The protective effect of special electromagnetic field treated water and far infrared rays on endotoxin-induced acute respiratory distress syndrome may result from their role in reducing the levels of IL-1<i>β</i> and IL-6 in serum and the expression level of p65 protein in lung tissue, in addition to reliving inflammatory response, lung coefficient, and lungs edema.
Moreover, we established a mouse model of lipopolysaccharide- and cecal ligation and puncture-induced ARDS treated with neutralizing antibodies (anti-IL-35 Ebi3 or anti-IL-35 P35); the results showed that lung injury occurred more often than in untreated models and the inflammatory cytokines CXCL-1, tumor necrosis factor alpha, IL-6, and IL-17A increased significantly after neutralizing antibody treatment in bronchoalveolar lavage fluid and serum.
The TNF-α rs1800629 locus A allele and the IL-6rs1800796 locus G allele were found to be risk factors for ARDS (adjusted OR = 1.452, 95% CI: 1.211-1.689, P < .001 and adjusted OR = 1.205, 95% CI: 1.058-1.358, P = .005, respectively).
We identified biological pathways that were enriched at each time point in subjects alive and extubated within 28 days after ARDS onset (alive/extubated<sub>Day28</sub>) versus those dead or persistently supported on mechanical ventilation at Day 28 (dead/intubated<sub>Day28</sub>).<b>Measurements and Main Results:</b> "M1-like" (classically activated) and proinflammatory gene sets such as IL-6/JAK/STAT5 (Janus kinase/signal transducer and activator of transcription 5) signaling were significantly enriched in AMs isolated on Day 1 in alive/extubated<sub>Day28</sub> versus dead/intubated<sub>Day28</sub> subjects.
Changes in tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-10 and vascular endothelial growth factor (VEGF) in serum and bronchoalveolar lavage fluid (BALF) in rats with acute respiratory distress syndrome (ARDS) and the intervention effect of dexamethasone were observed to explore the theoretical basis of dexamethasone in the treatment of ARDS.
BBR pretreatment also decreased the production of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and inhibited NF-κB signaling pathway activation in LPS-induced ARDS.
The aim of this meta-analysis was to assess the value of early IL-6 levels (within the first 24 h after trauma) for predicting post-traumatic complications [acute respiratory distress syndrome (ARDS), systemic inflammatory response syndrome (SIRS), sepsis, multiple organ failure (MOF), and multiple organ dysfunction syndrome (MODS)] and mortality.
The increased lung IL-6 in CS-exposed LPS-injured mice indicates that this potent cytokine, previously shown to predict mortality in patients with ARDS, may play a role in exacerbating lung injury in smokers and may have utility as a biomarker of tobacco-related lung injury.
Our data indicate that aSMase and IL-6 are not simply biomarkers of poor outcomes but pathogenic mediators of pulmonary vascular dysfunction in ARDS secondary to Gram-negative infections.
The four downregulated rno‑let‑7 miRNAs may be involved in the inflammatory process in the pathogenesis and progression of ARDS, via the synergistic regulation of their target genes, such as IL‑6.
We found that the forced DOK3 expression significantly attenuated LPS-induced pulmonary histological alterations, inflammatory cells infiltration, lung edema, as well as the generation of inflammatory cytokines TNFα, IL- 1β and IL-6 in BALF of LPS-induced ARDS mice.
However, in patients with P-CAP multivariate analysis adjusted for age, gender, co-morbidity, hospital of origin, and severity (pneumonia severity index, PSI) showed that the IL6 -174 GG genotype was protective against the development of ARDS (p = 0.002, OR = 0.25, 95% CI 0.07-0.79), septic shock (p = 0.006, OR = 0.46, 95% CI 0.18-0.79), and multiple organ dysfunction syndrome (p = 0.02, OR = 0.53, 95% CI 0.27-0.89).
Furthermore, tracheal aspirate levels of IL-6 were significantly increased in premature neonates with respiratory distress syndrome who had an adverse outcome (bronchopulmonary dysplasia/death).