Urinary kidney injury molecule 1 (uKIM-1) serves as a reliable marker for the early diagnosis of acute kidney injury (AKI). The rapid and facile detection of changes in uKIM-1 is essential for early AKI diagnosis, ultimately improving the prognosis of patients. In this study, we developed a fully printed photonic crystal-integrated microarray with photonic crystal-enhanced fluorescence properties, which can detect uKIM-1 levels at the point-of-care. We confirmed its efficacy in the early diagnosis of AKI using clinical urine specimens. Direct quantitative detection of uKIM-1 was achieved within 10 min. The lowest limit of detection is 8.75 pg·mL⁻¹ with an accuracy of 94.2%. The diagnostic efficacy was validated using 86 clinical urine samples, highlighting the high sensitivity and stability of the photonic crystal microarray. Consequently, a facile and reliable immunoassay was designed and prepared for the rapid quantitative detection of uKIM-1, which is crucial for the early identification and convenient detection of AKI in hospital or community settings. Rapid, convenient, cost-effective, and long-term monitoring of changes in uKIM-1 levels can assist clinicians in making timely adjustments to treatment regimens, preventing the transition from AKI to chronic kidney disease (CKD), improving the quality of life of patients with AKI, and reducing healthcare costs. It highlights the advantages of utilizing urine samples as a noninvasive and easily accessible medium for early detection and monitoring of kidney-related conditions.

Accumulating evidence has shown that long noncoding RNAs (lncRNAs) are involved in several biological processes, including immune responses. However, the role of lncRNAs in antiviral innate immune responses remains largely unexplored. Here, we identify an uncharacterized human lncRNA from influenza A virus (IAV) patients, antivirus and activate neutrophil ( AVAN ), that is significantly up-regulated upon virus infection. Mechanistically, nuclear lncRNA- AVAN positively regulates the transcription of forkhead box O3A (FOXO3a) by associating with its promoter and inducing chromatin remodeling to promote neutrophil chemotaxis. Furthermore, we also found that cytoplasmic lncRNA- AVAN directly binds tripartite motif containing 25 (TRIM25) and enhances the association of TRIM25 and Retinoic acid inducible gene-1 proteins (RIG-I) and the ubiquitylation of RIG-I, thereby promoting TRIM25- and RIG-I-mediated antiviral innate immune signaling. More importantly, we enforced the expression of AVAN in transgenic mice and found that it significantly alleviated IAV virulence and virus production. Collectively, these findings highlight the potential clinical implications of lncRNA- AVAN as a key positive regulator of the antiviral innate immune response and a promising target for developing broad antiviral therapeutics.

(1) Background: With the resurgence of brucellosis epidemics in China in recent years, the chances of a brucella coinfection with other common respiratory pathogens, such as the influenza virus, have increased dramatically. However, little is known about the pathogenicity or the mechanisms of brucella and influenza coinfections. (2) Methods: To clarify the interventions in the early stages of lung damage due to brucella and influenza coinfections, we evaluated the effect of the coinfection on disease progression and mortality using a coinfection model in WT mice and NLRP6^−/− mice, and we verified the function of NLRP6 in infection and proinflammation. (3) Results: The coinfection induced significant respiratory symptoms, weight loss, and a high mortality rate in WT mice. Influenza in the coinfection group significantly increased brucella proliferation in a synergistic manner. Meanwhile, a histological examination showed severe lung tissue destruction and excessive inflammatory responses in coinfected WT animals, and the expression of NLRP6 and IL-18 was dramatically increased in the lung tissues. Furthermore, NLRP6 deletion attenuated lung injuries and inflammation, a reduced bacterial load, and decreased IL-18 protein expression. (4) Conclusions: Our findings indicated that NLRP6 plays a critical role and might be a promising potential therapeutic target for brucella–influenza coinfections.