Abstract
Abstract According to the hygiene hypothesis, sensing bacteria in the gut is imperative to switching the immune system from Th2 to Th1, thus reducing potential for an asthma-like phenotype developing in the lungs. In the gut toll-like receptors 2 and 4 (TLR2, TLR4) are critical for sensing Gram positive and negative bacteria, respectively. Previous data indicate in the first two weeks of life when the immune system switch generally occurs and a microbial repertoire is established, these two receptors are significantly upregulated. This project's hypothesis is TLR2 and 4 are critical for microbial sensing in the gut, thus C57BL/6 mice deficient in TLR2, TLR4, or both (double knockout) should have a more asthmatic phenotype. Interestingly, after inducing asthma with cockroach antigen (CRA) in a specific pathogen-free environment, the TLR2-/-/4-/- treated with CRA had a significant increase in serum IgE compared to the C57BL/6 treated with CRA, while the TLR4-/- had increased IL-13 mRNA levels compared to the C57BL/6 treated with CRA. This indicates the lack of interplay of TLR2 and 4 may play a role in maintaining a Th2 phenotype in the lungs; consequently preventing the immune switch to a Th1 phenotype. Research supported by the Strategic Program for Asthma Research
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