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Fig. 2 | Allergy, Asthma & Clinical Immunology

Fig. 2

From: Co-exposure to lipopolysaccharide and desert dust causes exacerbation of ovalbumin-induced allergic lung inflammation in mice via TLR4/MyD88-dependent and -independent pathways

Fig. 2

Effects of testing samples on pathological changes in the lungs. a–l PAS stain; Bar = 80 μm. a WT ovalbumin (OVA); b TLR2−/− OVA; c TLR4−/− OVA; d MyD88−/− OVA: no pathological changes in lungs treated with OVA. e WT OVA + lipopolysaccharide (LPS); f TLR2−/− OVA + LPS: very slight proliferation of goblet cells (thin arrow) that have mucus stained pink with PAS in the airway epithelium, and peribronchiolar inflammation due to slight infiltration of inflammatory cells into the submucosa of airways. g TLR4−/− OVA + LPS; h MyD88−/− OVA + LPS: no pathological changes in lungs treated with OVA + LPS. i WT OVA + heated-Asian sand dust (H-ASD) + LPS: moderate proliferation of goblet cells (thin arrow) in the airway epithelium, and moderate to marked infiltration of inflammatory cells (arrow) into the submucosa of airways. j TLR2−/− OVA + H-ASD + LPS: slight to moderate proliferation of goblet cells (thin arrow) in the airway epithelium, and slight infiltration of inflammatory cells (arrow) into the submucosa of airways. k TLR4−/− OVA + H-ASD + LPS: very slight proliferation of goblet cells (thin arrow) in the airway epithelium, and very slight peribronchiolar inflammation (arrow). l MyD88−/− OVA + H-ASD + LPS: no significant pathological changes in airway epithelium or airway submucosa

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