Hongsheng Wang

Fibroblasts are heterogeneous stromal cells with remarkable lineage plasticity, generating distinct subsets that orchestrate either regenerative repair or fibrotic remodeling. However, how the pro-fibrotic fibroblast state is molecularly stabilized after activation remains poorly defined. Here, we identify the long noncoding RNA SNHG26 as an essential regulator of fibroblast fate maintenance and fibrogenic activity. SNHG26 is markedly enriched in CD90+ fibroblasts within human hypertrophic scars and keloids. Genetic deletion of Snhg26 in fibroblasts or antisense oligonucleotide–mediated silencing disrupts mesenchymal identity, suppresses extracellular matrix synthesis, and dramatically attenuates scar formation in murine and xenograft models. Single-cell transcriptomics reveal that loss of SNHG26 promotes a mesenchymal-to-papillary fibroblast transition, indicating that SNHG26 enforces lineage stability within the scar-forming fibroblast pool. Mechanistically, SNHG26 functions as a nuclear scaffold that binds the RNA-binding protein PTBP1, enabling PTBP1-directed alternative polyadenylation of AKT3 . This interaction favors distal polyadenylation site usage, generating a long 3′UTR AKT3 isoform with enhanced stability, thereby sustaining AKT3 expression and downstream pro-fibrotic signaling. Upstream, TNFα–ERK–STAT3 signaling induces SNHG26 transcription, linking chronic inflammation to persistent posttranscriptional activation of fibrogenic pathways. Collectively, these findings define a lncRNA-based regulatory checkpoint in which the SNHG26 –PTBP1–AKT3 axis stabilizes mesenchymal fibroblast identity and drives extracellular matrix accumulation. Targeting SNHG26 offers a promising therapeutic strategy for preventing pathological scar formation.

[This corrects the article DOI: 10.3389/fmicb.2026.1810237.].

Introduction: Non-tuberculous mycobacteria constitute a rapidly emerging class of opportunistic pathogens with escalating clinical significance globally. We recently characterized two novel species within the Mycobacterium gordonae complex-Mycobacterium camsae and Mycobacterium pumcae-both isolated from human cutaneous infections. Methods: Comprehensive phenotypic and transcriptomic analyses were conducted to elucidate their pathobiological properties. Comparative analysis included M. gordonae (closest phylogenetic relative), M. marinum (slow-growing reference), and M. abscessus (rapid-growing reference). Growth kinetics, intracellular survival, cytokine induction, and bacterial and host transcriptomic profiling were characterized. Results: Both novel species exhibited attenuated growth kinetics characteristic of the M. gordonae complex. Notably, M. pumcae demonstrated enhanced inflammatory potential resembling M. marinum , while M. camsae displayed more subdued host responses akin to M. gordonae . Bacterial transcriptomic profiling unveiled distinct adaptive strategies: M. pumcae preferentially upregulated stress response regulons and iron homeostasis pathways, whereas M. camsae emphasized cell envelope biosynthesis and core metabolic reconfiguration. Host transcriptomic analysis at 24 h post-infection revealed differential temporal dynamics: the rapid-growing M. abscessus predominantly triggered immunometabolic reprogramming pathways, while slow-growing mycobacteria ( M. camsae, M. pumcae , and M. gordonae ) were still eliciting robust innate immune recognition signatures. Discussion: This investigation provides the first systematic characterization of host-pathogen interactions within these newly described M. gordonae complex members, establishing a mechanistic foundation for understanding their distinct pathogenic trajectories and informing species-specific diagnostic and therapeutic approaches.

Background: Chronic diabetic ulcers exhibit a dysregulated immune microenvironment characterized by aberrant leukocyte responses and dysfunctional fibroblast activation. Identifying molecular regulators of fibroblast-driven immune responses may provide therapeutic targets to restore effective wound repair in these chronic wounds. Methods: Bulk RNA-seq (GSE199939) and scRNA-seq (GSE165816) datasets from human DFUs were integrated to identify alterations in MFGE8 expression in wound fibroblasts. These findings were validated by immunofluorescence staining and RT-qPCR in db/db mouse wounds. Cytokine screening assays were performed to identify upstream regulators of MFGE8 dysregulation. The effects of MFGE8 on fibroblast immune activity were assessed by RT-qPCR, Western blotting, ELISA, and Transwell migration assays. To evaluate its therapeutic potential in vivo , a single-dose of MFGE8-prestimulatedd fibroblasts were locally delivered into db/db mouse wounds, followed by wound healing assessment, immunofluorescence staining, and transcriptomic analysis. Results: MFGE8 was markedly downregulated in fibroblasts from DFUs. TNF-α and IL-1α robustly induced MFGE8 expression in dermal fibroblasts. Recombinant MFGE8 reprogrammed fibroblasts toward a pro-inflammatory phenotype, significantly increasing the expression of IL1B, IL6, CXCL8, CXCL1, and CCL2, and enhancing macrophage migration in vitro . In db/db mice, MFGE8-prestimulated fibroblasts increased macrophage infiltration, activated inflammatory and pro-repair transcriptional programs, and accelerated wound closure. Conclusion: These findings establish MFGE8 as a key regulator of fibroblast inflammatory competence and support a cell-based immunomodulatory strategy to promote healing in chronic diabetic wounds.

Mycobacterium nanjing sp. nov. Isolated from Cutaneous Infection, China

Background: In resource-limited areas, severe shortages of radiologists contribute to high rates of missed pulmonary tuberculosis (PTB) cases when relying solely on conventional chest X-ray (CXR). Although artificial intelligence–powered computer-aided detection (CAD) has proven effective in PTB diagnosis, its real-world performance remains underexplored. Objective: This study aimed to evaluate the real-world diagnostic yield of CAD technology as a triage tool for detecting PTB in primary health care facilities in high-burden areas. Methods: We conducted a retrospective paired-design diagnostic yield study using CXR images collected from 7 county- and 32 township-level health care facilities in Yichang city between 2022 and 2024 year. All images were retrospectively reprocessed with CAD software (JF CXR-1), and the original reports interpreted by radiologists at the time of patient admission were extracted. CAD and radiologist performances were compared using 2 primary evaluation indicators—diagnostic yield among diagnosed cases (DYD) and positive predictive value (PPV). Subgroup analysis (by region, age, sex, health care facility tier, and patient category) and sensitivity analysis were conducted to assess the robustness of the results. Results: Among 93,319 enrolled study patients, including 273 (0.3%) bacteriologically confirmed PTB cases, CAD demonstrated a substantially higher DYD (229/273, 83.9%) than radiologists (70/273, 25.6%), although the PPV was much lower (1.70% vs 10.31%). This high-sensitivity performance achieved an 85.5% (79,804/93,319) reduction (only 13,515 instead of 93,319 CXRs) in radiologist workload via selective review of CAD-positive images, without missing any radiologist-identified PTB cases. Furthermore, probability scores greater than 0.75 were a key threshold for identifying high-risk patients with PTB, and these patients were prioritized for radiologist review. Subgroup analysis further revealed that CAD outperformed radiologists in identifying PTB cases across all scenarios, despite some heterogeneity. CAD performance was significantly better in township-level medical facilities (DYD: 86.7%; PPV: 2%) than in county-level hospitals (DYD: 62.5%; PPV: 0.6%). Conclusions: CAD technology is valuable for detecting PTB in primary health care facilities. Combined with a tiered artificial intelligence prescreening with selective human review strategy, this approach effectively alleviates the workload of radiologists in resource-constrained regions, offering a scalable solution for tuberculosis prevention and control.

Two slow-growing nontuberculous mycobacterial strains were isolated from clinical skin lesions in Jiangsu, PR China, and identified as novel species within the genus Mycobacterium . The bacterial colonies exhibited scotochromogenic pigmentation and rod-shaped morphology, and they were classified as acid-fast bacilli. Phylogenetic analysis indicated that the two strains were closely related to Mycobacterium gordonae . The two strains, X7091 ^T and Z3061 ^T , exhibited average nucleotide identity and in silico DNA–DNA hybridization values below the threshold for species delineation when compared with other type strains of M. gordonae complex. Therefore, two novel Mycobacterium species are proposed: Mycobacterium camsae sp. nov., with the type strain being X7091 ^T (=CGMCC 1.90336 ^T =JCM 37414 ^T ), and Mycobacterium pumcae sp. nov., with the type strain being Z3061 ^T (=CGMCC 1.90337 ^T =JCM 37415 ^T ).

This study evaluated the diagnostic value and therapeutic efficacy assessment potential of the interferon-γ release assay T-SPOT.TB in cutaneous Mycobacterium marinum infections. A total of 145 patients diagnosed at the Institute of Dermatology, Chinese Academy of Medical Sciences (2020–2024), excluding tuberculosis cases, were retrospectively analysed. Clinical data including demographics, underlying diseases, pathology, microbiological culture, molecular identification, T-SPOT.TB results, treatment regimens, and outcomes were collected. T-SPOT.TB results before treatment, and at 3 and 6 months post-treatment, were compared to assess its diagnostic and monitoring utility. The baseline T-SPOT.TB positivity rate was 71% (95% CI: 63.2–77.8%). Among 17 patients retested at 3 months, positivity was 64.7% (p = 0.125), with median spot-forming cells (SFCs) significantly decreasing from 20.0 (IQR 8.5–41.0) to 8.0 (IQR 2.5–28.0) (p = 0.0007). Among 27 patients retested at 6 months, positivity was 59.3% (p = 0.344), with median SFCs decreasing from 12.0 (IQR 5.0–30.0) to 8.0 (IQR 3.0–13.0) (p = 0.0006). No significant difference in positivity rates was observed between 3 and 6 months post-treatment. The T-SPOT.TB assay shows significant diagnostic value for cutaneous M. marinum infections and facilitates early diagnosis. Declining SFC counts post-treatment provide useful reference for evaluating therapeutic response.