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] |