Mounting data suggest that environmental pollution due to airborne fine particles (AFPs) increases the occurrence and severity of respiratory virus infection in humans. However, it is unclear whether and how interactions with AFPs alter viral infection and distribution. We report synergetic effects between various AFPs and the H1N1 virus, regulated by physicochemical properties of the AFPs. Unlike infection caused by virus alone, AFPs facilitated the internalization of virus through a receptor-independent pathway. Moreover, AFPs promoted the budding and dispersal of progeny virions, likely mediated by lipid rafts in the host plasma membrane. Infected animal models demonstrated that AFPs favored penetration of the H1N1 virus into the distal lung, and its translocation into extrapulmonary organs including the liver, spleen, and kidney, thus causing severe local and systemic disorders. Our findings revealed a key role of AFPs in driving viral infection throughout the respiratory tract and beyond. These insights entail stronger air quality management and air pollution reduction policies.

The thymus has spatially distinct microenvironments, the cortex and the medulla, where the developing T-cells are selected to mature or die through the interaction with thymic stromal cells. To establish the immunological self in the thymus, medullary thymic epithelial cells (mTECs) express diverse sets of tissue-specific self-antigens (TSAs). This ectopic expression of TSAs largely depends on the transcriptional regulator Aire, yet the mechanism controlling Aire expression itself remains unknown. Here, we show that Jmjd6, a dioxygenase that catalyses lysyl hydroxylation of splicing regulatory proteins, is critical for Aire expression. Although Jmjd6 deficiency does not affect abundance of Aire transcript, the intron 2 of Aire gene is not effectively spliced out in the absence of Jmjd6, resulting in marked reduction of mature Aire protein in mTECs and spontaneous development of multi-organ autoimmunity in mice. These results highlight the importance of intronic regulation in controlling Aire protein expression.

LD is likely to be underrecognized in many countries. Due to the widespread existence ofL. pneumophilain natural and artificial water environments and to the lack of cross-protection against different strains,L. pneumophilais a potentially serious threat to human health.

Aim: Our work is to study the correlation between the virulence of different Legionella pneumophila in mouse model and its ability to activate NF-κB signaling pathway in vitro. Materials & methods: We measured the abilities of different strains of L. pneumophila to induce the activation of NF-κB signaling pathway in vitro. By using A/J mice, we also detected the virulence of different strains in vivo. Results & conclusion: We demonstrated that different strains of L. pneumophila induce different levels of activation to NF-κB signaling pathway in vitro. We also found that L. pneumophila strain induced higher NF-κB activation in vitro showed more severe weight losses, higher mortality, more severe lung inflammation and higher levels of serum cytokines production in mice. Graphical Abstract