The innate immune system plays a key role in modulating host immune defense during
bacterial disease. Upon sensing
pathogen-associated molecular patterns (
PAMPs), the multi-
protein complex known as the
inflammasome serves a protective role against bacteria burden through facilitating pathogen clearance and bacteria lysis. This can occur through two mechanisms: (1) the cleavage of pro-inflammatory
cytokines IL-1β/IL-18 and (2) the initiation of inflammatory cell death termed pyroptosis. In recent literature, AIM2-like Receptor (ALR) and
Nod-like Receptor (NLR)
inflammasome activation has been implicated in host protection following recognition of
bacterial DNA. Here, we review current literature synthesizing mechanisms of
DNA recognition by
inflammasomes during bacterial respiratory disease. This process can occur through direct sensing of
DNA or indirectly by sensing pathogen-associated intracellular changes. Additionally,
DNA recognition may be assisted through
inflammasome-
inflammasome interactions, specifically non-canonical
inflammasome activation of NLRP3, and crosstalk with the
interferon-inducible
DNA sensors Stimulator of
Interferon Genes (
STING) and
Z-DNA Binding Protein-1 (ZBP1). Ultimately,
bacterial DNA sensing by
inflammasomes is highly protective during respiratory disease, emphasizing the importance of
inflammasome involvement in the respiratory tract.