Introduction: Metagenomic next-generation sequencing (mNGS) has been increasingly used to detect infectious organisms and is rapidly moving from research to clinical laboratories. Presently, mNGS platforms mainly include those from Illumina and the Beijing Genomics Institute (BGI). Previous studies have reported that various sequencing platforms have similar sensitivity in detecting the reference panel that mimics clinical specimens. However, whether the Illumina and BGI platforms provide the same diagnostic performance using authentic clinical samples remains unclear.Methods: In this prospective study, we compared the performance of the Illumina and BGI platforms in detecting pulmonary pathogens. Forty-six patients with suspected pulmonary infection were enrolled in the final analysis. All patients received bronchoscopy, and the specimens collected were sent for mNGS on the two different sequencing platforms.Results: The diagnostic sensitivity of the Illumina and BGI platforms was notably higher than that of conventional examination (76.9% vs. 38.5%, p < 0.001; 82.1% vs. 38.5%, p < 0.001; respectively). The sensitivity and specificity for pulmonary infection diagnosis were not significantly different between the Illumina and BGI platforms. Furthermore, the pathogenic detection rate of the two platforms were not significantly different.Conclusion: The Illumina and BGI platforms exhibited similar diagnostic performance for pulmonary infectious diseases using clinical specimens, and both are superior to conventional examinations.

Recent studies suggest that improper resolution of acute neuroinflammation may lead to long-lasting low-grade chronic neuroinflammation and drive progressive neurodegeneration. However, the molecular mechanism underlying the transition from acute to chronic neuroinflammation remains unclear. The main purpose of this study was to search for potential pathways mediating LPS-elicited chronic neuroinflammation and resultant neurodegeneration. Using microglia cultures prepared from C57BL/6J, MAC1-deficient, and MyD88-deficient mice, the initial study showed that activation of TLR-4 is not sufficient for maintaining chronic neuroinflammation despite its essential role in LPS-initiated acute neuroinflammation. Opposite to TLR-4, our studies showed significantly reduced intensity of chronic neuroinflammation, oxidative stress, and progressive loss of nigral dopaminergic neurons in MAC1-deficient neuron/glial cultures or mice stimulated with LPS. Mechanistic studies revealed the essential role ERK1/2 activation in chronic neuroinflammation-elicited neurodegeneration, which was demonstrated by using an ERK1/2 inhibitor in neuron-glial cultures. Taken together, we propose a key role of the MAC1-NOX2-ERK1/2 signaling pathway in the initiation and maintenance of low-grade chronic neuroinflammation. Continuing ERK1/2 phosphorylation and NOX2 activation form a vicious feedforward cycle in microglia to maintain the low-grade neuroinflammation and drive neurodegeneration.