The ovalbumin (OVA)-alum mouse model, which induces a Th2-biased immune response, is commonly used to study allergic airway inflammation. However, the artificial nature of this model limits its relevance to environmental or infection-related airway diseases. The free-living environmental protozoan Acanthamoeba is a potential trigger of airway inflammation, but its immune mechanisms remain largely unknown. To compare these 2 models of airway inflammation, this study carried out microarray-based transcriptomic analysis of lung tissue obtained from mice with OVA-alum treatment or intranasal Acanthamoeba exposure. Compared to controls, OVA-alum treatment induced broad transcriptional changes involving >2,900 probes (fold change ≥1.5); Acanthamoeba exposure led to a substantially weaker response, with <500 probes affected at the same threshold. Unlike the OVA-alum–treated group, the Acanthamoeba-exposed mice showed minimal overlap with only 5 genes significantly downregulated, suggesting a distinct immune activation profile. Downregulation of genes related to the immunoglobulin variable region (Ighv1-58 and Igkv3-10) and eosinophil function (Rnase2a) in the Acanthamoeba group suggest suppression of a typical Th2/humoral response. Heatmap and clustering analysis demonstrated clear separation between the Acanthamoeba, OVA-alum, and control groups. Taken together, these results suggest that Acanthamoeba induces a unique airway immune response that is markedly different from traditional Th2-dominant inflammation, and may be a more suitable model for studying environmentally-induced or infection-related respiratory diseases.
Cockroaches can cause allergic sensitization in humans via contact with their feces or frass. Antibiotics can affect concentration of major allergen and total bacteria production in German cockroaches (Blattella germanica). This study examined the ability of antibiotic-treated German cockroaches to induce allergic airway inflammation and the effect of antibiotics on their lipopolysaccharide and Bla g1, 2, and 5 expression levels. Specifically, we measured the ability of German cockroach extract (with or without prior antibiotic exposure) to induce allergic inflammation in human bronchial epithelial cells and a mouse model of asthma. Bacterial 16S rRNA and lipopolysaccharide levels were lower in ampicillin-treated cockroaches than in the control group. The Bla g1, Bla g2, and Bla g5 expression in ampicillin-treated cockroaches decreased at both the protein and RNA levels. In human bronchial epithelial cell lines BEAS-2B exposed to the ampicillin-treated extract, expression levels of interleukin-6 and interleukin-8 were lower than that in the control group. The total cell count and eosinophil count in bronchoalveolar lavage fluid was also lower in mice exposed to the ampicillin-treated extract than in those exposed to normal cockroach extract. Mouse lung histopathology showed reduced immune cell infiltration and mucus production in the ampicillin group. Our results showed that ampicillin treatment reduced the symbiont bacterial population and major allergen levels in German cockroaches, leading to reduced airway inflammation in mice. These results can facilitate the preparation of protein extracts for immunotherapy or diagnostics applications.
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