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Based on these preliminary results, our published work (57, 7275, 7783) and a recent clinical study correlating TLR2, TLR4, and COX-2 overexpression in carotid artery plaques with the severity of disease (71), we postulate that constituents of CS, acting in concert with bacterial toxins and mast cell products, may amplify inflammatory response by engaging the H1R-TLR2/TLR4-COX2 axis (Figure 2)

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Tissue plasminogen activator has been identified as a negative biomarker for T2 immune responses in nasal polyps, and inactivation of tissue plasminogen activator leads to excessive fibrin deposition [110]

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