Detection of <i>Dialister micraerophilus</i> (p=0.01), <i>Eggerthella</i> sp type 1 (p=0.05) or <i>Mycoplasma hominis</i> (p=0.03) was associated with higher TNFα concentrations, and detection of <i>D. micraerophilus</i> (p<0.01)<i>, Eggerthella</i> sp type 1 (p=0.04)<i>, M. hominis</i> (p=0.02) or <i>Parvimonas</i> sp type 2 (p=0.05) was associated with significantly higher IL-1β concentrations.Seven bacterial taxa (<i>D. micraerophilus</i>, <i>Eggerthella</i> sp type 1, <i>Gemella asaccharolytica, Sneathia</i> sp, <i>Megasphaera</i> sp, <i>M. hominis</i> and <i>Parvimonas</i> sp type 2) were found to be highly correlated by principal component analysis (eigenvalue 5.24, explaining 74.92% of variability).
<i>Mycoplasma pneumoniae</i> is an atypical bacterial respiratory pathogen known to cause a range of airway inflammation and lung and extrapulmonary pathologies.We recently reported that an <i>M. pneumoniae</i>-derived ADP-ribosylating and vacuolating toxin called community-acquired respiratory distress syndrome (CARDS) toxin is capable of triggering NLRP3 (NLR-family, leucine-rich repeat protein 3) inflammasome activation and interleukin-1β (IL-1β) secretion in macrophages.
Mycoplasma salivarium and Mycoplasma pneumoniae cells activated murine bone marrow-derived macrophages (BMMs) to induce production of IL-1α, IL-1β, and IL-18.
In conclusion, we provide evidence that Hsp90/Sec22b promotes the unconventional secretion of IL-1β through an autophagosomal carrier during Mycoplasma hyopneumoniae infection.
These mediators include classical pro-inflammatory cytokines such as TGF-β, TNF-α, interferons, or IL-1β that are released upon bacterial challenge with <i>Streptococcus pneumoniae, Klebsiella pneumoniae</i>, or <i>Mycoplasma pneumoniae</i> as well as in viral infection with influenza A virus, pathogenic coronaviruses, or respiratory syncytial virus.