Relevance of Inflammatory Cytokine mRNA Expression of Tumour Necrosis Factor- Alpha (TNF α), Interleukin 17A (IL 17A) and Interleukin 6 (IL 6) in Indian Patients with Psoriasis.

Background: Psoriasis, a chronic, immune-mediated skin disorder, has systemic manifestations as well as an ample negative impact on the quality of life (QOL) of the patient. An abnormal proliferation of keratinocyte and dermal infiltration by immune cells is a characteristic feature. It involves components of both innate and adaptive immunity, and the interaction of T cells with macrophages. Keratinocytes and dendritic cells are mediated by the secreted cytokines. This study was taken up to look into changes at the molecular level that occur during the expression of three cytokines namely tumour necrosis factor-alpha (TNFα), interleukin 17A (IL-17A) and interleukin 6 (IL-6) in Indian patients with psoriasis. Methods: A case-control study was conducted with samples from 15 psoriasis vulgaris patients and 10 healthy control subjects. Clinical parameters were recorded. Blood samples were analysed for peripheral blood messenger ribonucleic acid (mRNA) expression of TNFα, IL-17A and IL-6 using real-time polymerase chain reaction (RT-PCR). Results: The mRNA expression of TNFα, IL-17A and IL-6 in psoriasis patients were increased as compared to that in normal subjects. Conclusions: The elevated levels of Interleukins indicates a systemic inflammatory process that is akin to the cutaneous inflammation. This study indicates that the targeted therapies against these cytokines are likely to be beneficial in Indian psoriasis patients.

Inflammatory mediators in various molecular pathways involved in the development of pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a type of interstitial lung disease (ILD) that is marked by scarring of lung tissue, ultimately leading to respiratory failure. The survival rate of IPF is disappointing and to date demonstrates a clinical quandary. The exact etiology of the disease remains under discussion. According to the recent hypothesis, inflammatory mediators cause severe damage to the alveolar epithelium leading to the impairment of the alveolar structure. The role of inflammation in the development of the IPF has been controversial for years. There are two schools of thought regarding the role of inflammation. One group of researchers claims that cell death and fibroblast dysfunction are the primary causes and inflammation is just a secondary cause of IPF. The other group claims inflammation to be the primary cause. Studies using human subjects have also reported inflammation as a critical element in IPF. Inflammatory cytokinesserve amajor rolein commencing theinflammatoryresponse in the lungs. Several cytokines are reported to be involved in different molecular mechanisms underlying IPF, someof which alsocontribute additionally by acting as growth factors. The present review addressed to explore the contribution of various inflammatory cytokines, growth factors, and various other inflammatory molecules activating the major molecular pathways involved during the development of IPF.

Radiation induced apoptosis and pulmonary fibrosis: curcumin an effective intervention?

Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by interstitial remodeling, leading to compromised lung function. Extra vascular fibrin deposition and abnormalities in the fibrinolysis are the major clinical manifestations of lung diseases such as acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS). ALI progresses to pulmonary fibrosis (PF) and makes patient's life miserable. Anti-fibrinolysis and apoptosis are involved in the progression of PF. Apoptotic markers are detectable within IPF lung tissue and senescent cell deletion can rejuvenate pulmonary health. Enhanced expression of p53 due to DNA damage is seen in irradiated lung tissue. The role of fibrinolytic components such as Urokinase Plasminogen activator (uPA), uPA receptor (uPAR) and Plasminogen activator inhibitor-1 (PAI-1) has been detailed in I. Curcumin is known to possess anti-inflammatory and anti-fibrotic effects. Radioprotective effect of curcumin enables it to attenuate radiation-induced inflammation and fibrosis. Understanding the mechanism of radioprotective effect of curcumin in radiation-induced PF and apoptosis can lead to the development of an effective therapeutic to combat acute lung injury and fibrosis.

Inflammatory and Fibrinolytic System in Acute Respiratory Distress Syndrome.

Acute respiratory distress syndrome (ARDS) is the most advanced form of acute lung injury (ALI). This is characterized by bilateral pulmonary infiltrates and severe hypoxemia. According to Berlin definition of ARDS, this is defined based on the timings, radiographic changes, edema formation, and severity on the PaO2/FiO2 ratio. During ARDS, the loss of integrity of the epithelium causes the septic shock. The degree of epithelial injury is the major prognostic marker of ARDS. In addition to this, inflammatory cell migration, fibro-proliferation, and activation of apoptosis also play an important role in the pathophysiology of ARDS. The alveolar epithelial cell is the prime target during injury where this cell either undergo apoptosis or epithelial-mesenchymal transition (EMT). Injury to the AECs triggers the changes in the DNA fragmentation and activation of certain apoptotic markers such as caspases at the same time some cells undergo biochemical changes and loses its epithelial morphology as well epithelial biomarkers and gain mesenchymal biomarkers and morphology. In both the cases, the fibrinolytic system plays an important role in maintaining the integrity of the disease process efficiently. This review highlights the research evidence of apoptosis and EMT in lung development, injury and its prognosis in ARDS thereby to develop an effective strategy for the treatment of ARDS.