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Chlamydia pneumoniae (C. pneumoniae) is a specialized intracellular parasitic pathogen capable of causing pneumonia, sinusitis, bronchitis, and other respiratory diseases, which pose significant public health challenges. Therefore, rapid, accurate, and sensitive diagnosis is crucial for the prevention and treatment of respiratory diseases caused by C. pneumoniae. In this study, we combined enzymatic recombination amplification (ERA) with the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein (Cas) 12a system (CRISPR/Cas12a) to develop a dual detection platform termed the Cpn-ERA-CRISPR/Cas12a dual system. This system integrates both the ERA-CRISPR/Cas12a fluorescence system and the ERA-CRISPR/Cas12a lateral flow system. Detection results can be measured using a fluorescence detector or observed with the naked eye on lateral flow strips. The fluorescence system and the lateral flow system detect C. pneumoniae in 30 minutes and 15 minutes, respectively. This dual system exhibits no cross-reactivity with the other seven pathogens, demonstrating high specificity, and achieves a sensitivity of 100 copies/µL. Additionally, the Cpn-ERA-CRISPR/Cas12a dual system was employed to analyze 39 clinical samples, comprising 19 positive and 20 negative samples. The detection rate for positive samples was 100%, with no positive results in the negative samples, indicating a high level of concordance with qPCR results. In summary, the Cpn-ERA-CRISPR/Cas12a dual system represents a novel tool for diagnosing C. pneumoniae and holds promising application potential in grassroots community hospitals. [ABSTRACT FROM AUTHOR]

Mycoplasma pneumoniae is a common cause of community-acquired pneumonia in which neutrophils play a critical role. Immune-responsive gene 1 (IRG1), responsible for itaconate production, has emerged as an important regulator of inflammation and infection, but its role during M. pneumoniae infection remains unknown. Here, we reveal that itaconate is an endogenous pro-inflammatory metabolite during M. pneumoniae infection. Irg1 knockout (KO) mice had lower levels of bacterial burden, lactate dehydrogenase (LDH), and pro-inflammatory cytokines compared with wild-type (WT) controls after M. pneumoniae infection. Neutrophils were the major cells producing itaconate during M. pneumoniae infection in mice. Neutrophil counts were positively correlated with itaconate concentrations in bronchoalveolar lavage fluid (BALF) of patients with severe M. pneumoniae pneumonia. Adoptive transfer of Irg1 KO neutrophils, or administration of β-glucan (an inhibitor of Irg1 expression), significantly attenuated M. pneumoniae pneumonia in mice. Mechanistically, itaconate impaired neutrophil bacterial killing and suppressed neutrophil apoptosis via inhibiting mitochondrial ROS. Moreover, M. pneumoniae induced Irg1 expression by activating NF-κB and STAT1 pathways involving TLR2. Our data thus identify Irg1/itaconate pathway as a potential therapeutic target for the treatment of M. pneumoniae pneumonia. Author summary: M. pneumoniae is a common human pathogen that causes community-acquired pneumonia. Neutrophil infiltration has been widely recognized as a characteristic of M. pneumoniae pneumonia; however, the interaction between neutrophils and M. pneumoniae is not completely understood. Here we demonstrate a critical role of the Irg1/itaconate metabolic pathway in neutrophils in the pathogenesis of M. pneumoniae pneumonia. We observe a positive correlation between neutrophil counts and itaconate levels in BALF from patients with severe M. pneumoniae pneumonia. We find that M. pneumoniae infection induces itaconate production in neutrophils, which dampens neutrophil bactericidal activity and impedes neutrophil apoptosis through inhibiting mitochondrial ROS (mtROS). Suppressing neutrophil itaconate production mitigates M. pneumoniae pneumonia in mice. We also find that M. pneumoniae induces Irg1 expression in neutrophils by activating NF-κB and STAT1 signaling pathways. Therefore, our findings suggest that targeting neutrophil itaconate production may be an effective therapeutic strategy for the treatment of M. pneumoniae pneumonia in humans. [ABSTRACT FROM AUTHOR]

Demethylcantharidin (DEM) is a widely used antitumor drug; however, its poor tumor targeting and serious organotoxicity limit its application. The aim of this study was to develop a new drug delivery system for efficient delivery of DEM. Nanoemulsion based lipid nanoparticles containing demethylcantharidin (DNLNs) were prepared by loading nanoemulsions into lipid nanoparticles. The cells proliferation, apoptosis, cycle, and uptake were investigated by Cell counting kit‐8 (CCK‐8), flow cytometry, and in situ fluorescence assays, respectively. Then, we established the H22 tumor‐bearing mouse model to evaluate the antitumor efficacy of DNLNs and further studied its organ toxicity and distribution. DNLNs significantly inhibited the proliferation and promoted apoptosis of H22 cells, and H22 cells could take up more DNLNs. Compared with DEM, DNLNs had certain tumor‐targeting properties, and the tumor inhibition rate increased by 23.24%. Moreover, DNLNs can increase white blood cell count and reduce organ toxicity. This study paves the way for nanoemulsion‐based lipid nanoparticle (NLNs)‐efficient DEM delivery to treat liver cancer. [ABSTRACT FROM AUTHOR]

The electrocatalytic carbon dioxide reduction reaction is an effective means of combating the greenhouse effect caused by massive carbon dioxide emissions. Carbon nitride in the graphitic phase (g-C3N4) has excellent chemical stability and unique structural properties that allow it to be widely used in energy and materials fields. However, due to its relatively low electrical conductivity, to date, little effort has been made to summarize the application of g-C3N4 in the electrocatalytic reduction of CO2. This review focuses on the synthesis and functionalization of g-C3N4 and the recent advances of its application as a catalyst and a catalyst support in the electrocatalytic reduction of CO2. The modification of g-C3N4-based catalysts for enhanced CO2 reduction is critically reviewed. In addition, opportunities for future research on g-C3N4-based catalysts for electrocatalytic CO2 reduction are discussed. [ABSTRACT FROM AUTHOR]