These results suggest that immediate prone positioning alleviated the degree of aspiration-induced lung injury, possibly through mitigating IL-6-mediated 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.
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.
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.
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.
Finally, we established that, in HBE cells, andrographolide reversed the CSE-induced EMT via decreasing IL-6 levels and, in an animal model, prevented CS-induced lung inflammation and small airway remodeling, indicating that it has potential clinical application for CS-induced pulmonary dysfunction and COPD.
Diffuse alveolar damage score and gene expression of markers associated with lung inflammation (interleukin-6), alveolar-stretch (amphiregulin), epithelial cell damage (club cell protein 16), and fibrogenesis (metalloproteinase-9 and type III procollagen), as well as diaphragm inflammation (tumor necrosis factor-α) and proteolysis (muscle RING-finger-1) were comparable between groups.
Genetic ablation of Il-17c resulted in a decreased recruitment of inflammatory cells into the tumor microenvironment, a decreased expression of tumor-promoting cytokines (e.g. interleukin-6 (IL-6)), and a reduced tumor proliferation in the presence of Haemophilus influenzae- (NTHi) induced COPD-like lung inflammation.
Results showed that NaHS improved lung inflammation through its inhibitory effect on iNOS expression, decreasing the levels of IL-6 and lipid peroxides and increasing TAC levels.
This suggests that antioxidant NAC attenuates IL-17A-induced pulmonary inflammation by restoring oxidant-antioxidant balance and attenuation of IL-6 in the lung.
Although participation of IL-6 in lung inflammation has been widely elucidated, the transcriptional regulation of its generation in alveolar type II cells stimulated by TNF-α remain unclear.
Accordingly, IL-6 and IL-33 neutralizing antibodies were used to explore which cytokine might play a key role in lung inflammation induced by BC and oBC.
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.
Taken together, the above results suggest that IL-36-mediated IL-6 and CXCL8 production in human lung fibroblasts and bronchial epithelial cells may be involved in pulmonary inflammation especially caused by bacterial or viral infections.
In the T<sub>H</sub>17 lung inflammation model, basophils are recruited to the inflamed lungs following CT challenge, and T<sub>H</sub>17 responses are significantly reduced in the absence of basophils or IL-6.
A mouse in vivo study of LPS-stimulated lung inflammation showed that phloretin effectively suppressed the levels of TNF-α, IL-1β, and IL-6 in lung tissue with low cytotoxicity.Phloretin was found to bind <i>M. tuberculosis</i> β-ketoacyl acyl carrier protein synthase III (mtKASIII) with high affinity (7.221 × 10⁷ M<sup>-1</sup>); a binding model showed hydrogen bonding of A-ring 2'-hydroxy and B-ring 4-hydroxy groups of phloretin with Asn261 and Cys122 of mtKASIII, implying that mtKASIII can be a potential target protein.
Surprisingly, vaccinated pigs showed enhanced virus shedding, lung inflammation and increased levels of systemic and lung interferon-α as well as elevated lung interleukin-6.
Collectively, these results support the ability of OSM to induce B cell activation and iBALT formation independently of IL-6 and highlight a role for IL-6 downstream of OSM in the induction of pulmonary inflammation.
Some inflammatory factors, such as tumor necrosis factor, interleukin 1 and interleukin 6, were upregulated in lung tissue of transgenic mice compared with that of wild-type mice, implying that long-term HER2 overexpression could induce serious lung inflammation and some precancerous lesions.
Expansion of CD4(+) CD25(+) and CD25(-) T-Bet, GATA-3, Foxp3 and RORγt cells in allergic inflammation, local lung distribution and chemokine gene expression.
To determine whether endogenous IL-6 contributes to mediate hypoxic PH and lung inflammation, we studied IL-6-deficient (IL-6-/-) and wild-type (IL-6+/+) mice exposed to hypoxia for 2 weeks.