Throat microbiota drives alterations in pulmonary alveolar microbiota in patients with septic ARDS.

OBJECTIVES: The translocation of intestinal flora has been linked to the colonization of diverse and heavy lower respiratory flora in patients with septic ARDS, and is considered a critical prognostic factor for patients. METHODS: On the first and third days of ICU admission, BALF, throat swab, and anal swab were collected, resulting in a total of 288 samples. These samples were analyzed using 16S rRNA analysis and the traceability analysis of new generation technology. RESULTS: On the first day, among the top five microbiota species in abundance, four species were found to be identical in BALF and throat samples. Similarly, on the third day, three microbiota species were found to be identical in abundance in both BALF and throat samples. On the first day, 85.16% of microorganisms originated from the throat, 5.79% from the intestines, and 9.05% were unknown. On the third day, 83.52% of microorganisms came from the throat, 4.67% from the intestines, and 11.81% were unknown. Additionally, when regrouping the 46 patients, the results revealed a significant predominance of throat microorganisms in BALF on both the first and third day. Furthermore, as the disease progressed, the proportion of intestinal flora in BALF increased in patients with enterogenic ARDS. CONCLUSIONS: In patients with septic ARDS, the main source of lung microbiota is primarily from the throat. Furthermore, the dynamic trend of the microbiota on the first and third day is essentially consistent.It is important to note that the origin of the intestinal flora does not exclude the possibility of its origin from the throat.

Icariin possesses chondroprotective efficacy in a rat model of dexamethasone-induced cartilage injury through the activation of miR-206 targeting of cathepsin K.

The present study aimed to investigate the articular cartilage and chondrocytes of dexamethasone (DXM)-induced cartilage injuries in rats in response to treatment with icariin, as well as the implicated molecular mechanism. Effects of icariin on bone metabolism and articular cartilage in experimental rats were investigated. Subsequently, the present study assessed dysregulated microRNA (miRNA) in the articular cartilage of experimental rats, and validated the significant miRNA and their targets. Finally, the effects of icariin on chondrocytes in experimental rats and the implicated molecular mechanism were explored. Quantitative polymerase chain reaction demonstrated that icariin significantly reversed DXM-induced bone degradation and stimulated bone regeneration. In addition, some notable changes in articular cartilage were also observed following continuous administration of icariin to DXM-treated rats, including enhanced cartilage area (revealed by safranin-O staining), substantial decrements in serum concentrations of deoxypyridinoline and C-terminal telopeptide of type II collagen, reduced expression of collagen type I and matrix metalloproteinase-13, as well as elevated expression of transforming growth factor-ß. Furthermore, miR-206 was determined to be significantly upregulated in the icariin group compared with the DXM-treated group. A luciferase assay further validated cathepsin K as the target RNA of miR-206. Additionally, icariin (100 µM) facilitated the viability of chondrocytes and reduced apoptotic chondrocytes. More importantly, icariin (100 µM) not only abolished the inhibition effect of DXM on miR-206 expression in chondrocytes, but also eliminated the enhancing effect of DXM on cathepsin K expression. Overall, the present study identified icariin as a novel therapeutic agent in DXM-induced cartilage injury in rats, and revealed that the activation of miR-206 targeting of cathepsin K may be responsible for the chondroprotective efficacy of icariin.