Table 1.

Nlrp6 in host defense following microbial infection.

Pathogen	Model used	Phenotype observed	Proposed mechanism of action	Inflammasome/NF-κB/IFN dependent	Refs.
Staphylococcus aureus	Pneumonia (IT)	Nlrp6−/− mice protected	Nlrp6 augments pyroptosis and necroptosis of neutrophils and macrophages, thereby reducing the number of phagocytes to clear bacteria. In addition, Nlrp6 deficiency enhances IFN-γ secretion in the lungs	Inflammasome dependent	12
Listeria monocytogens	Systemic infection (IV)	Nlrp6−/− mice protected	Nlrp6 inflammasome enhances IL-18 secretion, which is detrimental during Listeria infection	Inflammasome dependent	18
Salmonella typhimurium	Systemic infection (IV)	No change in phenotype		NA	18
Salmonella typhimurium	Systemic infection (IP)	Nlrp6−/− mice protected	Nlrp6 deficiency augments NF-κB-mediated neutrophil recruitment, which is important to limit Salmonella	Inflammasome independent, but NF-κB dependent	13
Escherichia coli	Systemic infection (IP)	Nlrp6−/− mice protected	Deletion of Nlrp6 enhances NF-κB-mediated neutrophil recruitment	Inflammasome independent, but NF-κB dependent	13
Clostridium rodentium	Enteritis model	Nlrp6−/− mice susceptible	Nlrp6−/− mice had a thin mucus layer as a result of defective goblet cell function. This facilitates prolonged adherence of C. rodentium	Inflammasome dependent	11
Encephalomyocarditis virus (EMCV), Norovirus	Systemic infection (EMCV: IP and oral; Norovirus: oral)	Nlrp6−/− mice susceptible	Nlrp6 recognizes cytosolic long dsRNA and activated mitochondrial antiviral signaling proteins (MAVS) to enhance the antiviral response. Nlrp6-Dhx15-MAVs axis augments the expression of interferon-stimulated genes to limit virus in the intestine	Inflammasome independent, but IFN dependent	36