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.
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.
Expansion of CD4(+) CD25(+) and CD25(-) T-Bet, GATA-3, Foxp3 and RORγt cells in allergic inflammation, local lung distribution and chemokine gene expression.
Expansion of CD4(+) CD25(+) and CD25(-) T-Bet, GATA-3, Foxp3 and RORγt cells in allergic inflammation, local lung distribution and chemokine gene expression.
PAR(1) knockout mice are protected from bleomycin-induced lung inflammation and fibrosis and this protection is associated with marked attenuation in CCL2 induction.
These results suggest that immediate prone positioning alleviated the degree of aspiration-induced lung injury, possibly through mitigating IL-6-mediated lung inflammation.
Two and three doses of MSCs reduced lung inflammation, levels of interleukin (IL)-4, IL-13, and eotaxin; total leukocyte, CD4<sup>+</sup> T-cell, and eosinophil counts in bronchoalveolar lavage fluid; and total leukocyte counts in bone marrow, spleen, and mediastinal lymph nodes.
We hypothesized that TLMPs trigger inflammasome activation and IL-1β production in bronchial and alveolar epithelial cells to induce airway and lung inflammation.
Also, autophagy-deficient ILC2s were adoptively transferred into Rag<sup>-/-</sup>GC<sup>-/-</sup> mice, which were then challenged with IL-33 and assessed for AHR and lung inflammation.
Intratracheal instillation of nZnO intensively aggravated LPS-induced lung inflammation that was accompanied by enhanced expression of interleukin-1β, interleukin-6, monocyte chemotactic protein-1αand granulocyte-macrophage colony stimulating factor.
Multiple lines of evidence suggest that the excessive activation of Toll-like receptor 4 (TLR4) plays an important role in this detrimental lung inflammation.
The rs12976445 SNP in miR-125a is associated with the risk of pneumonitis after in lung cancer patients undergoing the radiotherapy by regulating the expression of miR-125a and TGFB1.
Importantly, we demonstrate that PI3K inhibitor significantly suppressed IL-17 production and lung inflammation caused by HP-PRRSV <i>in vivo</i>, implicating that higher IL-17 level induced by HP-PRRSV might be associated with severe lung inflammation.
Since enhanced interleukin-6 (IL-6) expression has been reported in infants with BPD, it was hypothesized that a decrease in IL-6 may enhance lung inflammation and decrease hyperoxia-induced neonatal lung injury in mice.
Real-time quantitative PCR was used to analyze mRNA of IL-6 and tumor necrosis factor-α (TNF-α). hADSC treatment increased survival rate of septic mice with MV. hADSCs attenuated dysfunction of the liver and kidney and decreased lung inflammation and tissue injury of the liver and lung.
In vivo studies revealed that the indicators of pulmonary inflammation (pathology, inflammatory cell numbers) and related cytokines (IL-1β, IL-6, IL-33) mRNA expressions in CD11c-Map3k7<sup>-/-</sup> animals were significantly lower than wild-type animals after mice were instilled particles.
In contrast to oral application, intranasal pretreatment with EcN-Chim prior to poly-sensitization led to a significant reduction of lung inflammation (eosinophils, IL-5, and IL-13 in bronchoalveolar lavage) along with suppressed levels of allergen-specific serum IgE.
Thus, we propose that an important mechanism by which cAMP-mobilising prostanoid drugs limit PAH is by inhibiting IL-6-mediated pulmonary inflammation and remodelling via SOCS3 inhibition of IL-6 signalling.
While the contribution of IL-17/Th17 responses to both physiological and pathological lung inflammation is now well established, the cellular interactions, soluble factors, and signalling pathways that determine Th17 cell responses to fungal infection remain unclear.
In vivo studies revealed that the indicators of pulmonary inflammation (pathology, inflammatory cell numbers) and related cytokines (IL-1β, IL-6, IL-33) mRNA expressions in CD11c-Map3k7<sup>-/-</sup> animals were significantly lower than wild-type animals after mice were instilled particles.
Here, we report that MLN4924 can markedly reduce the expression of proinflammatory cytokines and chemokines such as IL-1β, IL-6, and CXCL-1 and neutrophilia in a mouse model of IL-17A adenovirus-induced pulmonary inflammation.