Table 1.
The good: inflammasome control of pathogen infection
Organism | PAMPS identified | Inflammasome activated | Inflammasome importance established in vivo? | Refs |
---|---|---|---|---|
Helminths | ||||
Schistosoma mansoni | n.d. | NLRP3 | Yes | [138] |
Bacteria | ||||
Mycobacterium tuberculosis | ESX-1 secretion system | NLRP3-dependent and -independent mechanism | Yes. In vivo IL-1 production is independent of caspase-1 | [17,139–142] |
Streptococcus pneumoniae | Pneumolysin | NLRP3 | Yes | [143,144] |
Streptococcus pyogenes | Streptolysin O | NLRP3 | Yes. Not important in vivo | [145] |
Streptomyces hygroscopicus | Nigericin | NLRP3 | n.a. | [146] |
Klebsiella pneumoniae | n.d. | NLRP3 | Yes | [147] |
Chlamycia pneumoniae | n.d. | NLRP3 | Yes | [148] |
Salmonella typhimurium | Flagellin and type III secretion system | NLRP3 and NLRC4 | Yes | [149,150] |
Francisella tularensis | DNA | AIM2 | Yes | [146,151,152] |
Legionella pneumophila | Flagellin | NLRC4 | Yes | [153] |
Listeria monocytogenes | Flagellin, Listeriolysin O, DNA | AIM2, NLRP3, NLRC4 | Yes* | [146,154,155] |
Pseudomonas aeruginosa | Flagellin, Type III secretion system | NLRC4 | Yes | [156–158] |
Shigella flexneri | Type III secretion system | NLRC4 | Yes | [157,159] |
Neisseria gonorrhoeae | Lipo-oligosaccharide | NLRP3 | No | [160] |
Staphylococcus aureus | Peptidoglycan Haemolysin | NLRP3 | Yes | [146,161–165] |
Virbrio vulnificus and Vibrio cholerae | Haemolysins | NLRP3 | No | [166] |
Bacillus anthracis | Anthrax lethal toxin | NLRP1 | Yes | [167–170] |
Escherichia coli | Type III secretion system, flagellin | NLRC4 | No | [157] |
Chlamydia trachomatis | Type III secretion system | NLRP3 | No | [171] |
Protozoa | ||||
Toxoplasma gondii | n.d. | NLRP1 | No | [172] |
Plasmodium species; falciparum, berghei, chabaudi | Haemozoin, MSU | NLRP3 | Yes† | [30,136,173] |
Fungal | ||||
Candida albicans | Hyphae, β-glucan | NLRP3 | Yes | [174] |
Aspergillus fumigatus | n.d., β-glucan | NLRP3 | No | [175,176] |
Saccharomyces cerevisiae | n.d., β-glucan | NLRP3 | n.a. | [174] |
Viruses | ||||
Sendai virus | RNA | NLRP3 | No | [177] |
Influenza virus | RNA, M2 ion channel | NLRP3 | Yes | [177–181] |
Adenovirus | DNA | NLRP3 | Yes | [182] |
Vaccinia virus | DNA, RNA | AIM2 | No | [23,155] |
Mouse cytomegalovirus | DNA | AIM2 | Yes | [155] |
Vesicular stomatis virus | 5′-triphosphate ssRNA | RIG-Ic, NLRP3 | Yes. Not important in vivo | [24,183] |
Encephalomyocarditis virus | RNA | NLRP3 | Yes. Not important in vivo | [24,183] |
Flagellin importance only determined.
In a Plasmodium berghei mouse model, NLRP3 has been suggested to protect from cerebral malaria in a NLRP3-dependent, but caspase-1, apoptosis speck protein (ASC) and interleukin (IL)-1β-independent manner [184].
The requirement of retinoid-inducible gene 1 (RIG-I) for vesicular stomatis virus (VSV)-induced IL-1 is unclear as, unlike the initial finding, it was reported recently to not be required [183].
PAMP: pathogen-associated molecular pattern; ESX: early secreted antigenic target, 6 kDa secretion system; MSU: monosodium urate; n.d.: not determined; n.a.: not applicable.