Our data showed that compared with the healthy controls, circulating Ang-2 level was higher in the patients with ARDS, and were usually supposed to be positively related to the severity of ARDS.
Positive findings indicate the implication of genetic polymorphisms of proinflammatory cytokines in premature birth; angiotensin converting enzyme in perinatal adaptation and angiotensin type 1 receptor in the closure of ductus arteriosus; surfactant proteins A and B in respiratory distress syndrome; interleukin (IL)-6 in sepsis, and IL-4-receptor alpha chain and IL-18 in NEC.
While the genes of the classic proinflammatory cytokines interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), IL-6, and IL-8, and inducible nitric oxide synthase (iNOS) were upregulated in septic non-ARDS or late ARDS patients, expressions of these genes in the acute phase of septic ARDS were most distinct.
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.
Increased A(1-9)/A(1-10) ratio suggests that angiotensin converting enzyme II (ACE2) activity is higher in patients who survived their ARDS insult while an increase in A(1-7)/A(1-10) ratio suggests that ACE activity is also higher in survivors.
Pulmonary edema, vascular exudation, and neutrophil accumulation were observed in the ARDS model mice, and the levels of inflammatory cytokines including TNF-α, IL-1b, IL-6, and IL-17 were significantly increased.
Plasma VEGF levels in patients with ARDS with the +936CT+TT genotype were significantly lower than in subjects with the +936CC genotype (median 49 (IQR 16-98) pg/ml vs 112 (IQR 47-162) pg/ml, p = 0.02).
The serum VEGF levels between the ARDS group and the non-ARDS group showed no significant difference (p > 0.05). sVEGFR1 in the ARDS group was significantly higher than that in the non-ARDS group (p < 0.0001), and sVEGFR2 in the ARDS group was significantly lower than that in the non-ARDS group (p < 0.0001).
In neonates, elevated SP-D levels in cord blood and on day 1 have been associated with prenatal risk factors and with an increased risk of respiratory distress syndrome and infections.
The levels of surfactant protein-A (SP-A) and surfactant protein-D (SP-D) in the serum of patients with septic acute respiratory distress syndrome (ARDS) were determined.
Serum SP-A level (n=134) was elevated in acute respiratory distress syndrome and in some cases of drowning, fire and MA fatalities, hyperthermia and chest traumas.
Finally, we confirmed the clinical relevance and found that IL-17 expression was elevated and associated with the disease severity in patients with ARDS.
Pulmonary edema, vascular exudation, and neutrophil accumulation were observed in the ARDS model mice, and the levels of inflammatory cytokines including TNF-α, IL-1b, IL-6, and IL-17 were significantly increased.
Increased A(1-9)/A(1-10) ratio suggests that angiotensin converting enzyme II (ACE2) activity is higher in patients who survived their ARDS insult while an increase in A(1-7)/A(1-10) ratio suggests that ACE activity is also higher in survivors.
Furthermore, one SP-A2 allele (1A0) shown to associate with low SP-A mRNA levels is found with higher frequency in a subgroup with respiratory distress syndrome.
To test whether plasma interleukin-1 receptor antagonist or variants within the gene encoding for interleukin-1ra (IL1RN), or proteins involved in regulating interleukin-1β levels or interleukin-1β response, are associated with pediatric acute respiratory distress syndrome or outcomes in mechanically ventilated children with parenchymal lung disease.
Downregulation of ACE2 is always associated with the ALI or ARDS induced by avian influenza virus, severe acute respiratory syndrome-coronavirus, respiratory syncytial virus and sepsis.
Besides, Trx-1, nuclear factor erythroid 2-related factor 2 (Nrf2) and Txnip expression were measured to explore how seawater induced oxidative stress and the mechanism by which AC-Res attenuated seawater inhalation-induced ARDS.