune Responses ◽  
Tissue Injury ◽  
Innate Immune ◽  
Organ Injury ◽  
Innate Immune Responses ◽  
Immune Mediators ◽  
Diabetes Status ◽  
The Impact ◽  
Physiologic Role

Abstract The coronavirus disease 2019 (COVID-19) pandemic has forced us to consider the physiologic role of obesity in the response to infectious disease. There are significant disparities in morbidity and mortality by sex, weight, and diabetes status. Numerous endocrine changes might drive these varied responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, including hormone and immune mediators, hyperglycemia, leukocyte responses, cytokine secretion, and tissue dysfunction. Studies of patients with severe COVID-19 disease have revealed the importance of innate immune responses in driving immunopathology and tissue injury. In this review we will describe the impact of the metabolically induced inflammation (meta-inflammation) that characterizes obesity on innate immunity. We consider that obesity-driven dysregulation of innate immune responses may drive organ injury in the development of severe COVID-19 and impair viral clearance.

scholarly journals The Possible Role of Neutrophils in the Induction of Osteoclastogenesis

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Carolyn G. J. Moonen ◽  
Teun J. de Vries ◽  
Patrick Rijkschroeff ◽  
Patrice E. Poubelle ◽  
Elena A. Nicu ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Polymorphonuclear Leukocytes ◽  
Alveolar Bone ◽  
Surface Expression ◽  
Rankl Expression ◽  
Experimental Conditions ◽  
Periodontal Tissues ◽  
Immune Mediators ◽  
Receptor Activator

The ligand of the receptor activator of NF-κB (RANKL) is a key molecule in the formation of osteoclasts, the key cells that cause the disease-associated alveolar bone resorption in periodontitis. We hypothesized that polymorphonuclear leukocytes (PMNs), found as the most prominent cells of inflamed periodontal tissues, could play an important role in providing signals to trigger osteoclastogenesis and thus activating pathological bone resorption in periodontitis. RANKL expression was investigated on circulatory PMNs (cPMNs) and oral PMNs (oPMNs) taken from both controls and periodontitis patients. On average, 2.3% and 2.4% RANKL expression was detected on the cPMNs and oPMNs from periodontitis patients, which did not differ significantly from healthy controls. Since cPMNs may acquire a more osteoclastogenesis-facilitating phenotype while migrating into the inflamed periodontium, we next investigated whether stimulated (with LPS, TNF-α, or IL-6) cPMNs have the capacity to contribute to osteoclastogenesis. Enduring surface expression of RANKL for short-lived cells as cPMNs was achieved by fixating stimulated cPMNs. RANKL expression on stimulated cPMNs, as assessed by flow cytometry and immunohistochemistry, was limited (6.48±0.72%,mean expression±SEM) after 24 and 48 hours of stimulation with LPS. Likewise, stimulation with TNF-αand IL-6 resulted in limited RANKL expression levels. These limited levels of expression did not induce osteoclastogenesis when cocultured with preosteoclasts for 10 days. We report that, under the aforementioned experimental conditions, neither cPMNs nor oPMNs directly induced osteoclastogenesis. Further elucidation of the key cellular players and immune mediators that stimulate alveolar bone resorption in periodontitis will help to unravel its pathogenesis.

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