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""Asthma is a widespread chronic health problem exacerbated by common viral and bacterial infections. Further research is required to understand how infection worsens asthma Otenabant control in order to advance therapeutic options in the future. Recent research has revealed that ��2-adrenergic receptor (��2-AR) agonists lose bronchodilatory efficacy because the receptor-mediated molecular pathways responsible for their beneficial actions are desensitized by infection. To date, most studies have focussed on viral infection, leaving the impact of bacterial infection on ��2-AR desensitization relatively under-investigated. We address this in this study. Utilizing an in vitro model of bacterial exacerbation in airway smooth muscle (ASM) cells, we show that activation of toll-like receptor 2 (TLR2; mimicking bacterial infection) in the presence of an inflammatory stimulus leads to ��2-AR desensitization. This occurs via TLR2-dependent upregulation of cyclooxygenase 2 (COX-2) mRNA expression and increased secretion of PGE2. Importantly, PGE2 causes heterologous Selleck Ribociclib ��2-AR desensitization and reduces cAMP production in response to short-acting (salbutamol) and long-acting (formoterol) ��2-agonists. Thus, bacterial infectious stimuli act in a PGE2-dependent manner to severely curtail the beneficial actions of ��2-agonists. The impact of ��2-AR desensitization is demonstrated by reduced gene expression of the critical anti-inflammatory molecule MKP-1 in response to ��2-agonists, as well as impaired bronchodilation in a mouse lung slices. Taken together, our results show that, like viruses, bacteria induce prostanoid-dependent ��2-AR desensitization on ASM cells. Notably, COX-2 inhibition with the specific inhibitor celecoxib represses PGE2 secretion, presenting a feasible pharmacological option for treatment of infectious exacerbation www.selleckchem.com/products/mi-773-sar405838.html in asthma in the future. ""Allergic reactions to hidden food allergens (e.g., unexpected ingredients) and cross-reacting food allergens can result in unexpected allergic reactions. A reaction to a hidden food allergen that is erroneously attributed to a different ingredient in a culprit food may lead to a misdiagnosis. Hidden or unexpected exposure to food allergens may occur from undeclared ingredients, from cross-contact with an allergen, or from exposures not expected to carry food proteins, such as kissing, from airborne proteins, or in medications and cosmetics. Patient education can reduce such reactions. Cross-reactivity may account for reactions to a variety of related foods of plant or animal origin that are caused by homologous proteins. Positive specific IgE tests to related foods are common, but do not necessarily indicate clinical allergy. True clinical cross-reactivity is more common (>35%) among tree nuts, fish, shellfish, certain mammalian milks, and certain fruits, than among grains and legumes (