<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.
BPIFB1 was localized in CF lung samples along with BPIFA1, MUC5AC, CD68 and NE and directly compared to histologically normal lung tissues and that of bacterial pneumonia.
IP6K1-mediated inorganic polyphosphate (polyP) production by platelets was essential for infection-induced neutrophil-platelet aggregate (NPA) formation and facilitated neutrophil accumulation in alveolar spaces during bacterial pneumonia.
A serum interleukin-6 level of greater than or equal to 93.0 pg/mL had 100.0% sensitivity and 99.14% specificity in discriminating bacterial pneumonia from respiratory syncytial virus pneumonia and Mycoplasma pneumoniae pneumonia.
Because IL-17A and IL-17F, ligands for IL-17 receptor antagonist (IL-17RA), have been shown to mediate neutrophil migration into the lung in response to LPS or Gram-negative bacterial pneumonia, we hypothesized that IL-17RA signaling was critical for acute lung injury in response to pulmonary influenza infection.
Because IL-17A and IL-17F, ligands for IL-17 receptor antagonist (IL-17RA), have been shown to mediate neutrophil migration into the lung in response to LPS or Gram-negative bacterial pneumonia, we hypothesized that IL-17RA signaling was critical for acute lung injury in response to pulmonary influenza infection.
Because IL-17A and IL-17F, ligands for IL-17 receptor antagonist (IL-17RA), have been shown to mediate neutrophil migration into the lung in response to LPS or Gram-negative bacterial pneumonia, we hypothesized that IL-17RA signaling was critical for acute lung injury in response to pulmonary influenza infection.
BPIFB1 was localized in CF lung samples along with BPIFA1, MUC5AC, CD68 and NE and directly compared to histologically normal lung tissues and that of bacterial pneumonia.
Efficacy and Safety of Intravenous-to-oral Lefamulin, a Pleuromutilin Antibiotic, for the Treatment of Community-acquired Bacterial Pneumonia: The Phase III Lefamulin Evaluation Against Pneumonia (LEAP 1) Trial.