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This study investigates the potential of novel probiotic strains, a 1:1 mix of Bifidobacterium longum RAPO and Lactiplantibacillus plantarum LRCC5264, to alleviate atopic dermatitis (AD). In vitro, the probiotics at 1 × 106 CFU/mL increased anti-inflammatory (interleukin-6; IL6) and reduced pro-inflammatory (IL9) cytokine expression in LPS-stimulated RAW 264.7 cells. In an 2,4-dinitrochlorobenzene-induced AD mouse model, treatment with the probiotics (1 × 106 CFU/day) for eight weeks exhibited significant reductions in dermatitis score, plasma immunoglobulin E, transepidermal water loss, and mRNA expression of ceramidase in the skin. Furthermore, the probiotic consumption suppressed Il9 mRNA expression in the skin and reduced eotaxin-1, eosinophil infiltration, and epidermal thickness. Gut microbiota analysis revealed probiotic consumption increased relative abundances of Alistipes and Ruminococcaceae_uncultured, with a negative association with immune responses and skin barrier functions. These results demonstrate the potential of the probiotic strains in modulating immune responses and the gut microbiota, suggesting their role as a dietary intervention strategy for managing AD.

The direct effects and antimicrobial activity of synthetic antimicrobial peptides (AMPs) obtained from dogs, including cBD, cBD103, and cCath, against P. aeruginosa wild-type strain PAO1 and canine keratinocytes were analyzed. Antibacterial effects on planktonic bacteria were assessed by determining the minimum bactericidal concentrations (MBCs) of AMPs and by a time-kill assay. Antibiofilm effects were assessed using the microtiter plate assay. We also evaluated the effects of AMPs on cell cytotoxicity and host immune response induced by stimulating canine epidermal keratinocyte progenitor (CPEK) cells with PAO1 and its LPS. cBD, cBD103, and cCath all exhibited dose-dependent antimicrobial and antibiofilm effects. In particular, 25 μg/mL cBD103 showed rapid bactericidal activity within 60 min and inhibited biofilm formation. In addition, pretreatment with cBD103 (25 µg/mL) and cCath (50 µg/mL) 1 h before stimulation significantly reduced the cytotoxicity of the CPEK cells by PAO1 and LPS-induced IL-6 and TNF-a expressions. cBD had little effect on the response to PAO1 and LPS in the cells. These results indicate the therapeutic potential of AMPs in P. aeruginosa skin infections. However, further studies on the mechanism of action of AMPs in keratinocytes and clinical trials are needed.

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Importance: Feline calicivirus (FCV)-associated viral systemic disease (VSD) is a severe systemic disease caused by virulent FCV strains and has a very poor prognosis. Objective: To evaluate the clinical characteristics of a nosocomial FCV-VSD outbreak involving 18 cats in Korea. Methods: Medical records of cats diagnosed with FCV-VSD from March to September 2018 at a referral veterinary hospital were reviewed. The patient's signalment, history, clinical features, diagnosis, treatment, and prognosis were evaluated. Results: Two outbreaks involving 18 cats diagnosed with FCV-VSD occurred over a 6-month period at a referral hospital in Korea. Anorexia, lethargy, fever, and limb edema were the most commonly observed clinical symptoms. Lymphopenia and macrothrombocytopenia were the most common hematological findings, and hyperbilirubinemia and increased levels of aspartate aminotransferase, creatine kinase, and serum amyloid A were the most frequent results of serum biochemistry. FCV was detected by reverse transcription polymerase chain reaction in 11 patients and the remaining 7 were suspected with FCV-VSD. The overall mortality rate was 72.2%. The hospital was closed and disinfected twice, and no additional outbreaks have occurred since the last patient. Conclusions and Relevance: The clinical and diagnostic characteristics and outcomes of FCV-VSD described in this study can be used to recognize and contain infectious diseases through quick action. To the best of the authors' knowledge, this is the first report of a nosocomial outbreak of FCV-VSD in Asia. [ABSTRACT FROM AUTHOR]