TNF Induces Laminin-332-Encoding Genes in Endothelial Cells and Laminin-332 Promotes an Atherogenic Endothelial Phenotype.

Laminins are essential components of the basement membranes, expressed in a tissue- and cell-specific manner under physiological conditions. During inflammatory circumstances, such as atherosclerosis, alterations in laminin composition within vessels have been observed. Our study aimed to assess the influence of tumor necrosis factor-alpha (TNF), a proinflammatory cytokine abundantly found in atherosclerotic lesions, on endothelial laminin gene expression and the effects of laminin-332 (LN332) on endothelial cells' behavior.

An Eco-Friendly Synthesis Approach for Enhanced Photocatalytic and Antibacterial Properties of Copper Oxide Nanoparticles Using Algal Extract.

Background: In the current scenario, the synthesis of nanoparticles (NPs) using environmentally benign methods has gained significant attention due to their facile processes, cost-effectiveness, and eco-friendly nature.

Methods: In the present study, copper oxide nanoparticles (CuO NPs) were synthesized using aqueous extract of  algae as a reducing, stabilizing, and capping agent. The synthesized CuO NPs were characterized by X-ray diffraction (XRD), UV-visible spectroscopy (UV-Vis), Fourier transform infrared spectroscopy (FTIR), dynamic light scattering (DLS), and field emission scanning electron microscopy (FE-SEM) coupled with energy-dispersive X-ray spectroscopy (EDS).

TMAO enhances TNF-α mediated fibrosis and release of inflammatory mediators from renal fibroblasts.

Trimethylamine-N-oxide (TMAO) is a gut microbiota-derived metabolite and TNF-α is proinflammatory cytokine, both known to be associated with renal inflammation, fibrosis and chronic kidney disease. However, today there are no data showing the combined effect of TMAO and TNF-α on renal fibrosis-and inflammation. The aim of this study was to investigate whether TMAO can enhance the inflammatory and fibrotic effects of TNF-α on renal fibroblasts.

RSAD2 is abundant in atherosclerotic plaques and promotes interferon-induced CXCR3-chemokines in human smooth muscle cells.

In atherosclerotic lesions, monocyte-derived macrophages are major source of interferon gamma (IFN-γ), a pleotropic cytokine known to regulate the expression of numerous genes, including the antiviral gene RSAD2. While RSAD2 was reported to be expressed in endothelial cells of human carotid lesions, its significance for the development of atherosclerosis remains utterly unknown. Here, we harnessed publicly available human carotid atherosclerotic data to explore RSAD2 in lesions and employed siRNA-mediated gene-knockdown to investigate its function in IFN-γ-stimulated human aortic smooth muscle cells (hAoSMCs).

Vascular smooth muscle cells in response to cholesterol crystals modulates inflammatory cytokines release and promotes neutrophil extracellular trap formation.

Background: The formation and accumulation of cholesterol crystals (CC) at the lesion site is a hallmark of atherosclerosis. Although studies have shown the importance of vascular smooth muscle cells (VSMCs) in the disease atherosclerosis, little is known about the molecular mechanism behind the uptake of CC in VSMCs and their role in modulating immune response.

Methods: Human aortic smooth muscle cells were cultured and treated with CC.

Effects of ageing and frailty on circulating monocyte and dendritic cell subsets.

Ageing is associated with dysregulated immune responses, resulting in impaired resilience against infections and low-grade inflammation known as inflammageing. Frailty is a measurable condition in older adults characterized by decreased health and physical impairment. Dendritic cells (DCs) and monocytes play a crucial role in initiating and steering immune responses.

Soluble LDL-receptor is induced by TNF-α and inhibits hepatocytic clearance of LDL-cholesterol.

Defective LDL-C clearance and hence its elevation in the circulation is an established risk factor for cardiovascular diseases (CVDs) such as myocardial infarction (MI). A soluble LDL-receptor (sLDL-R) has been detected in human plasma which correlates strongly with circulating LDL-C and classical conditions that promote chronic inflammation. However, the mechanistic interplay between sLDL-R, inflammation, and CVDs remains to be investigated.

algae-mediated copper oxide nanoparticles as a robust and recyclable catalyst for the degradation of noxious dyes from wastewater.

The present article explores the synthesis of copper oxide nanoparticles (CuO NPs) utilizing algal extract and examines the effect of various reaction parameters on the size and morphology of the nanoparticles. The samples were thoroughly characterized using XRD, FTIR, UV-vis, FE-SEM, and EDS techniques. The XRD analysis disclosed that the size of the synthesized nanoparticles could be controlled by adjusting the reaction parameters, ranging from 4.

Trimethylamine N-Oxide (TMAO) Mediates Increased Inflammation and Colonization of Bladder Epithelial Cells during a Uropathogenic Infection In Vitro.

Urinary tract infections (UTIs) are among the most common infections in humans and are often caused by uropathogenic (UPEC). Trimethylamine N-oxide (TMAO) is a proinflammatory metabolite that has been linked to vascular inflammation, atherosclerosis, and chronic kidney disease. As of today, no studies have investigated the effects of TMAO on infectious diseases like UTIs.

Interleukin-6 trans-signaling induced laminin switch contributes to reduced trans-endothelial migration of granulocytic cells.

Background And Aims: Laminins are essential components of the endothelial basement membrane, which predominantly contains LN421 and LN521 isoforms. Regulation of laminin expression under pathophysiological conditions is largely unknown. In this study, we aimed to investigate the role of IL-6 in regulating endothelial laminin profile and characterize the impact of altered laminin composition on the phenotype, inflammatory response, and function of endothelial cells (ECs).

TMAO Suppresses Megalin Expression and Albumin Uptake in Human Proximal Tubular Cells Via PI3K and ERK Signaling.

Trimethylamine-N-oxide (TMAO) is a uremic toxin, which has been associated with chronic kidney disease (CKD). Renal tubular epithelial cells play a central role in the pathophysiology of CKD. Megalin is an albumin-binding surface receptor on tubular epithelial cells, which is indispensable for urine protein reabsorption.

Role of Hemoglobin Content of Reticulocyte to Evaluate Anemia in Patients with Malignancy.

Anemia is common in patients with cancer and it's pathophysiology is complex and multifactorial . Conventional methods (Serum Iron, serum ferritin, TIBC, TSAT) to diagnosing iron deficiency anemia in cancer patients is affected by cancer type, duration, treatment, infection and inflammation related to cancer. RET-He measure the recent functional availability of iron and the correlation well with iron deficient / restricted erythropoiesis, and it is not affected by infection and inflammation related to cancer so it can be useful marker to rapidly rule out iron deficiency in cancer patients.

Inhibition of IL17A Using an Affibody Molecule Attenuates Inflammation in ApoE-Deficient Mice.

The balance between pro- and anti-inflammatory cytokines released by immune and non-immune cells plays a decisive role in the progression of atherosclerosis. Interleukin (IL)-17A has been shown to accelerate atherosclerosis. In this study, we investigated the effect on pro-inflammatory mediators and atherosclerosis development of an Affibody molecule that targets IL17A.

Human Renal Fibroblasts, but Not Renal Epithelial Cells, Induce IL-1β Release during a Uropathogenic Infection In Vitro.

Understanding how uropathogenic (UPEC) modulates the immune response in the kidney is essential to prevent UPEC from reaching the bloodstream and causing urosepsis. The purpose of this study was to elucidate if renal fibroblasts can release IL-1β during a UPEC infection and to investigate the mechanism behind the IL-1β release. We found that the UPEC strain CFT073 induced an increased IL-1β and LDH release from renal fibroblasts, but not from renal epithelial cells.

The Fibrotic Effects of TMAO on Human Renal Fibroblasts Is Mediated by NLRP3, Caspase-1 and the PERK/Akt/mTOR Pathway.

Trimethylamine N-oxide (TMAO), a product of gut microbiota metabolism, has previously been shown to be implicated in chronic kidney disease. A high TMAO-containing diet has been found to cause tubulointerstitial renal fibrosis in mice. However, today there are no data linking specific molecular pathways with the effect of TMAO on human renal fibrosis.

Faecal microbiota transfer in patients with microscopic colitis - a pilot study in collagenous colitis.

Objectives: Faecal microbiota transfer (FMT) consists of the infusion of donor faecal material into the intestine of patients with the aim to restore a disturbed gut microbiota.

Methods: In this pilot study (NCT03275467), the effect of three repeated FMTs (day 0, two weeks, four weeks) was studied and followed up for six months in nine collagenous colitis (CC) patients, using two stool donors.

Results: Five patients had an active disease at the time of baseline sampling.

Scleroedema of Buschke in conjunction with ovarian carcinoma: rare association of a rare disease.

Scleroedema is a rare clinical condition characterised by diffuse woody induration of skin commonly associated with diabetes mellitus, infections and monoclonal gammopathy. Its association with ovarian malignancy has not been reported. We report a case of a 56-year-old female with rapidly progressing skin thickening of limbs, face and trunk for 1 year and abdominal distension for 3 months.

Tuberculous meningitis: An unlikely cause of Guillain-Barre syndrome.

Guillain-Barre syndrome (GBS) is a life-threatening immune-mediated acute inflammatory polyneuropathy and is associated with various antecedent infections. Its association with tuberculosis is very uncommon with only a handful of cases being reported in the literature. It's association with tuberculous meningitis is even more scarce with only one case reported in literature till date.

Association of high-sensitivity C-reactive protein (hs-CRP) with non-alcoholic fatty liver disease (NAFLD) in Asian Indians: A cross-sectional study.

Background: Non-alcoholic fatty liver disease (NAFLD) is an important etiology for the development of chronic liver disease worldwide. Its pathophysiology includes chronic low-grade inflammation. There are limited studies on the association of inflammatory markers with NAFLD.

Hyperglycemia-induced posterior reversible encephalopathy syndrome: A rare cause of reversible blindness.

Posterior reversible encephalopathy syndrome (PRES) is an amalgam of clinical and radiological entities, which is reversible if diagnosed and treated promptly. It is characterized by varying neurological manifestation of seizure, headache, visual loss with typical magnetic resonance imaging findings of symmetric distribution of changes involving the parietooccipital lobes, which reflects vasogenic edema. The common causes include hypertension, renal failure, eclampsia, preeclampsia, sepsis, diabetic ketoacidosis, sepsis, cytotoxic drugs, and autoimmune disorders.

Activation of the JAK/STAT3 and PI3K/AKT pathways are crucial for IL-6 trans-signaling-mediated pro-inflammatory response in human vascular endothelial cells.

Background: IL-6 classic signaling is linked to anti-inflammatory functions while the trans-signaling is associated with pro-inflammatory responses. Classic signaling is induced via membrane-bound IL-6 receptor (IL-6R) whereas trans-signaling requires prior binding of IL-6 to the soluble IL-6R. In both cases, association with the signal transducing gp130 receptor is compulsory.

Expression and characterization of αvβ5 integrin on intestinal macrophages.

Macrophages play a crucial role in maintaining homeostasis in the intestine, but the underlying mechanisms have not yet been elucidated fully. Here, we show for the first time that mature intestinal macrophages in mouse intestine express high levels of αvβ5 integrin, which acts as a receptor for the uptake of apoptotic cells and can activate molecules involved in several aspects of tissue homeostasis such as angiogenesis and remodeling of the ECM. αvβ5 is not expressed by other immune cells in the intestine, is already present on intestinal macrophages soon after birth, and its expression is not dependent on the microbiota.

Fecal stream diversion and mucosal cytokine levels in collagenous colitis: A case report.

In this case report, we examined the levels of cytokines expressed before and during fecal stream diversion and after intestinal continuity was restored in a patient with collagenous colitis. We report the case of a 46-year-old woman with chronic, active collagenous colitis who either failed to achieve clinical remission or experienced adverse effects with the following drugs: loperamide, cholestyramine, budesonide, methotrexate and adalimumab. Due to the intractable nature of the disease and because the patient was having up to 15 watery bowel movements per day, she underwent a temporary ileostomy.

Enhanced levels of chemokines and their receptors in the colon of microscopic colitis patients indicate mixed immune cell recruitment.

Microscopic colitis (MC), comprising collagenous colitis (CC) and lymphocytic colitis (LC), is a common cause of chronic diarrhea. Various immune cell infiltrations in the epithelium and lamina propria are seen in MC immunopathology. We compared gene and protein expressions of different immune cell attracting chemokines and their receptors in colon biopsies from MC patients in active disease or histopathological remission (CC/LC-HR) with controls, using qRT-PCR and Luminex, respectively.