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small proportion of cells recovered by BAL @unnill 1960; Foresi, Bertorelli et al. 1990;
Koshino, Teshima et al. 1993; Macfarlane, Kon et al. 2000). Provocation studies have shown
the early asthma response is associated with increased histamine, tryptase, prostaglandinD2,
prostaglandin F2, thromboxane and leukotrienes which are released by these two cell types
(Murray, Tonnel et al. 1986; Wenzel, Fowler et al. 1988; Liu, Hubbard et al. l99l; Chilton,
Averill et al. 1996; Kavuru, Dweik et al. 1999). Adhesion molecules such as intracellular
adhesion molecule I (ICAM l) and lymphocyte function-associated antigen I (IJA 1) were
also increased (Williams, Johnson et al. 1992). The cytokines associated with an allergic
profile - IL3, IIA,ILI and GM-CSF -
and their receptors in cell surfaces were measured in
high amounts (Virchow, Walker et al. 1995; Chung and Barnes 1999; Hamid, Tulic et al.
2003). Increases have also been seen in IL9 and ILl3 which have been associated with mucus
hypersecretion and IgE regulation (Louahed, Toda et al. 2000; Shimbara, Christodoulopoulos
et al. 2000; louahed, Zhou et al. 2001) as well as increased interleukin 11 (Lll) and
interleukin 17 (lLl7) that have pro-fibrotic activity @inarsson, Geba et al. 1995; Minshall,
Chakir et al. 2000; Molet, Hamid et al. 2001). On the other hand, decreased interleukin 10
(L10), an anti-inflammatory cytokine, was seen during acute asthma and this returned to
levels similar to controls with recovery (Borish, Aarons et al. 1996). Chemokines have been
demonstrated as present and rising with airway challenges including eotaxin, monocyte
chemoattractant protein and rantes as well as TGFp which has been noted to have a role in the
subepithelial fibrosis (Hamid, Tulic et al. 2003). With specific challenges, such as using
ragweed antigen, specific IgE and IgA have also been shown to be increased in
bronchoalveolar lavage fluid @eebles, Hamilton et al. 2001). Similar to the findings from the
biopsy studies, with treatment of either IHCS or oral corticosteroids, while there was a
reduction of eosinophil, mast and epithelial cell numbers in lavage fluid, the eosinophilic
proteins did not reduce and there was not a direct correlation between the inflammatory cell
decrease and improvement in symptoms or bronchial hyper-responsiveness @uddridge, Ward
et al. L993; Booth, Richmond et al. 1995; Djukanovic, Homeyard et al.1997; Olivieri, Chetta
et al. t997).
The paediatric literature in this area has been more recent but has largely been in agreement
with the findings in adults. The increase in eosinophilic inflammation and eosinophil proteins
were seen (Barbato, Panizzolo et al. 2001; Just, Fournier et al.2002; Najafi, Demanet et al.
2003), as well as increased neutrophils which were associated with persistent symptoms (Just,
Fournier et al. 2OO2), 'difficult to treat' asthma (de Blic, Tillie-Irblond et al. 2004; Payne,
Qiu et al. 2OO4) and status asthmaticus (Lamblin, Gosset et al. 1998; Tonnel, Gosset et al.
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