Active clinical trials for "Inflammation"

Background: - When bacteria enter the lungs, serious infections can occur. Researchers want to learn more about the process of inflammation in the lungs by studying lung cells and the products that they make. Lung cells are influenced by infections, smoking, and molecules made within the body. Researchers also want to learn more about one of these molecules, called microRNA (or micro ribonucleic acid). Objective: - To better how the body responds to infection. Also, to understand which cells in the lung secrete microRNA and how they may influence other lung cells. Eligibility: - Healthy, non-smoking adults ages 18-45. Design: Participants will be screened with a medical history and physical exam. They will have blood and urine tests and an electrocardiogram. Participants will have blood drawn from an arm vein. They will have an intravenous catheter (small plastic tube) placed in a vein. All participants will have bronchoscopy with bronchoalveolar lavage. They will be numbed with medicine. A thin flexible tube will be placed through the nasal passages or the mouth into the airways of the lung. Some participants will have bronchoscopy with bronchoalveolar lavage (rinsing the airways with salt water) in order to obtain cells from lung. The water will then be suctioned out. Some participants will have two bronchoscopies; during the first procedure, endotoxin, a molecule found in bacteria is squirted into a small portion of the lung. Endotoxin is a molecule that acts like an infection but isn t one. After 6 to 48 hours, bronchoscopy with with bronchoalveolar lavage will be done to look at the lung s response to endotoxin. Participants heart rhythm and rate, temperature and blood oxygen level will be monitored during the procedures. Participants will be called the next day to see how they are feeling.

This prospective randomized pilot trial will evaluate a multiple intervention program of prevention in lifelong smokers aiming at reduction of chronic inflammation status through treatment with low-dose acetylsalicylic acid (ASA), smoking cessation with cytisine, targeted modification of diet and physical activity, in addition to early diagnosis with annual ultra low-dose spiral computed tomography (LDCT).

An estimated 1500 people in Sweden will annually be diagnosed with head and neck cancer (HNC). Five year survival is approximately 69%. Long-term sequelae are common and in particular nutritional problems and fatigue. Radiotherapy (RT) is the cornerstone of treatment, either as single modality treatment or combined modality treatment. RT can induce immune responses at the site of tumor. It has been demonstrated that RT can lead to a strong systemic immune response . We have previously shown that an increase of conventional measures of systemic immune response to RT varied significantly across individuals. We predict that local immune response plays a major role in the antitumor effect. We also predict that a strong systemic immune response contributes to malnutrition and influence on survival. And malnutrition may lead to a worse response to RT. The overall aim of this multicenter observational longitudinal study is to prospectively identify immunological and metabolic variables that affect the outcome of HNC patients. We will systematically investigate the local and systemic immune response induced by RT as well as explore alterations in metabolite composition induced by disease and treatment through global metabolite profiling. A platform for studies on immuno-metabolic changes in HNC patients has been established in the Uppsala-Orebro and Northern regions. Approximately 370 patients per year are eligible. Findings in this study can have implications on the development of personalized therapy in patients with HNC. The long-term benefit of the study will be the identification of measures for improved patient surveillance in order to improve the general and nutritional outcomes.

This study is focused on assessing gastrointestinal-level improvements by which green tea limits metabolic endotoxemia. It is expected that catechin-rich green tea will improve gut barrier function to prevent endotoxin translocation and associated low-grade inflammation. Outcomes will therefore support dietary recommendations for green tea to alleviate obesity-related inflammatory responses. Specifically, the study is expected to demonstrate that a green tea confection snack food can attenuate metabolic endotoxemia in association with restoring gastrointestinal health.

Cystic Fibrosis (CF) is a disease that affects salt and water transport in multiple organs. Many CF patients suffer from abdominal pain and this could be due to intestinal inflammation. However, so far we do not know how many of the CF patients actually do have intestinal inflammation when looking at intestinal specimens. There is a proven connection between chronic inflammation and developing colorectal cancer and over the years more CF patients are developing colorectal cancer. Thus, it becomes increasingly important to look for the presence of intestinal inflammation in CF patients since early treatment may improve their symptoms and reduce the risk for colorectal cancer.

This study will examine adipose tissue inflammation and adipokine expression and serum markers of inflammation and adipokine levels in patients with growth hormone (GH) deficiency before and after treatment.

The intrinsic connection between inflammation and tumor promotion is well characterized and is a key pathogenic event in patients with colorectal cancer (CRC), the second most common cause of tumor-related death in western countries. Environmental factors and chronic inflammation represent the major causes of intestinal carcinogenesis. In fact, patients suffering from inflammatory bowel diseases, including Crohn's disease and Ulcerative Colitis (UC), have high risk of developing colitis-associated CRC with poor prognoses. Therefore, targeting the cancer-associated inflammation may offer new avenues for cancer treatment. In fact, several anti-inflammatory drugs, have been used for prophylaxis and have shown efficacy in contrasting cancer, despite various adverse side effects. Thus, there is an urgent need to discover novel cancer-associated mechanisms to develop alternative therapies that may reduce aberrant inflammatory responses without interfering with physiological defenses against infection and functional anti-tumor immunity. A novel approach promoting anti-tumor immunity has been recently proposed after the discovery of potent, endogenous, specialized pro-resolving mediators (SPMs), including lipoxins, resolvins, protectins, and maresins, mainly derived from omega-3 polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) via COX, LOX and CYP450 pathways, mediated by MFSD2A. Due to the potent bioactivity of SPMs in resolving inflammation and because of the correlation between inflammation and cancer, the roles of these lipid mediators have attracted great attention for their potential therapeutic role in cancer treatment, including CRC. Nevertheless, the understanding of the endogenous mechanisms that limit the inflammatory response during CRC development is incomplete and requires further investigation. Based on the preliminary results indicating that dysfunctional MFSD2A-dependent pro-resolving pathways may foster CRC development, the investigators aim to define the functional role of MFSD2A in orchestrating pro-resolving pathways in the intestinal endothelium of metastatic and not metastatic CRC patients. This is a cross-sectional single-center observational study involving patients with CRC. The investigators will enroll 15 patients with colorectal cancer (CRC) stratified by tumor stage (T0 / T1-T4, M0 / M1, N0 / N1 / N2) undergoing surgery in the Gastroenterology and Digestive Endoscopy unit within Gastro Center (IRCCS Ospedale San Raffaele). Human Intestinal Microvascular Endothelial Cells (HIMEC) will be generated from each sample of cancer surgical specimens, while the healthy cells will be derived from the healthy margins of the colorectal resection of the same CRC patients. MFSD2A will be overexpressed or silenced and the investigators will evaluate its biological effects in both tumor-derived HIMECs and healthy tissue-derived HIMECs through transcriptomics and lipidomics analysis. The investigators will also exploit a possible novel therapy based on the delivery of MFSD2A encoding plasmid-conjugated liposomes.

The purpose of this study is to evaluate how supplementation will alter the skin and the gut barrier and inflammation in those with rosacea.

Patients with multi-bracketed fixed orthodontic treatment are at increased risk of developing white spot lesions (WSL) and gingivitis. Various preventive strategies have been examined to prevent the development of WSLs. During initial non-surgical periodontal therapy, the use of subgingival air-polishing with erythritol powder has shown promising results in reducing deep pockets and gingival inflammation. The efficacy of its use as monotherapy in preventing WSLs and gingival inflammation in patients during orthodontic treatment, has not yet been tested. The primary objective of the present study is to compare the effectiveness of an air-polishing device used as monotherapy versus ultrasonic instrumentation (the current gold standard procedure) in preventing white spot lesions (WSL) and gingivitis among young patients undergoing multi-bracketed fixed orthodontic treatment.

Widely expressed in the sensory nerve endings of the skin, Transient Receptor Potential Vanilloid 1 (TRPV1) is a receptor that plays an important role in the perception of pain and pruritus but also in skin inflammation, primarily by inducing the local release of several neuropeptides. Although the mechanisms by which TRPV1-sensitizing inflammatory mediators in damaged skin have received considerable attention, the role of TRPV1 in psoriasis has so far been little explored. However, two studies have reported that ablation of sensory nerves expressing TRPV1 reduced psoriasiform skin inflammation, demonstrating the neuronal contribution to inflammation in psoriasis. However, the expression of TRPV1 is not limited to neurons alone. TRPV1 is also expressed by epidermal keratinocytes and skin microvessels. For example, in 2018, transcriptomic analysis of psoriatic patient skins (by definition devoid of neuron nuclei) revealed that TRPV1 expression was increased in the skin of psoriatic patients suffering from itching (pruritus). Regarding human keratinocytes, it is recognized that the activation of TRPV1 present on their surface induces the release of pro-inflammatory factors such as cyclooxygenase-2. In addition, the investigators have demonstrated that TRPV1 has a pivotal role in the keratinocyte production of inflammatory mediators, which is mediated by the protease-activated receptor-2 (PAR-2). However, the role of vascular TRPV1 in inflammation is not described. The investigators hypothesize that in addition to neuronal TRPV1, non-neuronal TRPV1 receptors of non-neuronal cells (keratinocytes and endothelial cells) may be involved in the vicious circle of the inflammatory process characteristic of psoriasis. Putting TRPV1 at the center of the deregulation of the homeostatic balance including epithelial, neuronal and vascular inflammation in psoriasis is totally innovative.