Rationale: Klebsiella pneumoniae (K. pneumoniae, KP) are divided into two types: classic K. pneumoniae (cKP) and hypervirulent K. pneumoniae (hvKP). hvKP causes liver abscess and metastatic infection. Here, we report one case with pyogenic liver abscess (PLA) and endogenous endophthalmitis (EE) due to a relatively rarely reported serotype of K. pneumoniae in China. Patient Concerns: An 80-year old man presented with nausea, vomiting, and epigastric discomfort for 2 weeks. Diagnoses: PLA was identified by CT scan and abdominal ultrasound. Urgent ophthalmologic consultation was performed. B-scan ocular ultrasound was done and he was diagnosed as EE. Interventions: Antibiotic treatment, intravitreal injection of eyes and eye drops were given. Percutaneous needle aspiration, evisceration, and drainage of the right eye were performed. Outcomes: Cultures of the blood, the aspirated pus from the liver abscess, and the contents of the eyeball all yielded K. pneumoniae with a positive string test. The capsular serotype was K64. According to the existence of multiple virulence genes and the severe invasive clinical manifestation, this strain is regarded as a hvKp strain. Multilocus sequence typing (MLST) revealed the sequence type (ST) of this strain was K64-ST1764. Antimicrobial resistance genes, bla_NDM-1 and bla_KPC-2, were not detected in the genome. The patient lost his eyesight but his symptoms subsided. During 15 months follow-up, the result was satisfactory. Lessons: Here, we report one case with PLA due to a relatively rarely reported serotype of K. pneumoniae in China. This K64 K. pneumoniae strain is confirmed as hvKp by multiple methods. It is noteworthy that the sequence type is K64-ST1764 instead of the commonest ST11. Moreover, this strain is not considered a K. pneumoniae carbapenemase-producing K. pneumoniae (KPC-Kp) or a carbapenem-resistant K. pneumoniae (CRKP) as it is usually. Further follow-up and research are required to investigate this strain.

Tissue‐resident memory T (T_RM) cells are a recently discovered subpopulation of memory T cells that reside in non‐lymphoid tissues such as the intestine and skin and do not enter the bloodstream. The intestine encounters numerous pathogens daily. Intestinal mucosal immunity requires a balance between immune responses to pathogens and tolerance to food antigens and symbiotic microbiota. Therefore, intestinal T_RM cells exhibit unique characteristics. In healthy intestines, T_RM cells induce necessary inflammation to strengthen the intestinal barrier and inhibit bacterial translocation. During intestinal infections, T_RM cells rapidly eliminate pathogens by proliferating, releasing cytokines, and recruiting other immune cells. Moreover, certain T_RM cell subsets may have regulatory functions. The involvement of T_RM cells in inflammatory bowel disease (IBD) is increasingly recognized as a critical factor. In IBD, the number of pro‐inflammatory T_RM cells increases, whereas the number of regulatory subgroups decreases. Additionally, the classic markers, CD69 and CD103, are not ideal for intestinal T_RM cells. Here, we review the phenotype, development, maintenance, and function of intestinal T_RM cells, as well as the latest findings in the context of IBD. Further understanding of the function of intestinal T_RM cells and distinguishing their subgroups is crucial for developing therapeutic strategies to target these cells.

The clinicopathological features of early gastric cancer (EGC) with mixed-type histology (differentiated and undifferentiated) are incompletely understood, and the capacity of endoscopic submucosal dissection (ESD) to treat mixed-type cancer remains controversial. This systematic review analyzed the rate of lymph node metastasis (LNM) in mixed-type EGC. We gathered articles published up to February 21, 2021, that analyzed the relationship between LNM and mixed-type EGC from Embase, PubMed, and Web of Science. The primary outcome was the LNM rate associated with different histological types of EGC, and the secondary outcomes were the odds ratios (ORs) for LNM risk factors among EGC patients. From the 24 studies included in this meta-analysis, the overall rate of LNM in predominantly differentiated mixed-type (MD) EGC was 12%, whereas the LNM rate in predominantly undifferentiated mixed-type (MU) EGC was 22%. We further divided these studies into 2 groups according to the depth of invasion. In mixed-type mucosal EGC, the pooled LNM rate was 15%; in submucosal EGC, the rate was 33% for MU, which was higher than the rates for pure types (pure differentiated type, 13%; pure undifferentiated type, 21%; p<0.05). The LNM rate of MD was 20%, it was higher than those of the pure differentiated type and nearly the same as pure undifferentiated type. Other pooled statistics showed that submucosal invasion, pure undifferentiated EGC, and mixed-type EGC were independent risk factors for LNM. This meta-analysis showed that MD submucosal EGC has a high rate of LNM and is highly correlated with LNM; thus, the management of MD EGC as purely differentiated EGC according to the indications for ESD is inappropriate, and the mixed type should be added as a parameter in these indications.

Background: Inflammatory bowel disease (IBD) is a common chronic inflammatory illness affecting the gastrointestinal tract. Cholangiocarcinoma (CCA) comprises a group of highly heterogeneous cancers originating from the biliary tract. Epidemiological evidence suggests a positive correlation between IBD and CCA. However, the pathological mechanisms are unestablished. This research aimed to identify common biomarkers and immune infiltration features in IBD and CCA to support early detection and development of targeted therapies. Methods: Based on transcriptomic data from the GEO and TCGA databases, candidate genes were obtained by integrating differentially expressed genes (DEGs) with key modules derived from weighted gene co-expression network analysis (WGCNA). Hub genes were subsequently screened using four machine learning algorithms. A comprehensive validation of the hub genes (LCN2 and DUOX2) was performed through receiver operating characteristic (ROC) curve analysis, survival analysis, immune infiltration profiling (CIBERSORT), and drug sensitivity assessment. Results: By overlapping DEGs with key WGCNA modules, thirteen candidate genes were obtained. Eight common hub genes (CCL11, CCL20, DUOX2, DUOXA2, LCN2, NOS2, PDZK1IP1, and TRIM40) were ultimately selected through integrated ML approaches. ROC analysis demonstrated that LCN2 and DUOX2 exhibited excellent diagnostic performance for both IBD and CCA, as reflected by high area under the curve values. Conclusion: This research confirmed that LCN2 and DUOX2 are key shared genes in the comorbidity of IBD and CCA. It also highlighted the distinct immune infiltration features between the two diseases. These findings provide novel perspectives on the pathogenesis of IBD and CCA, thereby offering a basis for early screening of CCA in individuals with IBD.

Autoimmune gastritis (AIG) is a chronic disease characterized by specific immune damage to the gastric mucosa. Previous studies have mostly focused on the single immune pathway mainly mediated by T cells, but the synergistic role of humoral immunity in disease progression cannot be ignored. This article systematically reviews the immunological mechanism of AIG, and analyzes the inflammatory cascade immune mechanism centered on the self-attack of gastric parietal cells mediated by CD4 ⁺ T, with the pro-inflammatory roles of Th1/Th17 cells and defective suppressive function of Tregs as a supplement. This article emphasizes the imbalance between humoral and cellular immunity, including the pathogenic potential of autoantibodies and the synergistic role of T-B cells in promoting inflammation. Furthermore, while existing animal models (including genetic modification, lymphopenic, and non-lymphopenic models) can replicate features of human AIG such as gastric gland atrophy, they exhibit significant limitations regarding the mechanism of T-B cell collaboration, differences in cancer risk, and species specificity. This article systematically clarifies that AIG results from an imbalance between cellular and humoral immunity, providing a theoretical basis for targeted immunotherapy strategies.