In the present study, we aim to investigate the association of promoter-region polymorphisms IL-6 (-174G/C) rs1800795 and TNF-α (-308G/A) rs1800629 with pneumonia-induced sepsis.
GM-CSF neutralization compromised the bacterial control under sub-optimal isoniazid/rifampicin treatment in TNFα-deficient mice, leading to exacerbated lung inflammation with necrotic granulomatous structures and high numbers of intracellular M. tuberculosis bacilli.
Polymorphism of the TNF gene, particularly the -238A allele and a related haplotype, revealed the most striking and consistent association with pneumonia in univariate analyses.
Ttp-/- mice with elevated (9.5±0.6 fold) basal TNF-α showed further increase (12.2±0.9 fold, p<0.02) in TNF-α release and acute lung inflammation within a week post-irradiation.
The faster growing strains elicited more tumor necrosis factor α and interleukin 1β than the slower growing strains, even after heat killing, and caused accelerated death of infected guinea pigs (∼9 weeks vs 24 weeks) associated with increased lung inflammation/pathology.
Polymorphisms in the central major histocompatibility complex (MHC) (particularly TNF and adjacent genes) associate with several immunopathological diseases and with susceptibility to pneumonia.
In this work, a new, highly sensitive lab on a chip (LOC) immunoassay has been designed, developed, and characterized for tumor necrosis factor α (TNF-α), a protein biomarker that causes lung inflammation due to RCS exposure.
<i>In vitro</i> experiments were conducted to evaluate binding of EVs to HMW HA and uptake of EVs by human monocytes.<b>Measurements and Main Results:</b> Administration of HMW HA ameliorated the impairment of alveolar fluid clearance, protein permeability, and acute inflammation from <i>E. coli</i> EVs or pneumonia and reduced total bacteria counts after <i>E. coli</i> pneumonia.HMW HA bound to <i>E. coli</i> EVs, inhibiting the uptake of EVs by human monocytes, an effect associated with reduced TNFα (tumor necrosis factor α) secretion.Surprisingly, HMW HA increased <i>E. coli</i> bacteria phagocytosis by monocytes.<b>Conclusions:</b> EVs induced and released during severe bacterial pneumonia were inflammatory and induced ALI, and HMW HA administration was effective in inhibiting the uptake of EVs by target cells and decreasing lung injury from <i>E. coli</i> EVs or bacterial pneumonia.
The aim of the present study was to further characterize the role of alveolar macrophages (AM) in acute human lung inflammation by evaluating their capacity to produce pro-inflammatory cytokines such as tumour necrosis factor (TNF)-alpha, interleukin (IL)-6 and IL-8.
While IFN-γ, IL-2, and TNF-α have been previously noted, the finding of elevated levels of the innate cytokines GM-CSF and IL-1β could suggest that these, as well as IL-13, are early and specific markers for pulmonary coccidioidomycosis.<b>IMPORTANCE</b> Coccidioidomycosis, commonly known as Valley fever, is a common pneumonia in the southwestern United States.
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).
In individuals with pneumonia, Mann-Whitney U exact tests suggested an association (P<.05) between the formation of a first PU and a slight increase in plasma concentrations of tumor necrosis factor-alpha (TNF-α), and a decrease in urine concentrations of TNF-α, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interleukin (IL)-15 after onset of pneumonia.
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.
Serum Tumor Necrosis Factor-<i>α</i> and Interferon-<i>γ</i> Levels in Pediatric <i>Mycoplasma pneumoniae</i> Pneumonia: A Systematic Review and Meta-Analysis.
Cox survival analysis was used to determine the association of corticosteroids at study entry and as a time-varying covariate, corticosteroid-sparing agents (immunomodulators and antitumor necrosis-alpha [TNF] inhibitors), and pneumococcal vaccination with the development of all-cause pneumonia.