Inflammatory cell secretion

Acute-phase proteins are a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction (or acute-phase response). In response to injury, local inflammatory cells secrete a number of cytokines into the bloodstream, the most notable of which are the interleukins (IL-1, IL-6, IL-8) and TNF-a. The liver responds by producing a large number of acute-phase reactants or reducing the production of others. 

When exposure is repeated, the allergen binds between two adjacent IgE molecules. This causes release of inflammatory mediators (histamine, leukotrienes, chemotactic factors). These act locally and cause smooth muscle contraction, increased vascular permeability, mucous gland secretion, and infiltration of inflammatory cells (neutrophils and eosinophils). However, histamine can also be released by non-IgE-mediated mechanisms (e.g., due to exposure to certain fungi). 463... 

This is the enzyme that converts Leukotriene C4(LTC4) to Leukotriene D4 (LTD4) upon its secretion from inflammatory cells. 

Logan MR, Odemuyiwa SO, Moqbel R Understanding exocytosis in immune and inflammatory cells the molecular basis of mediator secretion. J Allergy Clin Immunol 2003 111 923-932. 

Dysfunction of the endothelium allows lipoproteins, predominantly low-density lipoprotein (LDL) cholesterol, and inflammatory cells, namely monocytes and T lymphocytes, to migrate from the plasma to the sub-endothelial space. Monocyte-derived macrophages ingest lipoproteins to form foam cells. Macrophages also secrete growth factors that promote smooth muscle cell migration from the media to the intima. A fatty streak consists of lipid-laden macrophages and smooth muscle cells and is the earliest type of atherosclerotic lesion. 

Corticosteroids are the most potent anti-inflammatory agents available for the treatment of asthma. The efficacy of corticosteroids is due to their ability to affect multiple inflammatory pathways, resulting in the suppression of inflammatory cell activation and function, prevention of microvascular leakage, decreased mucus production, and upregulation of P2-adrenergic receptors.10,18 Clinically, corticosteroids decrease airway inflammation, decrease AHR, decrease mucus production and secretion, and improve the response to P2-agonists.18 Corticosteroids for the treatment of asthma are available in inhaled, oral, and injectable dosage forms. 

Eosinophils may be increased in some patients, particularly during exacerbations. Activated inflammatory cells release a variety of mediators, most notably leukotriene B4, interleukin-8, and tumor necrosis factor-a (TNF-a). Various proteinases, such as elastase, cathepsin G, and proteinase-3, are secreted by activated neutrophils. These mediators and proteinases are capable of sustaining inflammation and damaging lung structures. 

In the central airways (the trachea, bronchi, and bronchioles greater than 2 to 4 mm in internal diameter), inflammatory cells and mediators stimulate mucus-secreting gland hyperplasia... 

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. 

The regulation of mast-cell activity by biologically active peptides is an area of research, the rapid growth of which has been sparked in part by this intense interest in the interactions between neural, endocrine and immune systems [4, 26, 41] and in part by the recognition that activation of mast-cell secretion as a purely allergic IgE-dependent event is undoubtedly too restrictive. The involvement of the mast cell in the inflammatory response, for example, has for years been suspected to involve a number of non-immunologic, IgE-inde-pendent factors [24,42], Direct evidence for peptide involvement, however, has... 

Articulated joints between bones, for example at the knee, are covered in a capsule enclosing a space, which contains synovial fluid. The lining of the capsule is composed by the synovial membrane it is this synovium that becomes inflamed in rheumatoid arthritis (RA). Secretions produced by inflammatory cells (lymphocytes, macrophages... 

Cellular pathophysiology of asthma. Top, Cross-section of the normal airway and the asthmatic ain/vay. Mediators released during the inflammatory process associated with asthma cause bronchoconstriction, mucus secretion, and mucosal inflammation and edema. These changes reduce the size of the airway lumen and increase resistance to airflow, which leads to wheezing and shortness of breath. Bottom, The multitude of inflammatory cells (macrophages, eosinophils, mast cells, neutrophils) and neurotransmitters implicated in asthma pathophysiology. 

The corticosteroids have an array of actions in several systems that may be relevant to their effectiveness in asthma. These include inhibition of cytokine and mediator release, attenuation of mucus secretion, up-regulation of (3-adrenoceptor numbers, inhibition of IgE synthesis, attenuation of eicosanoid generation, decreased microvascular permeability, and suppression of inflammatory cell influx and inflammatory processes. The effects of the steroids take several hours to days to develop, so they cannot be used for quick relief of acute episodes of bronchospasm. 

Apart from histamine, leukotiienes liberated during inflammation are more powerful bronchoconstrictor and longer acting. Leukotrienes also increase bronchial mucus secretion and increase vascular permeability. All the leukotrienes are derived from 5-lipoxygenase pathway of arachidonic acid and are synthesized by a variety of inflammatory cells in the airways e.g. eosinophils, mast cells, basophils and macrophages. The LTB, exert many... 

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