Caspase-11 Plays a Protective Role in Pulmonary Acinetobacter baumannii Infection.
Wei WangYue ShaoShengjun LiNa XinTingxian MaChenghai ZhaoMin SongPublished in: Infection and immunity (2017)
Activation of caspase-11 by some Gram-negative bacteria triggers the caspase-1/interleukin 1β (IL-1β) pathway, independent of canonical inflammasomes. Acinetobacter baumannii is a Gram-negative, conditionally pathogenic bacterium that can cause severe pulmonary infection in hospitalized patients. A. baumannii was revealed to activate canonical and noncanonical inflammasome pathways in bone marrow-derived macrophages (BMDMs). Pulmonary infection of caspase-11-/- mice with A. baumannii showed that caspase-11 deficiency impaired A. baumannii clearance, exacerbated pulmonary pathological changes, and enhanced susceptibility to A. baumannii These data indicate that the caspase-11-mediated innate immune response plays a crucial role in defending against A. baumannii.
Keyphrases
- acinetobacter baumannii
- multidrug resistant
- cell death
- gram negative
- induced apoptosis
- immune response
- drug resistant
- pulmonary hypertension
- pseudomonas aeruginosa
- endoplasmic reticulum stress
- signaling pathway
- dendritic cells
- adipose tissue
- toll like receptor
- machine learning
- early onset
- data analysis
- drug induced
- big data