2009
DOI: 10.1038/icb.2009.86
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Inhibition of eosinophil migration by lactoferrin

Abstract: Eosinophilic granulocytes are innate effector cells that are important in immune responses against helminth parasitic infections and contribute towards the pathology associated with allergic inflammatory conditions, including allergic rhinitis and asthma. Their recruitment to inflammatory sites occurs in response to chemotactic and activation signals, such as eotaxin and interleukin-5, and is a tightly controlled process. However, the mechanisms that counterbalance these positive chemoattractive processes, the… Show more

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Cited by 79 publications
(66 citation statements)
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“…Mast cells contribute to the induction and/or maintenance of eosinophilic inflammation by a variety of mechanisms, including IgE-dependent and IgE-independent processes (Pawankar et al, 2007). The recruitment of these mast cells to inflammatory sites occurs in response to chemotactic and activation signals (Bournazou et al, 2010). The intercellular adhesion molecule (ICAM)-1, a member of the immunoglobulin gene superfamily of adhesion molecules, is expressed on the surface of a variety of cells, including vascular endothelial cells, epithelial cells, alveolar macrophages, and fibroblasts (Calderon and Lockey, 1992;Guzman et al, 1994;Montefort et al, 1994).…”
Section: Introductionmentioning
confidence: 99%
“…Mast cells contribute to the induction and/or maintenance of eosinophilic inflammation by a variety of mechanisms, including IgE-dependent and IgE-independent processes (Pawankar et al, 2007). The recruitment of these mast cells to inflammatory sites occurs in response to chemotactic and activation signals (Bournazou et al, 2010). The intercellular adhesion molecule (ICAM)-1, a member of the immunoglobulin gene superfamily of adhesion molecules, is expressed on the surface of a variety of cells, including vascular endothelial cells, epithelial cells, alveolar macrophages, and fibroblasts (Calderon and Lockey, 1992;Guzman et al, 1994;Montefort et al, 1994).…”
Section: Introductionmentioning
confidence: 99%
“…Mast cells contribute to the induction and/or maintenance of eosinophilic inflammation by a variety of mechanisms, including IgE-dependent and IgE-independent processes (Pawankar et al, 2007). The recruitment of these mast cells to inflammatory sites occurs in response to chemotactic and activation signals (Bournazou et al, 2010). Minimal persistent inflammation is a physiopathological phenomenon referring to the presence of an inflammatory cell infiltrate (eosinophils and neutrophils) associated with the expression of intercellular adhesion molecule-1 (ICAM-1) in the epithelial cells of the mucosa exposed to the allergen in the absence of clinical symptoms.…”
Section: Introductionmentioning
confidence: 99%
“…Indeed, it was already described that a great amount of various infl ammatory mediators could be released during the active period of an allergic infl ammation even from a small area of the body (like rhinoconjunctivitis) causing a generalized and long-lasting activation of neutrophils (KALLENBACH et al, 1992;SZABÓ et al, 2000). LF released by activated neutrophils may mediate numerous compensatory effects to inhibit allergic infl ammations, decreasing mast cell degranulation, tryptase activity, eosinophils' migration, and promoting the Th1-type immune responses (ELROD et al, 1997;HE et al 2003;DE LA ROSA et al, 2008;BOURNAZOU et al, 2010). Our other fi nding, that IL-17 was more frequently detectable and its levels were higher (although not signifi cantly) both in the serum and breast milk of allergic mothers, supports the previous observation that some patients with pollen-induced allergic rhinitis may have high serum IL-17 levels outside of the pollen season (CIPRANDI et al, 2008).…”
Section: Resultsmentioning
confidence: 99%