Table 1.
Physical diseases associated with NLRP3 inflammasome | Stimulator | Pathology/Implication of NLRP3 on physical disease | Prevelence of Depression | References |
---|---|---|---|---|
Metabolic Disorders | ||||
Type II Diabetes Mellitus | Hyperglycemia Fatty acids |
β cell death, Insulin resistance | 26% |
Zhou et al. (2010),Mason et al. (2012) Evans et al.(2005) |
Obesity | Fatty acids | Decrease insulin sensitivity | 20%–30% | Wen et al. (2011), Vandanmagsar et al. (2011), Evans et al.(2005) |
Cardiovascular disease | Cholesterol crystals | Inflammation / polymorphism in the NLRP3 locus and concordance with fibrinogen gene variants | 17%–27% | Duewell et al. (2010), Mason et al. (2012), Evans et al.(2005) |
Autoimmuno Diseases | ||||
Rheumatoid Arthritis | ? | Chronic inflammation of the synovium / Increased expression of NLRP3 | 13%–20% | Kastbom et al. (2008), Mason et al. (2012), Sheehy et al. (2006) |
Systemic lupus erythematosus (SLE) | U1-snRNP | Inflammatory response causes cell death and organ failure | 22.5%–42% | Bachen et al. (2009), Shin et al. (2012), Nery et al. (2007) |
Alzheimer’s disease | Amyloid β | Nlrp3−/ − microglia demonstrated a significant reduction in the proinflammatory mediators when treated with amyloid-β | 30%–50% | Mitroulis et al. (2010), Mason et al. (2012), Evans et al. (2005), Halle et al. (2008) |
Multiple Sclerosis (MS) | ? | Nlrp3 found to play a role in the progression of disease in an experimental autoimmune encephalomyelitis model | 25%–50% | Gris et al. (2010), Mason et al. (2012), Fischer et al. (2012) |
Infection / Environmental Disease | ||||
HIV | HIV | Activation of immune system against the virus | 5%–30% | Pontillo et al. (2012), Evans et al. (2005) |
Asthma | Allergen? | A substaital reduction in inflammation and leukocyte recruitment to the lung in Nlrp3−/ − and IL-1R−/ − mice compared to WT mice | 18% | Besnard et al. (2011), Mason et al. (2012) |
Chronic obstructive pulmonary disorders | Inflammation (uric acid ?) | Chronic bronchitis and emphysema | 10%–42% |
Eisner et al. (2005) Gasse et al. (2009), Mason et al. (2012) |
Healthy Subject | ||||
General population | 10.3% (12-month) 7.1% (Lifetime) |
Caferella et al. (2012) Kessler et al. (1994), Evans et al. (2005) |
Listed are the systemic diseases associated with NLRP3, as well as the different types of danger substances that lead to IL-1β release (or activate caspase-1). The prevalence of depression in populations with these different diseases is much higher (up to 30% or even higher) than that of the general population, which is 10.3%.
(Bachen et al., 2009; Besnard et al., 2011; Cafarella et al., 2012; Duewell et al., 2010; Eisner et al., 2005; Evans et al., 2005; Fischer et al., 2012; Gasse et al., 2009; Gris et al., 2010; Halle et al., 2008; Kastbom et al., 2008; Kessler et al., 1994; Mason et al., 2012; Mitroulis et al., 2010; Nery et al., 2007; Pontillo et al., 2012; Sheehy et al., 2006; Shin et al., 2012; Vandanmagsar et al., 2011; Wen et al., 2011; Zhou et al., 2010).