Main Article Content
Toll-like receptors (TLR3), which respond to viral pathogenic molecules, further identify genetic content like dsRNA as their ligand. Upon activation induces signaling via Poly(I: C) compound, an artificial simulation of viral dsRNA that initiates innate response & pathogenesis of viral inflammation. Our purpose was to evaluate, TLR3 ligand changed AHR inflammation in an atopic paradigm that has already been developed. Our purpose was to see how a TLR3 ligand changed AHR inflammation in a pre-established allergic inflammation paradigm.
Poly (I: C) agonist was given for sensitization (i.p.) and challenge (i.n.) to Swiss albino mice for five days along with PBS & ovalbumin (OVA). AHR and pro-inflammatory cytokine expression in the mouse airway were evaluated in vivo, and bronchial structural damage was estimated using H&E staining of lung tissue. The TLR3/dsRNA complex inhibitor reduced the TLR3 agonist-induced AHR and cytokine production.
Poly (I: C) was given for sensitization (i.p.) and challenge (i.n.) to Swiss albino mice for 5 days along with PBS & ovalbumin (OVA). In-vivo study shows AHR, cytokine (NF-κB, IL-1β) expression, bronchial structural damage after H&E staining. The new TLR3/dsRNA inhibitor Calbiochem reduced AHR, leukocytecounts in bronchoalveolar lavage, cytokine expression, and histological damage as compared to ovalbumin & control mice.
This study showed optimized ovalbumin and Poly(I.C) compounds induced enhanced viral asthma features in bronchial epithelial cells. Calbiochem (TLR3/dsRNA
complex inhibitor), prevents NF-κB and IL-1β expression in comparison with dexamethasone (DEX) and can be a significant therapeutic compound for viral asthma exacerbations management.