Journal
INFLAMMATION
Volume 40, Issue 4, Pages 1382-1392Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10753-017-0581-x
Keywords
Allergic airway inflammation; Autophagy; Phosphoinositide 3-kinases; Toll-like receptor 2
Categories
Funding
- Natural Science Foundation of China [81170030, 81270082, 81300027]
- National Education Ministry of China [20113420110006]
- Annual Research Project of Anhui Province [10021303028]
- Key Lab of Geriatric Molecular Medicine of Anhui Province [1206c0805028]
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Toll-like receptors (TLRs) are innate pattern recognition receptors that play a critical role in allergic inflammation, yet their contribution to autophagy in asthma remains poorly defined. Here, we investigate the role of Toll-like receptor 2 (TLR2) in phosphoinositide 3-kinases/protein kinase B (PI3K/Akt) pathway-mediated autophagy in ovalbumin-induced airway inflammation in mice. Wild-type (WT) and TLR2-knockout (TLR2(-/-)) C57BL/6 mice were ovalbumin-sensitized and ovalbumin-challenged. In ovalbumin-challenged WT mice, enhanced expression of TLR2 in lung tissue, remarkable inflammatory cell infiltrates, goblet cell hyperplasia, and increased mucus production were observed. The number of inflammatory cells and interleukin-13 (IL-13) levels increased, while interferon-gamma (IFN-gamma) levels decreased in bronchoalveolar lavage fluid. Expression of PI3K, phospho-Akt, Beclin-1 and LC3-II was enhanced significantly. These changes were mitigated dose-dependently in 3-methyl adenine-treated mice. In contrast, similar but weaker changes were found in ovalbumin-challenged TLR2(-/-) mice, and the changes were not significantly attenuated by 3-methyl adenine treatment. These results indicate that TLR2 confers a pivotal role in allergic airway inflammation via regulating the PI3K/Akt signaling pathway-related autophagy in mice.
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