Ulcerative colitis, a major form of inflammatory bowel disease (IBD) associated with chronic colonic inflammation, may
be induced via overreactive innate and adaptive immune responses. Restoration of gut microbiota abundance and diversity
is important to control the pathogenesis. Lactobacillus spp., well-known probiotics, ameliorate IBD symptoms via various
mechanisms, including modulation of cytokine production, restoration of gut tight junction activity and normal mucosal
thickness, and alterations in the gut microbiota. Here, we studied the effects of oral administration of Lactobacillus rhamnosus
(L. rhamnosus) KBL2290 from the feces of a healthy Korean individual to mice with DSS-induced colitis. Compared to the
dextran sulfate sodium (DSS) + phosphate-buffered saline control group, the DSS + L. rhamnosus KBL2290 group evidenced
significant improvements in colitis symptoms, including restoration of body weight and colon length, and decreases in the
disease activity and histological scores, particularly reduced levels of pro-inflammatory cytokines and an elevated level of
anti-inflammatory interleukin-10. Lactobacillus rhamnosus KBL2290 modulated the levels of mRNAs encoding chemokines
and markers of inflammation; increased regulatory T cell numbers; and restored tight junction activity in the mouse colon.
The relative abundances of genera Akkermansia, Lactococcus, Bilophila, and Prevotella increased significantly, as did the
levels of butyrate and propionate (the major short-chain fatty acids). Therefore, oral L. rhamnosus KBL2290 may be a useful
novel probiotic.
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Systemic candidiasis, which is mainly caused by Candida albicans,
is a serious acute fungal infection in the clinical setting.
In a previous study, we reported that compound 22h (designated
as AB-22 in this study), a vinyl sulfate compound, is a
fast-acting fungicidal agent against a broad spectrum of fungal
pathogens. In this study, we aimed to further analyze the
in vitro and in vivo efficacy of AB-22 against filamentation,
biofilm formation, and virulence of C. albicans. Under in vitro
hyphal growth-inducing condition, AB-22 effectively inhibited
germ tube formation and hyphal growth, which are required
for the initiation of biofilm formation. Indeed, AB-22
significantly suppressed C. albicans biofilm formation in a
dose-dependent manner. Moreover, AB-22 treatment inhibited
the normal induction of ALS3, HWP1, and ECE1, which
are all required for hyphal transition in C. albicans. Furthermore,
AB-22 treatment increased the survival of mice systemically
infected with C. albicans. In conclusion, in addition
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biofilm formation in C. albicans, which could collectively contribute
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Low-density lipoprotein (LDL) was recently reported to be an
opsonin, enhancing the phagocytosis of group A Streptococcus
(GAS) by human monocytic leukemia U937 cells due to the
binding of LDL to some GAS strains. We postulated that LDL
might also promote the opsonophagocytosis of Pseudomonas
aeruginosa by U937 cells since this bacterium interacts with
LDL. In this study, P. aeruginosa (CMCC10104), U937 cells,
and human LDL were used in phagocytosis assays to test our
hypothesis. Escherichia coli strain BL21, which does not interact
with LDL, was used as a negative control. Colony counting
and fluorescence microscopy were used to determine the
bacterial quantity in the opsonophagocytosis assays. After
incubation of U937 cells and P. aeruginosa with LDL (100
μg/ml) for 15 and 30 min, phagocytosis was observed to be
increased by 22.71% and 32.90%, respectively, compared to
that seen in the LDL-free group. However, LDL did not increase
the phagocytosis of E. coli by U937 cells. In addition,
we identified CD36 as a major opsonin receptor on U937 cells,
since an anti-CD36 monoclonal antibody, but not an anti-
CD4 monoclonal antibody, almost completely abolished the
opsonophagocytosis of P. aeruginosa by U937 cells.
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