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Fig. 5 | Allergy, Asthma & Clinical Immunology

Fig. 5

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. 5

Effects of testing samples on IgE and IgG1 production in serum. According to the manufacturer’s protocol, 1 U of the anti-OVA IgG1 is defined as 160 ng of the antibody. Wild type (WT), toll like receptor (TLR)2−/−, TLR4−/−, myeloid differentiation primary response gene 88 (MyD88)−/−, four kinds of mouse were divided into six groups which were treated intratracheally with saline (control), LPS (50 ng LPS); heated-Asian sand dust (H-ASD) (0.1 mg H-ASD); ovalbumin (OVA), OVA + lipopolysaccharide (LPS), OVA + H-ASD + LPS. Four times at 2-week intervals. All values were expressed as mean ± SEM. *P < 0.05 vs. control; †P < 0.05 vs. LPS; §P < 0.05 vs. H-ASD; &P < 0.05 vs. OVA; #P < 0.05 vs. OVA + LPS; αP < 0.05 vs. WT within the same group; βP < 0.05 vs. TLR2−/− within the same group; γP < 0.05 vs. TLR4−/− within the same group

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