Role in Allergic Diseases

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There is increasing evidence that IL-10 secretion may be defective in patients with asthma.1,47 Lower concentrations of IL-10 are found in bronchoalveolar lavage fluid of asthmatic patients than in normal control subjects48 and there is a reduction in the number of macrophages expressing IL-10 in induced sputum.49 There is a reduced secretion of IL-10 from alveolar macrophages obtained by bronchoalveolar lavage from asthmatic patients compared to normal controls, and this is at the level of gene expression.8 This reduced expression of IL-10 is correlated with an increased production of proinflammatory cytokines, such as TNF-a and GM-CSF, and the chemokine MIP-1a from these cells. This suggests that a defect in IL-10 synthesis may be result in exaggerated and more prolonged inflammatory responses in asthmatic airways (Fig. 3). Furthermore, since IL-10 appears to act as a feedback inhibitor of antigen presentation by mononuclear cells, this may also account for the observation that macrophages from asthmatic patients are less effective at inhibiting T cell proliferative responses.50 The production of IL-10 from peripheral blood monocytes is reduced in allergic compared to normal subjects after influenza A infection, suggesting an impaired ability to mount an anti-inflammatory response in allergy.51 Similarly, IL-10 production from peripheral blood mononuclear cells is reduced in children who develop atopy.52 IL-10 levels are reported to be normal in patients with mild

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Figure 3. Macrophages rapidly release many inflammatory proteins in response to activating stimuli, such as lipopolysaccharide (LPS), many of which are regulated by nuclear factor-KB (NF-kB). The same activating stimuli increase release of IL-10, but this occurs later and results in inhibition of these inflammatory proteins through inhibition of NF-kB. In allergic disease there is defective production of IL-10, so that the inflammatory response is less suppressed leading to amplification of and prolongation of inflammation.

Figure 3. Macrophages rapidly release many inflammatory proteins in response to activating stimuli, such as lipopolysaccharide (LPS), many of which are regulated by nuclear factor-KB (NF-kB). The same activating stimuli increase release of IL-10, but this occurs later and results in inhibition of these inflammatory proteins through inhibition of NF-kB. In allergic disease there is defective production of IL-10, so that the inflammatory response is less suppressed leading to amplification of and prolongation of inflammation.

asthma, however53 and IL-10 release from peripheral blood monocytes is increased during the late response to allergen54 and in bronchoalveolar lavage after allergen challenge.53 Nasal allergen challenge in patients with seasonal allergic rhinitis reduces the concentrations of IL-10 in nasal lavage, however, in line with most of the studies in asthma.55 In atopic dermatitis an increase in IL-10 expression in the epidermis has been described.56

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Coping with Asthma

Coping with Asthma

If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.

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