Effects of airborne pollen on allergic rhinitis and asthma across different age groups in Beijing, China.

In the context of global warming and rapid urbanization, pollen has become a significant public health concern for Chinese citizens. However, there is a paucity of epidemiological research on the impact of pollen on allergen-linked diseases, such as allergic rhinitis and asthma, in China. Using data from the Beijing Chaoyang Hospital between 2013 and 2019, which included allergic rhinitis and asthma incidence, meteorological records, and air pollution data, we employed a Generalized Additive Model (GAM) to examine the relationship between overall and type-specific pollen concentrations in relation to varying population exposures. We found that increased overall pollen concentrations significantly increased the risks of allergic rhinitis and asthma in diverse populations. Notably, the risk of allergic rhinitis was higher than that of asthma at equivalent pollen concentrations. Seasonal trends indicated that spring pollen peaks, primarily from trees, were associated with a lower risk of both allergic rhinitis and asthma than autumn peaks, predominantly from weeds. This study underscores the importance of identifying pollen species that pose heightened risks to different demographic groups across seasons, thereby providing targeted interventions for public health agencies.

Desuccinylation of pyruvate kinase M2 by SIRT5 contributes to antioxidant response and tumor growth.

Tumor cells trends to express high level of pyruvate kinase M2 (PKM2). The inhibition of PKM2 activity is needed for antioxidant response by diverting glucose flux into the pentose phosphate pathway and thus generating sufficient reducing potential. Here we report that PKM2 is succinylated at lysine 498 (K498) and succinylation increases its activity. SIRT5 binds to, desuccinylates and inhibits PKM2 activity. Increased level of reactive oxygen species (ROS) decreases both the succinylation and activity of PKM2 by increasing its binding to SIRT5. Substitution of endogenous PKM2 with a succinylation mimetic mutant K498E decreases cellular NADPH production and inhibits cell proliferation and tumor growth. Moreover, inhibition of SIRT5 suppresses tumor cell proliferation through desuccinylation of PKM2 K498. These results reveal a new mechanism of PKM2 modification, a new function of SIRT5 in response to oxidative stress which stimulates cell proliferation and tumor growth, and also a potential target for clinical cancer research.