Inflammatory cells cytokines

Ben-Baruch, A. (2003). Host microenvironment in breast cancer development Inflammatory cells, cytokines and chemokines in breast cancer progression Reciprocal tumor-microenvironment interactions. Breast Cancer Res. 5, 31-36. 

Rom WN. 1991. Relationship of inflammatory cell cytokines to disease severity in individuals with occupational inorganic dust exposure. Am J Ind Med 19 15-27... 

Inflammation is considered the key feature of the immune system response to injury. The main symptoms of inflammations are redness, swelling, pain, and heat. The body s immime system commonly controls the inflammation itself When the inflammations become imcon-trollable, the body becomes diseased, leading to chronic discomfort [109]. This chronic inflammation is the major component of various chronic diseases, including inflammatory bowel disease, rheiunatoid arthritis, osteoporosis, and allergies [110,111]. Along with activation and proliferation of inflammatory cells, cytokines and chemokines are produced in excessive quantities in chronic inflammatory diseases. The primary targets of the anti-inflammatory compounds are the inhibition of inflammatory cell recruitment and proinflammatory mediator production [112]. 

In addition to antioxidant activity, there are specific a-tocopherol-dependent functions that normalize cellular functions in a variety of cells. a-Tocopherol plays a critical role through its ability to inhibit the activity of protein kinase C, a central player in many signal transduction pathways. Specifically, it modulates pathways of platelet aggregation, endothelial cell nitric oxide production, monocyte/macrophage superoxide production, and smooth muscle cell proliferation. Regulation of adhesion molecule expression and inflammatory cell cytokine production by a-tocopherol has also been reported. However, most of the information in this area has been obtained from in vitro studies. More studies in hiunans are needed to relate a-tocopherol intakes and tissue concentrations to optimal tissue responses. 

There are two isoforms of COX in animals COX-1 (figure a), which carries out normal, physiological production of prostaglandins, and COX-2 (figure b), which is induced by cytokines, mitogens, and endotoxins in inflammatory cells and is responsible for the production of prostaglandins in inflammation. 

In summary, recent years have seen the emergence of encouraging data for antibodies in clinical development that are directed against proinflammatory cytokines, inflammatory cells or co-stimulatory molecules. In particular, anti-TNFa therapies have set a new standard for symptom control and prevention of joint destruction in RA. 

In the late phase response, activated airway cells release inflammatory cytokines and chemokines, recruiting inflammatory cells into the lungs. The late phase response occurs 4 to 6 hours after the initial allergen challenge and results in a less intense bronchoconstriction as well as increased airway hyperresponsiveness and airway inflammation.6... 

Although infection with C. parvum is considered predominantly secretory, histopathologic studies have revealed varying degrees of villous atrophy and infiltration of inflammatory cells beneath the epithelial mucosa [85, 86], Prostaglandins, which are known to induce cAMP-mediated apical chloride secretion and inhibit electroneutral sodium chloride and water absorption in enterocytes, have been demonstrated to be elevated in a porcine model of cryptosporidiosis [87], Inflammatory cytokines such as IL-1, IL-8 and TNF-a are induced in intestinal epithelial cell lines infected with Cryptosporidium and in animal models of cryptosporidiosis and have been postulated to play a role in pathogenesis [88, 89], Expression of TNF-a and IL-1 mRNA in the majority of jejunal biopsies of adult volunteers after experimental infection were also observed, although this did not correlate with the enteric symptoms [90]. 

The development of respiratory hypersensitivity requires an induction phase where exposures to the sensitizer lead to an interaction with immune cells and the eventual development of specific effecter immune molecules (e.g., antibodies) and cells (e.g., T lymphocytes) [5], The induction phase can require months to years of exposure before there is a detectable immune response and/or onset of symptoms typical of respiratory hypersensitivity, including asthma. Classic IgE mediated responses have been described as Th2 cell dominant responses. A subset of CD4+ T cells known as Th2 cells push the immune response to the development of IgE and IgG4 antibodies in humans along with secretion of cytokines that attract and activate inflammatory cells such as eosinophils. 

CC Chemokine Receptor 2 (CCR2) is a member of the G protein-coupled receptor (GPCR) superfamily that serves as the receptor for monocyte chemoattractant proteins 1-4 (MCP-1 to -4), a group of pro-inflammatory chemotactic cytokines (chemokines). CCR2 is the primary chemokine receptor on inflammatory monocytes, and is also expressed on T-cells, dendritic cells, and endothelial cells. Upon ligand engagement, CCR2 mediates both cellular movement and activation. 

Once inflammatory cells have infiltrated into the tissue, they respond to chemotactic gradients established by cytokines and chemokines, which origin from sites of injury or infection. These... 

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