To optimize the animal model of asthma through TLR4 receptor antagonism mechanism as bacterial infections frequently cause asthma exacerbation. TLR4 responds to bacterial stimulation, putting toll-like receptors (TLRs) at the frontline of our microbial defense. This study showed how TLR4 stimulation and TLR4/MD2 complex inhibition were utilized for AHR allergic asthma management in a mouse model. Swiss albino mice were induced with the administration of PBS, LPS, and ovalbumin; later, two compounds activated the TLR4 receptor underlying mechanism for asthma induction. It was 23 days protocol in which animals were sensitized (i.p). It challenged intranasally (i.n.) and treatment given on the 21st & 22nd day followed by euthanasia and samples (BALF & lungs tissues) collected on day 23rd. Further analysis such as TLC/DLC & lung histopathology of asthma parameters in toxic & treatment groups compared to the standard group was performed. Bronchial smooth muscle hyperplasia and goblet cells swelling developed in poisonous groups. The bronchoalveolar lavage fluid (BALF) analysis demonstrated a significant increase in inflammatory infiltration and bronchial architectural damage. In contrast, bovine serum albumin delivery causes allergic airway irritation. The bacterial asthma exacerbation caused by LPS drug rise was decreased by treatment with a TLR4/MD2 complex inhibitor, which significantly reduced cell inflow in BALF. The airway-stabilizing action of TLR4 antagonist drugs suggests that TLR4-MD2 problematic inhibitor drug shown positive therapeutic potential compared to standard medications and could be used to treat microbial-induced allergic asthma exacerbations in the future.
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