Interleukin-35 is upregulated in response to influenza virus infection and secondary bacterial pneumonia.

Postinfluenza pneumococcal pneumonia is an important cause of global morbidity and mortality. What causes this increased susceptibility is not well elucidated. IL-35 is a newly described cytokine in infectious tolerance. A murine model was established to study postinfluenza pneumococcal pneumonia and evaluate the role of IL-35 in host defense against postinfluenza pneumococcal pneumonia. Pulmonary IL-35 was rapidly up-regulated during murine influenza infection, which was partially mediated by type I IFN-α/ß receptor signaling pathway. Secondary pneumococcal infection led to a synergistic IL-35 response in influenza-infected mice. Clinical analysis showed that IL-35 levels were significantly elevated in the patients with influenza infection compared with healthy individuals and influenza infection could induce IL-35 production from human peripheral blood mononuclear cells. These data suggest that IL-35 contributes to the increased susceptibility to secondary pneumococcal pneumonia at least in part by inhibiting the early immune response.

Numerical Investigation on Static and Rotor-Dynamic Characteristics of Convergent-Tapered and Divergent-Tapered Hole-Pattern Gas Damper Seals.

To study the influence of taper seal clearance on the static and rotor-dynamic characteristics of hole-pattern damper seals, this paper develops three-dimensional transient computational fluid dynamic methods, which comprise single-frequency and multi-frequency elliptical orbit whirl model, by the transient solution combined with a mesh deformation technique. Through the investigations, it is illustrated that: (1) In the present paper, the leakage rates of convergent-tapered hole-pattern damper seals are less than divergent-tapered hole-pattern damper seals for the same average seal clearance, and the maximum relative variation reaches 16%; (2) Compared with a constant clearance hole-pattern damper seal, the maximum relative variation of the rotor-dynamic coefficients is 1,865% for nine taper degrees in this paper; (3) Convergent-tapered hole-pattern damper seals have smaller reaction forces and effective damping coefficient, larger cross-over frequency, and direct stiffness coefficient, while divergent-tapered damper seals have the opposite effects; (4) Divergent-tapered hole-pattern damper seals alleviate the rotor whirl because of a larger effective damping coefficient when the rotor system has large natural frequency and small eccentricity. Convergent-tapered damper seals provide both sealing and journal bearing capabilities at the same time, and are more advantageous to the stability of the rotor system when rotor eccentricity is the main cause of rotor instability.

HMGB1 regulates IL-33 expression in acute respiratory distress syndrome.

The development and progression of acute respiratory distress syndrome (ARDS) has been shown to be regulated by cytokines. IL-33 and HMGB1 are conventionally considered as nuclear proteins and have a proinflammatory role. Studies have confirmed that HMGB1 has a significant role in ARDS, but few studies have provided direct evidence to confirm that IL33 is involved in ARDS. The purpose of our study was to determine whether IL-33 is elevated in ARDS and the relationship between IL-33 and HMGB1 in ARDS. We established a mouse model of LPS-induced lung inflammation/injury. Serum, bronchoalveolar lavage fluid (BALF) and lung tissues were obtained to determine the related indicators. IL-33 levels in both the serum, BALF and lungs were significantly increased at 24h after LPS administration compared to the control group. We also found that HMGB1 and other Th1 cytokine/chemokine levels in serum and BALF were also significantly elevated, but the Th2 cytokine levels in serum and BALF didn't increase. To further study the relationship between IL-33 and HMGB1, mice were pretreated with glycyrrhizin (an inhibitor of HMGB1) prior to LPS administration. We found that the expression of IL-33 and HMGB1 were markedly lower than those in the LPS group and the lung injury was ameliorated. The levels of other Th1 cytokines and chemokines in serum and BALF were also significantly decreased. The results showed that IL-33 is likely a major factor in ARDS, and the release of HMGB1 may be correlated with up-regulation of IL-33 expression.