BackgroundThis study was designed to explore the epidemiological and clinical profiles of respiratory syncytial virus (RSV) infection in neonates from the Suzhou area of China, taking into consideration how climate factors influence disease.MethodsFrom 2010 to 2014, nasopharyngeal aspirates (NPA) collected from hospitalized neonates with lower respiratory tract infections (LRIs) were screened for seven common respiratory viruses including RSV by direct immunofluorescence assay. Human bocavirus, human metapneumovirus, and mycoplasma pneumoniae were detected by polymerase chain reaction.ResultsOf the 1803 hospitalized neonates analyzed, 20.74 % were found to be infected with RSV. Interestingly, 30 subjects were identified as being coinfected with other viruses. The rate of RSV infection was highestduring thewinter and early spring seasons; however, infection was negatively associated with monthly mean temperature (rs = −0.821, P < 0.0001), total rainfall (rs = −0.406, P = 0.002), and sum of sunshine (rs = −0.386, P = 0.001). Monthly mean temperature was the only independent factor associated with RSV activity, as determined using multivariate regression analysis. Compared with non-RSV neonates, neonates with RSV infection presented more frequently with tachypnea,moist rales, and abnormal chest X-rays requiring supplemental oxygen and extended hospitalization postpartum. Neonatal admittance into the NICU was determined based on prematurity and coinfection with other viruses; two independent risk factors for RSV disease, as determined by multivariate logistic analysis.ConclusionsImportant as a major cause of LRIs in hospitalized neonate, we found that the subtropical climate of the Suzhou area was associated with RSV activity. The identified risk factors ofsevere disease in neonates with RSV infection should be taken into consideration when implementing disease health interventions.

The nuclear pore complex (NPC) is the sole and selective gateway for nuclear transport and its dysfunction has been associated with many diseases. The metazoan NPC subcomplex RanBP2, which consists of RanBP2 (Nup358), RanGAP1-SUMO1 and Ubc9, regulates the assembly and function of the NPC. The roles of immune signaling in regulation of NPC remain poorly understood. Here, we show that in human and murine T cells, following TCR stimulation, protein kinase C-θ (PKC-θ) directly phosphorylates RanGAP1 to facilitate RanBP2 subcomplex assembly and nuclear import and, thus, the nuclear translocation of AP-1 transcription factor. Mechanistically, TCR stimulation induces the translocation of activated PKC-θ to the NPC, where it interacts with and phosphorylates RanGAP1 on Ser504 and Ser506. RanGAP1 phosphorylation increases its binding affinity for Ubc9, thereby promoting sumoylation of RanGAP1 and, finally, assembly of the RanBP2 subcomplex. Our findings reveal an unexpected role of PKC-θ as a direct regulator of nuclear import and uncover a phosphorylation-dependent sumoylation of RanGAP1, delineating a novel link between TCR signaling and assembly of the RanBP2 NPC subcomplex.

Chronic inflammation is associated with cancer. CXCL8 promotes tumor microenvironment construction through recruiting leukocytes and endothelial progenitor cells that are involved in angiogenesis. It also enhances tumor cell proliferation and migration. Metformin, type II diabetes medication, demonstrates anticancer properties via suppressing inflammation, tumor cell proliferation, angiogenesis, and metastasis. This study intended to address the role of metformin in regulation of CXCL8 expression and cell proliferation and migration. Our data indicated that metformin suppressed LPS-induced CXCL8 expression in a dose-dependent manner through inhibiting NF-κB, but not AP-1 and C/EBP, activities under the conditions we used. This inhibitory effect of metformin is achieved through dampening LPS-induced NF-κB nuclear translocation. Cell migration was inhibited by metformin under high dose (10 mM), but not cell proliferation.

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