Since the emergence of the COVID-19 pandemic, the effects of SARS-CoV-2 have been extensively researched. While much is already known about the acute phase of the infection, increasing attention has turned to the prolonged symptoms experienced by a subset of individuals, commonly referred to as long COVID-19 patients. This study aims to delve deeper into the immune landscape of patients with prolonged symptoms by implementing single-cell mRNA analysis. A 71-year-old COVID-19 patient presenting with persistent viral pneumonia was recruited, and peripheral blood samples were taken at 3 and 2 years post-acute infection onset. Patients and control peripheral blood mononuclear cells (PBMCs) were isolated and single-cell sequenced. Immune cell population identification was carried out using the ScType script. Three months post-COVID-19 patients’ PBMCs contained a significantly larger immature neutrophil population compared to 2-year and control samples. However, the neutrophil balance shifted towards a more mature profile after 18 months. In addition, a notable increase in the CD8+ NKT-like cells could be observed in the 3-month patient sample as compared to the later one and control. The subsequent change in these cell populations over time may be an indicator of an ongoing failure to clear the SARS-CoV-2 infection and, thus, lead to chronic COVID-19 complications.

Background: The adenoids, primary sites of microbial colonization in the upper airways, can influence the development of various conditions, including otitis media with effusion (OME). Alterations in the adenoid microbiota have been implicated in the pathogenesis of such conditions. Aim: This study aims to utilize 16S rRNA genetic sequencing to identify and compare the bacterial communities on the adenoid surfaces of children with OME and children with healthy middle ears. Additionally, we seek to assess the differences in bacterial diversity between these two groups. Materials and Methods: We collected adenoid surface swabs from forty children, divided into two groups: twenty samples from children with healthy middle ears and twenty samples from children with OME. The V3-V4 hypervariable region of the bacterial 16S rRNA gene was amplified and sequenced using the Illumina MiSeq platform. Alpha and beta diversity indices were calculated, and statistical analyses were performed to identify significant differences in bacterial composition. Results: Alpha diversity analysis, using Pielou’s index, revealed significantly greater evenness in the bacterial communities on the adenoid surfaces of the healthy ear group compared with the OME group. Beta diversity analysis indicated greater variability in the microbial composition of the OME group. The most common bacterial genera in both groups were Haemophilus, Fusobacterium, Streptococcus, Moraxella, and Peptostreptococcus. The healthy ear group was primarily dominated by Haemophilus and Streptococcus, whereas the OME group showed higher abundance of Fusobacterium and Peptostreptococcus. Additionally, the OME group exhibited statistically significant higher levels of Alloprevotella, Peptostreptococcus, Porphyromonas, Johnsonella, Parvimonas, and Bordetella compared with the healthy ear group. Conclusion: Our study identified significant differences in the bacterial composition and diversity on the adenoid surfaces of children with healthy middle ears and those with OME. The OME group exhibited greater microbial variability and higher abundances of specific bacterial genera. These findings suggest that the adenoid surface microbiota may play a role in the pathogenesis of OME. Further research with larger sample sizes and control groups is needed to validate these results and explore potential clinical applications.

Background: The upper respiratory tract harbors diverse communities of commensal, symbiotic, and pathogenic organisms, originating from both the oral and nasopharyngeal microbiota. Among the primary sites of microbial colonization in the upper airways are the adenoids. Alterations in the adenoid microbiota have been implicated in the development of various conditions, including secretory otitis media. Aim: This study aims to employ 16S rRNA genetic sequencing to identify the most common bacteria present on the surface of adenoids in children with otitis media with effusion and compare them with children without pathologies in the tympanic cavity. Additionally, we seek to determine and compare the bacterial diversity in these two study groups. Materials and Methods: A total of nineteen samples from the adenoid surfaces were collected, comprising two groups: thirteen samples from children without middle ear effusion and six samples from children with secretory otitis media. The libraries of the V3–V4 hypervariable region of the bacterial 16S rRNA gene was made and sequenced using MiSeq platform. Results: The most prevalent phyla observed in both groups were Proteobacteria, Firmicutes, and Bacteroidetes. The most common bacterial genera identified in both groups were Haemophilus, Streptococcus, Moraxella, Fusobacterium, and Bordetella, with Fusobacterium and Moraxella being more prevalent in the groups that had no middle ear effusion, while Haemophulus and Streptococcus were more prevalent in the otitis media with effusion group, although not in a statistically significant way. Statistical analysis shows a trend towards bacterial composition and beta diversity being similar between the study groups; however, due to the limited sample size and unevenness between groups, we should approach this data with caution. Conclusion: The lack of prolific difference in bacterial composition between the study groups suggests that the role of the adenoid microbiome in the development of otitis media with effusion may be less significant.

Background and Objectives: the upper respiratory tract harbors the highest bacterial density in the whole respiratory system. Adenoids, which are located in the nasopharynx, are a major site of bacterial colonies in the upper airways. Our goal was to use culture-independent molecular techniques to identify the breadth of bacterial diversity in the adenoid vegetations of children suffering from chronic rhinosinusitis and obstructive sleep apnea. Materials and methods: in total, 21 adenoid samples were investigated using amplification and sequencing of the V3-V4 hypervariable region of the bacterial 16S rRNA gene. Results: among the most common bacterial species found were Veillonella atypica, Fusobactrium nucelatum, Shaalia odontolytica, and Moraxella catarrhalis. Veillonella atypica and Fusbacteriumnucelatum dominated the microbiome in all 21 samples, attributing to more than 60% of all detected genetic material. Conclusions: since both Veillonella atypica and Fusobacterium nucleatum are, predominantly, oral cavity and dental microorganisms, our findings may suggest oral microbiome migration deeper into the oropharynx and nasopharynx where these bacteria colonize adenoid vegetations.

Background: The adenoid surface serves as a potential bacterial reservoir for upper respiratory tract pathologies, including Adenoid Hypertrophy (AH) and Otitis Media with Effusion (OME). While dysbiosis is implicated in the pathogenesis of these conditions, it remains unclear whether the microbiome of children with otitis media differs significantly from those with simple hypertrophy when compared against a healthy baseline. This study aimed to characterize the adenoid microbiome in children with adenoid hypertrophy with and without middle ear effusion, contrasting them with a healthy control group. Methods: We conducted a cross-sectional case–control study involving 58 pediatric participants divided into three groups: adenoid hypertrophy, adenoid hypertrophy and otitis media with effusion and healthy controls. Nasopharyngeal swabs were collected, and bacterial community composition was analyzed using 16S rRNA gene V4 sequencing. Alpha and beta diversity metrics, taxonomic composition, and differential abundance were evaluated. Results: Alpha diversity was significantly reduced in both disease groups compared to healthy controls (p < 0.001), indicating a collapse of microbial richness and evenness. Beta diversity analysis revealed a distinct separation between healthy and diseased cohorts; however, the microbial profiles of the AH and AH with OME groups were nearly identical. Taxonomic analysis demonstrated that disease was characterized by the depletion of health-associated commensals, specifically Veillonella, Actinomyces, and Gemella, and a concomitant expansion of Fusobacterium, Haemophilus, and Streptococcus. Conclusions: Adenoid hypertrophy is associated with a profound dysbiotic shift characterized by the loss of protective commensal flora and the dominance of pathobionts. The lack of significant microbial differentiation between the AH and AH with OME groups suggests that the adenoid surface acts as a centralized reservoir of dysbiosis, the composition of which is conserved regardless of the presence of middle ear effusion. These findings highlight the importance of restoring the commensal microbiome in the management of chronic adenoid disease.

Chemotherapy with cisplatin (CDDP) and etoposide (ETO) is the standard treatment for gastroenteropancreatic neuroendocrine carcinoma (GEP-NEC). Despite high initial response rates, treatment-related toxicity and acquired resistance remain significant clinical challenges. No molecularly targeted therapies are currently established for this aggressive cancer. Here, we evaluated Aurora kinase inhibition with alisertib (ALI) as a synthetic lethality strategy in ARID1A-deficient GEP-NEC. Subcutaneous and orthotopic xenograft models were established in immunodeficient mice using the GEP-NEC-derived NT-38 cell line, and the therapeutic efficacy of ALI was compared with CDDP + ETO. Tumor responses were assessed by immunohistochemistry, Western blotting, and RNA sequencing. To confirm ARID1A dependency, transient knockdown was induced in the pancreatic neuroendocrine NT-18LM cell line, demonstrating that ALI sensitivity is significantly enhanced in ARID1A-deficient cells. ALI achieved antitumor efficacy comparable to chemotherapy and was well tolerated, with minimal weight loss relative to CDDP + ETO. Distant metastases, an early feature of GEP-NEC, developed in five animals over six weeks, two of which were treated with ALI and three controls. Transcriptomic profiling revealed convergence of both treatments on signal transduction, focal adhesion, receptor tyrosine kinase, and VEGFA-VEGFR2 signaling, while ALI uniquely enriched pathways related to pancreatic secretion, lipid metabolism, protein processing in the endoplasmic reticulum, and extracellular matrix organization. These findings establish Aurora kinase inhibition as mechanistically distinct and selectively effective in ARID1A-deficient GEP-NEC. Given its efficacy, favorable tolerability, and ARID1A-dependent specificity, ALI may represent a promising alternative to platinum-based chemotherapy, offering a strong rationale for further development of mechanism-driven combination strategies for GEP-NEC.