Pentraxin 3

Streptococcus suis serotype 2 (SS2) is a noteworthy zoonotic pathogen that has been responsible for large economic losses in pig production and a great threat to human health. Pentraxin 3 (PTX3) is an essential regulator of the innate immune response to bacterial pathogens; however, its role during SS2 infection is not fully understood. In this study, we found that the SS2 strain HA9801 induced a significant inflammatory response in the mouse air pouch model; this response was amplified by the treatment of exogenous PTX3 simultaneously in terms of the results of inflammatory cell recruitment and proinflammatory cytokine IL-6 production. In addition, PTX3 facilitated the phagocytosis of macrophage Ana-1 against SS2 strain HA9801. The supplementation of exogenous PTX3 significantly reduced the bacterial loads in a dose-dependent manner in lungs, livers and bloods of SS2-infected mice compared to the samples with HA9801 infection alone; this finding indicated that PTX3 may facilitate the bacterial clearance through enhancing the host inflammatory response during SS2 infection. Both PTX3 and SS2 capsular polysaccharide (CPS2) were required for the robust inflammatory response, implying that the host PTX3 protein and SS2 surface CPS2 modulate the host innate immune response in concert. All of these results suggested that PTX3 is a potential novel biological agent for the SS2 infection; however, the recommended dose of PTX3 must be evaluated strictly to avoid inducing an excessive inflammatory response that can cause serious tissue injury and animal death.

AimPentraxin-3, high sensitive CRP (HsCRP) and adropin were investigated in cord blood of infants of mothers with gestational diabetes mellitus (IDM) to evaluate the exposure of fetus to inflammation and whether there is any correlation with clinical findings.MethodsForty IDM and forty three infants whose mother did not have diabetes were included in this prospective study. Adropin, pentraxin-3 and HsCRP levels were measured in the cord blood samples. Echocardiographic measurements were performed in the first three days of life.ResultsAdropin and pentraxine-3 levels were significantly lower and HsCRP levels were significantly higher in IDM group. Echocardiographic measurements of myocardial hypertrophy were negatively correlated with adropin.ConclusionAlterations in these markers in IDM supports the hypothesis of in utero fetal exposure to inflammation caused by gestational diabetes mellitus. Potentially, cord blood adropin might be used as a predictor for complications of diabetes.