Attenuation of lung inflammation indicative of acute lung injury, such as alveolar hemorrhage, interstitial thickening, and the presence of alveolar exudate, together with reduced levels of the inflammatory mediators TNFα, IL-1β, IL-6, KC, and MCP-1, strongly suggests amelioration of the pathological immune response in the lungs to promote resolution of the infection.
Aging can increase the expression of MCP-1,CINC-1 and CINC-2α in patients with pneumonia, which may lead to increased risk of pneumonia in the elderly.
A significant increase in the number of alveolar macrophages and infiltrating neutrophils in the lungs and elevation in monocyte chemoattractant protein-1 (MCP-1) in BALF suggested the induction of pulmonary inflammation in the silica exposed rats.
NLE inhibited the recruitment of inflammatory cells and the expression of monocyte chemoattractant protein-1 (MCP-1) in the lungs of mice with CS- and LPS-induced pulmonary inflammation.
PAR(1) knockout mice are protected from bleomycin-induced lung inflammation and fibrosis and this protection is associated with marked attenuation in CCL2 induction.