Recent pan-cancer analyses have identified Complement Factor H (CFH) expression as an immune-related and prognostic biomarker. However, interpretation of CFH transcriptional data requires consideration of isoform specificity. The CFH gene encodes both full-length factor H (FH) and the biologically active splice isoform factor H-like 1 (FHL-1), which differ in structure and tissue localization. Common transcriptional and knockdown approaches do not distinguish between these isoforms, potentially introducing biological heterogeneity into diagnostic and prognostic assessments. Isoform-resolved analyses may therefore enhance the specificity and clinical utility of CFH-based biomarkers in oncology.

The cornea is the outermost layer of the eye, most vulnerable to injury including from chemical exposure, either environmental, industrial or chemical weapons. For example, exposure of the eye to sulfur mustard (SM) can cause mustard gas keratopathy, resulting in devastating consequences for vision. Available treatments for corneal mustard keratopathy are either ineffective, or if used for a prolonged time, have deleterious side effects. Here, we aimed to harness the anti-inflammatory and anti-angiogenic peptide angiotensin-(1-7), known as Ang-(1-7), that is derived from the renin-angiotensin system (RAS). We designed and developed a protein-like polymer (PLP) displaying a brush of norleucine modified Ang (1-7) peptides (NLE Ang (1-7) PLP), which is a more potent derivative of Ang-(1-7), for administration as an eye drop. In a mouse model of nitrogen mustard (NM)-induced corneal injury, topical treatment and intraperitoneal (i.p.) injection of NLE Ang (1-7) PLP persistently minimized: (i) corneal haze; (ii) edema; (iii), expression of pro-inflammatory and pro-angiogenic genes; and (iv) neovascularization and conjunctivalization as evidenced after a prolonged treatment and recovery period. Collectively, our observations have demonstrated the efficacy of this novel polymer proteomimetic based eye drop treatment in reducing chemical agent-induced corneal injury as well as indicating its potential application in other ocular surface diseases associated with inflammation and angiogenesis.

A 29-year-old man presented to Department of Ophthalmology, Affiliated Hospital of Nantong University with a 14-day history of redness and decreased vision in the right eye. Uncorrected visual acuity in the right eye was 0.02 (not improvable with correction). Slit-lamp examination revealed mutton-fat keratic precipitates on the corneal endothelium, anterior chamber inflammation, and two iris masses. Systemic evaluation suggested cervical lymph node tuberculosis, and empirical anti-tuberculosis therapy was initiated. After one month of treatment, the original iris lesion regressed, but new nodules developed. A diagnosis of iris tuberculous granuloma was suspected, and surgical excision of the iris lesions was performed. Histopathological examination demonstrated granulomatous nodules with chronic inflammatory cell infiltration. Furthermore, polymerase chain reaction analysis of vitreous fluid was positive for Mycobacterium tuberculosis DNA, confirming the diagnosis of iris tuberculous granuloma. Following continued systemic anti-tuberculosis therapy, the best-corrected visual acuity improved from 0.02 to 0.8, and the intraocular inflammation was completely controlled.

Pseudomonas aeruginosa (PA)-induced bacterial keratitis represents one of the most severe corneal infections usually accompanied by prominent inflammatory infiltration. Clinical fluoroquinolone-based therapies yield unfavorable therapeutic outcomes due to the insufficient ocular bioavailability and compromised anti-inflammatory efficacy. In the present work, we report a molecularly engineering strategy to conjugate ciprofloxacin (Cip) with a self-immolative carbonyl sulfide (COS)/hydrogen sulfide (H2S) donating motif. The resulting prodrug (termed ASCip) could spontaneously self-assemble into nanosheets in aqueous solution, thereby improving ocular surface retention and drug bioavailability. Importantly, ASCip could be specifically activated by aminopeptidase N (APN), which is overexpressed at the inflammatory sites, enabling the controlled and simultaneous release of Cip and H2S, to realize antibacterial and anti-inflammatory effects. In vitro evaluations of this carrier-free nanoantibiotic revealed potent antibacterial activity against PA upon APN activation, favorable biocompatibility, and significant anti-inflammatory effects via modulating the inflammatory mediators and promoting macrophage polarization towards the anti-inflammatory M2 phenotype. In a murine model of PA-infected keratitis, the nanoantibiotic efficiently eradicated pathogens, attenuated ocular inflammation, and remarkably accelerated corneal repair, providing a promising strategy to improve the efficacy of fluoroquinolone-based therapies against bacterial keratitis. More importantly, the strategy developed provides a versatile way to co-deliver COS/H2S with other functional motifs.

Severe bacterial enteritis causes significant clinical manifestations and has a widespread impact, while conventional antibiotic treatments have exacerbated antimicrobial resistance, underscoring the urgent need for effective therapeutic alternatives. To address this critical gap, we develop a biohybrid therapeutic platform that combines antibacterial ergothioneine-capped gold nanoclusters (EGT-Au NCs) with Spirulina for oral delivery. EGT alone has no antibacterial activity, yet the engineered EGT-Au NCs exhibit antibacterial efficacy approaching that of conventional antibiotics, while also minimizing the risk of resistance. Beyond their potent antibacterial activity, EGT-Au NCs display exceptional biocompatibility, negligible hemolytic toxicity, enhanced anti-inflammatory and antioxidant properties that collectively promote host recovery. By harnessing the natural gastrointestinal adhesion and prolonged retention of Spirulina (EGT-Au NCs@SP), this system enhances localized antimicrobial efficacy. In vivo studies confirm the EGT-Au NCs@SP platform exhibits robust antibacterial performance, effective inflammation suppression, and enhanced intestinal repair in Salmonella Typhimurium infection models. Mechanistic investigations demonstrate that EGT-Au NCs exert a sophisticated antibacterial mechanism, actively disarming bacteria by impairing flagellar assembly, disrupting biofilm formation, attenuating bacterial virulence, and significantly reducing epithelial invasion. Notably, Salmonella Typhimurium strains that acquired resistance to conventional antibiotics remainsensitive to EGT-Au NCs. This multifunctional biohybrid nanoplatform represents a safe and effective oral therapeutic strategy, offering a promising alternative to antibiotics for combating gastrointestinal infections and antimicrobial resistance.

Masquerade syndrome is a collective term for various ocular diseases presenting with clinical features resembling intraocular inflammation. Delays in definitive diagnosis and treatment can not only lead to irreversible vision loss but also impact the patient's prognosis regarding survival. We report the case of a 26-year-old male patient who presented with impaired vision in the right eye, which had persisted for six months; neuroretinitis was diagnosed. Although infectious neuroretinitis was suspected, tests for pathogens such as Mycobacterium tuberculosis, Toxoplasma, Toxocara, and Bartonella were all negative. Treatment with betamethasone eye drops alone resulted in a fluctuating course of improvement and worsening of the neuroretinitis. Ten months after the initial visit, the patient's headache-which had begun one month prior-worsened and was accompanied by vomiting and a pulsating sensation, leading to a consultation with our department of neurosurgery. Magnetic resonance imaging (MRI) revealed a lobulated mass extending from the right midbrain to the right thalamus, causing narrowing of the cerebral aqueduct and hydrocephalus. Four days after the neurosurgical consultation, the patient underwent endoscopic third ventriculostomy (ETV) and a brain biopsy, leading to a definitive diagnosis of germinoma. The headache improved the day after surgery, and by one month after the operation, the hydrocephalus had resolved, while neuroretinitis also showed improvement. The patient received carboplatin and etoposide (CARE) treatment in the second, third, and fourth months post-surgery, whole-ventricle radiotherapy (24 Gy/15 fractions) in the fifth and sixth months, and ifosfamide (IFO), cisplatin (CDDP), and etoposide (VP-16) (ICE) treatment in the seventh, ninth, and 11th months. No recurrence of the brain tumor has been observed since then. At the final follow-up visit five years post-surgery, the neuroretinitis had resolved. When neuroretinitis is observed in a young patient and infectious causes have been ruled out, intracranial germinoma should be considered in the differential diagnosis.

Ocular involvement is common in systemic rheumatic diseases and may precede or reflect systemic activity, serving as an important diagnostic clue. Inflammation can affect any ocular structure, with presentations ranging from mild to vision-threatening. Early recognition is critical, as ocular findings can guide diagnosis and management. A systematic approach combining clinical evaluation, imaging, and laboratory testing is essential to identify disease-specific patterns. Advances in immunomodulatory and biologic therapies have improved outcomes. Optimal care requires a multidisciplinary approach, with close collaboration among ophthalmologists, rheumatologists, and other specialists to ensure accurate diagnosis, coordinated treatment, and preservation of visual function.

Sjögren disease (SjD) is an autoimmune disease driven by autoimmune CD4[+]T cells that leads to an immune-mediated loss of lacrimal glands (LG). Meibomian glands are lipid-producing glands in the eyelids that help prevent tear evaporation. While the role of T cells in LG-mediated destruction is well established, it is unknown whether pathogenic T cells can cause MG dysfunction (MGD). Herein, we investigated whether autoimmune CD4[+]T cells induce MGD and characterized the pathophysiologic mechanisms using an adoptive transfer model. T cells were isolated from CD25KO (KO[CD4]) or wild-type (WT[CD4]) mice and transferred into Rag1KO mice. In comparison, KO cells were co-adoptively transferred with WT regulatory T cells (KO[CD4] + WT[Tregs]). Our results demonstrate that CD25KO CD4[+]T recipients had MG dropout, CD4[+]IFN-γ[+] infiltration, increased MHC II presentation within the periglandular area, MG fibrosis, decreased lipid production, and upregulation of pathways related to inflammation, including Type II interferon signaling. Rag1KO, WT[CD4], and KO[CD4] + WT[Tregs] recipients exhibited minimal inflammation in the periglandular MG area. These results indicate that autoimmune CD4[+]T cells are sufficient to cause MGD, and healthy young regulatory T cells can prevent T-cell-mediated damage. Our findings provide mechanistic insights into the pathogenesis of autoimmune SjD and could impact how patients are managed in the clinic.

The cornea is among the most densely innervated tissues in the body and depends on intact sensory and autonomic innervation to maintain epithelial integrity, tear film homeostasis, and ocular surface defense. Corneal nerve injury may occur after surgery, infection, inflammation, trauma, or systemic disease and can lead to reduced corneal sensitivity, impaired epithelial healing, dry eye, neuropathic pain, and neurotrophic keratopathy. Effective management requires both treatment of the underlying cause and restoration of a microenvironment permissive for reinnervation. This review examines the mechanisms underlying corneal nerve injury and repair, with emphasis on therapeutic strategies relevant to clinical translation. These include anti-inflammatory and immunomodulatory agents, growth factors and cytokines, blood-derived products, extracellular matrix-based therapies, stem cell- and secretome-based approaches, surgical neurotization, and physical stimulation modalities. We also highlight emerging challenges in the field, including the gap between structural nerve regeneration and functional recovery, limitations in clinical evidence, and barriers to therapeutic accessibility and implementation.