Involvement of TLR4 and PPAR-α Receptors in Host Response and NLRP3 Inflammosome Activation, Against Pulmonary Infection with Pseudomosas Aeruginosa

Colonization with Pseudomonas aeruginosa (PA), the most common pathogen isolated mainly in patients with cystic fibrosis, is particularly difficult to eradicate and is associated with acceleration of decline in lung function and with poorer prognosis. PA LPS is recognized by toll like receptors 4 (TLR4) and has been shown to induce lung inflammation in vivo. In addition, regulation of this process is essential for proper pathogen clearance and to prevent excessive inflammatory response resulting in tissue damage. One potential regulator of these process are the peroxisome proliferator-activated receptors (PPARs), and in particular PPARα Thus, the purpose of the present study was to evaluate the the effects of the absence of TLR4 and PPARα receptors in the pulmonary innate immunity response to PA and in the consequent inflammatory response and in the activation of the macromolecular complex of the NLRP3 inflamosome.