Additionally, IL-6 genotype was related to the length of oxygen (O(2)) supplementation and hospital stay, IL-10 genotype to the frequency of pneumonia, and TGF-beta1 genotype to O(2) saturations at presentation.
Altogether, our data demonstrate that IL-10 produced by M-MDSCs is required for bacterial clearance, reduction of lung tissue damage, and host survival during KP35 pneumonia.
Exposure to PQ significantly increased total WBC, neutrophil, eosinophil, lymphocyte, and monocyte counts, IL-10, interferon gama (INF-γ), nitrite (NO<sub>2</sub>), and malondialdehyde (MDA) levels, but catalase (CAT), superoxide dismutase (SOD), and thiol levels were decreased (<i>p</i> < 0.05 to <i>p</i> < 0.00).<i>Z. multiflora</i> and dexamethasone treatment significantly improved all behavioral as well as lung changes induced by inhaled PQ (<i>p</i> < 0.05 to <i>p</i> < 0.01).<b>Conclusion:</b><i>Z. multiflora</i> treatment improved learning and memory impairment as well as lung inflammation and oxidative stress induced by inhaled PQ.
In an in vivo model of pneumonia developing shock, IgM-enriched immunoglobulins administered as rescue treatment enhance the anti-inflammatory response by increasing blood levels of IL-10 and reducing TNF-α in BAL fluid.
In this study, we used a lung-specific, tetracycline-inducible IL-10 overexpression-transgenic (IL-10 OE) mouse to study the effects of IL-10 overexpression on Pseudomonas aeruginosa-induced lung inflammation and corresponding survival in mice.
Individual treatment with LZD (50 mg/kg for two times/day) resulted in improvement of body weight, chest imaging, bronchoscopic manifestations, histological parameters, and IL-10 concentration in plasma (<i>P<</i>0.01), decreasing pulmonary auscultation, and reduction of IL-8, IL-6, CRP, and TNF-α concentrations in plasma (<i>P<</i>0.01) compared with the pneumonia model group at 48 and 168 h. Compared with LZD group, co-administration of hUMSCs (1 × 10<sup>6</sup>/kg for two times at 6 and 72 h after MRSA instillation) and LZD further increased the body weight (<i>P<</i>0.05).
Interestingly, we observed that all BI patients with high frequency of IL-10(+) B cells on day 1 displayed an episode of pneumonia, and had a longer duration of mechanical ventilation and ICU stay compared to BI patients with low proportion of IL-10(+) B cells.
MDSC accumulation and serum IL-10 levels were significantly elevated in the children with asthma compared with the budesonide-treated alleviated group, normal healthy controls, and pneumonia controls (p<0.05), whereas those in the latter three groups showed no statistical differences (p>0.05).
Notably, sensitization of IL-10-deficient mice with OVA/Alum/CpG resulted in the development of neutrophilic lung inflammation associated with IFNγ production.
Our data suggest that AE inhibited LPS-induced lung inflammation by attenuating inflammatory cytokines and oxidative stress markers in mice and human cell culture via enhanced IL-10 production.
Our in vivo results demonstrated that Gln treatment reduced ET release (as indicated by cell-free-DNA content and myeloperoxidase activity), decreased lung inflammation (reductions in interferon-γ and increases in interleukin-10 levels), and improved lung morpho-function (decreased static lung elastance and alveolar collapse) in comparison with ARDS animals treated with saline.
Polymorphisms in B lymphocyte growth and differentiation factors, including IL-6 and IL-10, Fcg RIIa receptors, as well as genetic variants of ACE, angiotensin-converting enzyme, also are associated with increased susceptibility for pneumonia.
The expression levels of IL-6, IL-8, and IL-10 were significantly higher in inpatients with AVP compared to children hospitalized with tracheomalacia or MPP.
The frequency of the IL-10 -819 T/T genotype was significantly higher in patients with postoperative pneumonia than in patients without pneumonia (p = 0.0323).
The persistence of reduced HLA-DR expression amidst increasing levels of IL-10 in NP+ patients suggest that cell-mediated immune function is being suppressed.