Atopic dermatitis (AD) is a chronic inflammatory skin disease with repeated exacerbations of eczema and pruritus. Probiotics
can prevent or treat AD appropriately via modulation of immune responses and gut microbiota. In this study, we evaluated
effects of Lactobacillus acidophilus (L. acidophilus) KBL409 using a house dust mite (Dermatophagoides farinae)-induced
in vivo AD model. Oral administration of L. acidophilus KBL409 significantly reduced dermatitis scores and decreased
infiltration of immune cells in skin tissues. L. acidophilus KBL409 reduced in serum immunoglobulin E and mRNA levels
of T helper (Th)1 (Interferon-γ), Th2 (Interleukin [IL]-4, IL-5, IL-13, and IL-31), and Th17 (IL-17A) cytokines in skin tissues.
The anti-inflammatory cytokine IL-10 was increased and Foxp3 expression was up-regulated in AD-induced mice with
L. acidophilus KBL409. Furthermore, L. acidophilus KBL409 significantly modulated gut microbiota and concentrations
of short-chain fatty acids and amino acids, which could explain its effects on AD. Our results suggest that L. acidophilus
KBL409 is the potential probiotic for AD treatment by modulating of immune responses and gut microbiota of host.
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Mycobacterium tuberculosis (M. tuberculosis) is a highly pathogenic
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the leading cause of mortality from single infections. Redox
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stresses. The antioxidant sulforaphane (SFN) has been
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REOviruses (Respiratory Enteric Orphan viruses) are ubiquitous, non-enveloped viruses containing 10 segments of double-stranded RNA (dsRNA) as their genome. They are common isolates of the respiratory and gastrointestinal tract of humans but are not associated with severe disease and are therefore considered relatively benign. An intriguing characteristic of reovirus is its innate oncolytic potential, which is linked to the transformed state of the cell. When immortalized cells are transfected in vitro with activated oncogenes such as Ras, Sos, v-erbB, or c-myc, they became susceptible to reovirus infection and subsequent cellular lysis, indicating that oncogene signaling pathways are exploited by reovirus. This observation has led to the use of the virus in clinical trials as an anti-cancer agent against oncogenic tumors. In addition to the exploitation of oncogene signaling, reovirus may further utilize host immune responses to enhance its antitumor activity in vivo due to its innate interferon induction ability. Reovirus is, however, not entirely benign to immunocompromised animal models. Reovirus causes so-called “black feet syndrome” in immunodeficient mice and can also harm neonatal animals. Because cancer patients often undergo immunosuppression due to heavy chemo/radiation-treatments or advanced tumor progression, this pathogenic response may be a hurdle in virus-based anticancer therapies. However, a genetically attenuated reovirus variant derived from persistent reovirus infection of cells in vitro is able to exert potent anti-tumor activity with significantly reduced viral pathogenesis in immunocompromised animals. Importantly, in this instance the attenuated reovirus maintains its oncolytic potential while significantly reducing viral pathogenesis in vivo.
Live attenuated Japanese encephalitis (JE) virus SA14-14-2 produced in primary dog kidney cells (PDK) was adapted to African green monkey kidney cells, Vero. In an effort to gain insight into the molecular basis of the biological characteristics of the isolated SA14-14-2 (Vero) strain, the 1,500 nucleotide sequence encoding the envelope (E) gene which possesses major neutralizing epitopes was determined and dompared with the sequences of two other attenuated JE virus strains, SA14-14-2 (PHK) and SA14-14-2 (PDK). The amino acid sequence of the C-terminal region (a.a. 280-500) of the SA14-14-2 (Vero) E gene was found to be identical to those of strains SA14-14-2 (PHK) and SA14-14-2 (PDK), while the N-terminal region (a.a. 1-279) showed sequence variation. The distribution of mutations in the N-terminal region was nearly the same among the three attenuated strains, suggesting that the N-terminal sequences might be related with virus-host cell specificity. However, it was found that Lys and Val (a.a.138 and 176, respectively), known to be responsible for attenuation, are still conserved in SA14-14-2 (Vero). Animal testing showed that SA14-14-2 (Vero) has a neurovirulence phenotype similar to that of the parent SA14-14-2 (PDK) strain in suckling mice. The SA14-14-2 (Vero) grew very efficiently in Vero cells enough to support vaccine production. The growth characteristics of SA14-14-2 (Vero) in Vero cell and conservation of attenuation determinant of neurovirulence support that SA14-14-2 (Vero) could be developed as a new vaccine strain for human use.