Allergic disease airway inflammation

De Haar, C., et al., Ultrafine carbon black particles cause early airway inflammation and have adjuvant activity in a mouse allergic airway disease model, Toxicol. Sci. 87, 2, 409, 2005. 

Th2 cytokine IL-10 is an antiinflammatory cytokine that suppresses the secretion of proinflammatory cytokines (Dll), allergen-induced airway inflammation, and nonspecific airway responsiveness (T9). IL-13 shares a receptor component, signaling pathways, and many biological activities with IL-4. In fact, IL-13 is also an antiinflammatory cytokine and plays a unique role in the optimal induction and maintenance of IgE production and IgE-mediated allergic responses when IL-4 production is low or absent (DIO, W12). Moreover, IL-13 or IL-4 shows a synergistic effect with TNF-a or IL-5 on eosinophil activation (L20). Recently, IL-11 was found to be involved in the chronic remodeling seen in asthmatic airways and is associated with increasing severity of the disease (Ml6). 

As noted in the discussion above, respiratory viral infections are now acknowledged as potent co-stimulants of airway inflammation in atopic children, and may be an important co-factor in driving allergic respiratory disease towards persistence. The use of recently available anti-virals in children may provide a useful prophylactic approach for reduction of the impact of these infections in asthma pathogenesis. 

METZGER, W.J., ZAVALA, D RICHERSON, H.B., MOSELEY, P IWAMOTO, P MONICK, M SJOERDSMA, K. HUNNINGHAKE, G.W. (1987) Local allergen challenge and bronchoalveolar lavage of allergic asthmatic lungs description of the model and local airway inflammation. American Review of Respiratory Disease, 135,433 440. 

Colitis [71,72] periodontitis [73] asthma [74] dry eye disease [76] inflammatory pain [77] ischemia-reperfiision injury [75] allergic airway inflammation [78]. 

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