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Mucosal inflammation

Proteinaceous phytochemicals can contain toxic epitopes that elicit defense responses for example gliaden and glutein peptides which cause celiac disease and other mucosal disorders (Tighe and Ciclitira, 1995 Van de Wal et al, 1999). The mucosal inflammation caused by feeding carnivorous Atlantic salmon diets with soybean meal decreases rates of nutrient absorption (Nordrum et al, 2000), whereas the detrimental influence of such diets is much less pronounced when fed to omnivorous fish, such as catfish and tilapia. [Pg.171]

Multiple factors play a role in the development of AOM. Viral infection of the nasopharynx impairs eustachian tube function and causes mucosal inflammation, impairing mucociliary clearance and promoting bacterial proliferation and infection. Children are predisposed to AOM because their eustachian tubes are shorter, more flaccid, and more horizontal than adults, which make them less functional for drainage and protection of the middle ear from bacterial entry. Clinical signs and symptoms of AOM are the result of host immune response and damage to cells caused by inflammatory mediators such as tumor necrosis factor and interleukins that are released from bacteria.4... [Pg.1062]

Mucositis Inflammation of mucous membranes, typically within the oral and esophageal mucosa. Mucositis is usually associated with certain chemotherapy agents and radiation therapy involving mucosal areas. [Pg.1571]

Saetta M, Di Stefano A, Maestrelli P, et al Arway mucosal inflammation in occupational asthma induced by toluene diisocyanate. Am Rev Respir Dis 145 160-168, 1992... [Pg.685]

Arentz-Hansen et al. (2004) ( continuation of Lundin et al, 2003) 9 CD subjects who had history of oats exposure ( 5/9 from same study population) Derivation of polyclonal T cell lines In vitro duodenal mucosal cultures were challenged with either pepsin or Avenin-reactive T cell lines recognized avenin peptides in the context of HLA-DQ2 A substantial proportion of the avenin-reactive T cell appears to be specific to avenin Some CD patients have avenin-reactive mucosal T cells that can cause mucosal inflammation... [Pg.246]

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. [Pg.459]

Asthma is a chronic inflammatory condition characterized by bronchial hyper-responsiveness and reversible airway obstruction. Cytokine release from a variety of cell types such as eosinophils, lymphocytes and other inflammatory cells produces epithelial sloughing, plasma protein extravasation from the tracheobronchial microcirculation and airway remodeling. Bronchial mucosal inflammation is present in all patients. The primary goal of asthma management is to maintain control of the disease process by reducing symptoms and improving lung function. [Pg.201]

Cover TL, Blaser MJ (1996) Helicobacter pylori infection, a paradigm for chronic mucosal inflammation pathogenesis and implications for eradication and prevention. Adv Intern Med 41 85-117... [Pg.173]

Durham, S.R. 1998. Mechanisms of mucosal inflammation in the nose and lungs. Clin Exp... [Pg.81]

Hackett et al. (1987) and by ORNL), 46%, and 69%, respectively, were reported. In addition, gastric lesions (mucosal inflammation, edema, necrosis, and mucosal sloughing) were found at all doses, and teratogenic effects (fetal stunting and supernumerary ribs) were observed at the highest dose. On the basis of gastric lesions and mortality, the lowest-observed-adverse-effect level (LOAEL) for this study was 0.07 mg/kg per day. [Pg.103]

In chronic studies, male and female rats and mice tolerated up to 2.5 ppm chlorine gas for 6 h/day, 5 days/week for 2 years (CUT, 1993 Wolf et al, 1995). Concentration-dependent lesions confined to the nasal passages were observed in all animals. These lesions were most severe in the anterior nasal cavity and included respiratory and olfactory epithelial degeneration, septal fenestration, mucosal inflammation, respiratory epithelial hyperplasia, squamous metaplasia and goblet cell hypertrophy and hyperplasia, and secretory metaplasia of the transitional epithelium of the lateral meatus. Body weight was depressed compared to controls but no early deaths occurred. A similar lack of lower respiratory tract effects was seen in monkeys exposed to 2.3 ppm chlorine for 6 h/day, 5 days/week, for 1 year (Klonne et al, 1987). At these concentrations, chlorine is effectively scrubbed in the anterior nasal passages as indicated by the absence of lesions in the lung. [Pg.317]

Dr. Douglas J. Weiss is a Professor at the College of Veterinary Medicine at the UrMversity of Minnesota. Over the years, he has been extensively involved in both teaching and research at the College. He has received a number of awards for his teaching. His research interests include platelet activation mechanisms in thrombotic diseases, mechanisms of acute lung injury and mucosal inflammation. He has published extensively on his research. [Pg.379]

Oral administration of gentamicin in low dosages to reduce the intestinal flora is rarely practiced, although it is probably as effective as neomycin. In the presence of intestinal mucosal inflammation more than 10% of the dose can be absorbed. [Pg.1503]

The use of indometacin suppositories can be associated with rectal irritation, mucosal inflammation, or necrosis with bleeding (29). The local effect on the gastric mucosa is less important than the systemic one, and suppositories do not cause fewer gastric lesions than oral formulations (30). [Pg.1741]

Allergic Mucosal Inflammation 64 7.1.4 Do Mast Cells Initiate ... [Pg.53]

C.H., Holgate, S.T. and Howarth, P.H. (1993). Immunolocalization of cytokines in the nasal mucosa of normal and perennial rhinitic subjects the mast cell as a source of IL-4, IL-5 and IL-6 in human allergic mucosal inflammation. J. Immunol. 151, 3853-3865. [Pg.74]

Laitinen, L.A., Laitinen, A. and Haahtela, T. (1993b). Airway mucosal inflammation even in patients with newly diagnosed asthma. Am. Rev. Respir. Dis. 147, 697-704. [Pg.96]


See other pages where Mucosal inflammation is mentioned: [Pg.598]    [Pg.81]    [Pg.36]    [Pg.1068]    [Pg.361]    [Pg.396]    [Pg.141]    [Pg.273]    [Pg.270]    [Pg.276]    [Pg.459]    [Pg.425]    [Pg.446]    [Pg.464]    [Pg.478]    [Pg.60]    [Pg.61]    [Pg.206]    [Pg.302]    [Pg.339]    [Pg.60]    [Pg.63]    [Pg.64]    [Pg.67]    [Pg.94]    [Pg.116]    [Pg.162]    [Pg.191]   


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Mucosal

Mucositis

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