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Figure 7: Representative photomicrographs showing guinea pig airway wall samples obtained from controls ((a), (e), (i), (m), (q), and (u)), OVA-exposed ((b), (f), (j), (n), (r), and (v)), OVA-exposed MK treated ((c), (g), (k), (o), (s), and (w)), and OVA-exposed D treated ((d), (h), (l), (p), (t), and (x)) stained with LUNA ((a) to (d)—×1000) and immunohistochemistry for eotaxin detection ((e) to (h)—×1000), RANTES detection ((i) to (l)—×1000), IGF-I detection ((m) to (p)—×1000), fibronectin detection ((q) to (t)—×1000), and NF-κB detection ((u) to (x)). Control groups show a scarce number of eosinophils, eotaxinpositive cells, RANTES positive cells, IGF-I positive cells, fibronectin positive cells, and NF-κB positive cells. In contrast, the airway wall of OVA-exposed animals shows intense eosinophilic infiltration (b), a large number of eotaxin positive cells (f), RANTES positive inflammatory cells (j), IGF-I positive inflammatory cells (n), fibronectin positive inflammatory cells (r), and NF-κB positive inflammatory cells. Both treatments (MK and D) in ovalbumin-exposed animals reduced all these parameters.