Changjong Moon

Lee E, et al. J Vet Sci. 2027 ;28:e2. https://doi.org/10.4142/jvs.26210

Patients with atopic dermatitis (AD) often suffer from mental health issues such as depression. Crosstalk between proinflammatory cytokines and hippocampal circuits may be a potent risk factor for behavioral abnormalities in depression, including anxiety, and mood disorders, which negatively controlled hippocampal neurogenesis via the upregulation of several proinflammatory cytokines. However, the mechanisms by which AD notably contribute to the development of depression are poorly understood. We found that increased IL-6 and soluble IL-6Rα (sIL-6Rα) in the peripheral blood specifically disrupted the blood-brain barrier and triggered depressive symptoms in NC/Tnd mice with spontaneous AD. The skin severity and depressive behavior correlated with markedly reduced numbers of doublecortin (DCX)-positive immature neurons in the hippocampus. Parabiotic pairs of mice with AD and unaffected mice showed disruption of hippocampal neurogenesis in the unaffected mice. Injection of neutralizing mAb against IL-6 significantly improved depressive behavioral signs and hippocampal neurogenesis. Furthermore, house dust mite-induced dermatitis gave rise to no depressive phenotypes in IL-6-deficient mice. Single-cell RNA sequencing analysis showed high expression of IL-6Rβ, unlike IL-6Rα, in hippocampal cells isolated from NC/Tnd mice. Addition of IL-6 and sIL-6Rα to neuronal progenitor cells cultured from the murine hippocampal dentate gyrus significantly reduced the number of DCX-positive cells, whereas IL-6 alone had no effect. Overall, these findings suggest that increased peripheral blood IL-6 and sIL-6Rα following atopic inflammation inhibits hippocampal immature neurogenesis via IL-6Rβ and is a critical risk factor for the development of mood and behavioral disorders in AD.

Kim J, et al. J Vet Sci. 2026 ;27:e71. https://doi.org/10.4142/jvs.25286

Jang H, et al. J Vet Sci. 2026 ;27:e35. https://doi.org/10.4142/jvs.26012

The Philippine Darag native chicken demonstrates favorable health and welfare indicators that are comparable to those of slow-growing Redbro broiler chickens. This study analyzed the histomorphometric characteristics of the small intestinal segments in these 2 breeds over an 8-week growth period. Small intestinal samples were collected weekly from both breeds from week 1 to week 8. Tissues were fixed and stained with hematoxylin and eosin, and analysis was performed using ImageJ to quantify villus height (VH), crypt depth (CD), villus-to-crypt ratio, epithelial thickness (ET), mucosal thickness (MT), and tunica muscularis thickness. The effects of age and breed, as well as their correlations with body weight, relative organ weight, and total feed consumption, were evaluated using a mixed-effects model, Pearson’s correlation, and multiple linear regression. Additionally, a binomial logistic regression model was applied to examine the occurrence of zigzag villi patterns. All histomorphometric parameters exhibited a significant increase with age. Redbro displayed earlier and more rapid intestinal development, whereas Darag demonstrated slower yet more comprehensive maturation across parameters. The zigzag villi pattern emerged earlier in Redbro, particularly in the jejunum. The identified age- and breed-specific differences in small intestinal development suggest that intestinal adaptation may contribute to variations in growth performance and may indicate potential advantages to Darag in low-input production systems. Furthermore, the significant correlations of VH, CD, ET, and MT with production indices indicate that growth performance is influenced by a complex interaction of absorptive capacity, intestinal health, and motility, rather than solely by villus surface area.

Bartonella species, which are globally distributed gram-negative facultative intracellular bacteria, can infect a diverse range of hosts. Rodents are crucial for the maintenance and dissemination of Bartonella spp., several of which are pathogenic to humans. Although Bartonella infections have been studied in various animals, Bartonella genetic diversity in wild rodents and their fleas has not been investigated. This study examined Bartonella prevalence and genetic diversity in wild rodents and fleas from South Korea in 2023-2024. Bartonella was predominantly detected in the rodent species, Apodemus agrarius. A total of 278 rodent blood and spleen samples, along with 22 pools derived from 33 fleas, were analyzed for the presence of Bartonella DNA. Quantitative real-time PCR (qPCR), targeting the small stable RNA A gene, identified Bartonella spp. in 133 rodents (47.84%) and 11 flea pools (50%). Phylogenetic analysis was conducted using partial sequences of the Bartonella citrate synthase gene and the 16S-23S rRNA internal transcribed spacer region. Sequencing and phylogenetic analysis using the maximum likelihood method identified eight Bartonella spp. in these rodents, including Bartonella grahamii and Bartonella elizabethae, which are pathogenic to humans. Bartonella taylorii was the species most frequently detected in the rodents. Half of the flea pools analyzed using qPCR were positive for Bartonella spp. Bartonella grahamii and taylorii were identified as the dominant species in fleas. These findings suggest that in South Korea, wild rodents serve as natural reservoirs for a diverse range of Bartonella spp., with fleas enhancing the risk of zoonotic disease transmission to humans, necessitating caution to prevent infection. This study outlines a potential vector-host relationship concerning Bartonella spp. transmission and persistence in South Korea.

Background: Neuroplasticity and synaptic homeostasis are essential in regulating neuronal activity and behavioral functions within the hippocampus. Alzheimer’s disease (AD) is characterized by progressive cognitive decline, pathological accumulation of amyloid β (Aβ) plaques and tau neurofibrillary tangles, neuroinflammation, and synaptic dysfunction. However, the temporal progression of neuroplasticity-related impairments in the hippocampus, a region particularly vulnerable to AD pathology, is not completely understood. Methods: This study examined age-dependent changes in behavioral performance and hippocampal structural plasticity in the 5×FAD (five familial Alzheimer’s disease) mouse model at 3, 6, and 12 months of age. Results: The 5×FAD mice exhibited progressive impairments in fine motor coordination and hippocampal-dependent working memory compared to control. Corresponding increases were observed in the accumulation of Aβ and phosphorylated tau, glial activation, and inflammatory cytokine production in the hippocampus across all time points. Golgi staining revealed significant age-related reductions in dendritic complexity, including fiber crossing counts, total dendritic length, and branch points in the cornu ammonis 1 (CA1) and dentate gyrus (DG) hippocampal subregions. Dendritic spine density and morphology exhibited significant alterations in the CA1 apical/basal and DG subregions with advancing age. Furthermore, the expression of synaptic proteins, including activity-regulated cytoskeleton-associated protein (Arc) and postsynaptic density protein-95 (PSD-95), significantly declined at 6 and 12 months of age. Conclusions: Our findings suggest a potential relationship between AD-related protein pathology, neuroinflammation, and structural plasticity impairments in the hippocampus. Collectively, these changes may contribute to disrupted synaptic transmission and behavioral deficits associated with AD pathology.