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. 2014 May 1;161(1):38–43. doi: 10.1016/j.imlet.2014.04.012

Table 2.

Mechanisms of PTX3 in inflammation and innate immunity.

Effects exerted by PTX3 Suggested and/or reported mechanisms by PTX3 References
Protection against infections - Facilitates phagocytosis of pathogens through complement, complement receptor and Fcγ receptor
- Enhances viral clearance, suppresses neutrophil infiltration and inflammatory mediators in MHV-1 induced lung injury
- Exerts reversible effects depending on bacteria burden (K. Pneumoniae), suppressing neutrophil infiltration and increasing TNFα level in higher inoculation, while facilitating neutrophil infiltration and un-affecting TNFα level in lower inoculation
[64], [68]
[67]
[71]
Protection against acute myocardial infarction - Reduces no-reflow area, IL-6 level, neutrophil infiltration and C3 deposition [72]
Protection after ischemic stroke - Reduces blood–brain barrier (BBB) damage, and participates in the resolution of edema and glial scar formation [74]
Protection against lung injury - Reduces neutrophil infiltration, cell death and fibrin deposition in LPS-induced ALI [75], [81]
Protection against LPS damage - Controls IL-10 production, and enhances nitric oxide production from macrophages in a model of endotoxemia [69]
Protection against acute kidney injury - Prevents leukocyte recruitment and abrogates acute renal failure [77]
Detrimental effects - Facilitates neutrophil infiltration and proinflammatory cytokine levels (TNFα, IL-1β, CCL2; CXCL1) in a model of intestinal ischemia and reperfusion
Increases IL-1β, CCL2 and CXCL1 mRNA level in ventilation-induced lung injury
[78], [79]

[80]