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Airborne lipopolysaccharide activates airway epithelial cells through mitogen-activated protein kinase activation, cyclooxygenase-2 expression, and prostaglandin synthesis.
Toll-like receptor (TLR)-4 is a transmembrane-signaling receptor that recognizes lipopolysaccharide (LPS), the lipoprotein of gram-negative bacteria, and induces production of proinflammatory mediators such as tumor necrosis factor, interleukin-6, and prostaglandins. In a murine airway epithelial cell line, BEAS-2B, we investigated the response of BEAS-2B cells and a human airway epithelial cell line, A549, to airborne LPS in terms of activation of cell cycle progression, cyclooxygenase (COX)-2 expression, and prostaglandin synthesis. BEAS-2B cells differentiated into mucin-producing cells after LPS stimulation. LPS increased cell proliferation, which was mediated by CDK4 up-regulation. LPS stimulated the release of prostaglandin E(2) and prostaglandin F(2alpha), which was inhibited by pretreatment with the COX-2-specific inhibitor 5-({[4-((5-methyl-1,3-thiazol-4-yl)carbamoyl)phenyl]methylene}amino)imidazole-2-carbonitrile. On the other hand, A549 cells were resistant to LPS stimulation, but they responded to airborne LPS by a substantial increase of thymidine uptake, suggesting that airborne LPS may be an inducer of airway epithelial cell proliferation. Airborne LPS may act as a potent mitogen for airway epithelial cells, and, moreover, airborne LPS may play an important role in airway remodeling associated with chronic pulmonary diseases. has been also shown in other animal models such as rat, mouse, rabbit and pig ([@B13]; [@B22]). The increased gut permeability is usually the key factor associated with the augmentation of the intestinal antigen permeation leading to the development of the food allergy. In this study, 8 weeks of dietary TOS supplementation
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