• Korean Journal of Veterinary Research
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• v.56 no.2
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• pp.57-66
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• 2016

The gut epithelial barrier, which is composed of the mucosal layer and the intestinal epithelium, has multiple defense mechanisms and interconnected regulatory mechanisms against enteric microbial pathogens. However, many bacterial pathogens have highly evolved infectious stratagems that manipulate mucin production, epithelial cell-cell junctions, cell death, and cell turnover to promote their replication and pathogenicity in the gut epithelial barrier. In this review, we focus on current knowledge about how bacterial pathogens regulate mucin levels to circumvent the epithelial mucus barrier and target cell-cell junctions to invade deeper tissues and increase their colonization. We also describe how bacterial pathogens manipulate various modes of epithelial cell death to facilitate bacterial dissemination and virulence effects. Finally, we discuss recent investigating how bacterial pathogens regulate epithelial cell turnover and intestinal stem cell populations to modulate intestinal epithelium homeostasis.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.3
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• pp.331-343
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• 1998

Sublethal dose of bacterial lipopolysaccharide (LPS) would induce protection against cardiac ischemic/reperfusion (I/R) injury. This study examines the following areas: 1) the temporal induction of the cardio-protection produced by LPS; and 2) the relations between a degree of protection and the myocardial prostacyclin ($PGI_2$) production. Rats were administered LPS (2 mg/kg, i.v.), and hearts were removed 1, 4, 8, 14, 24, 48, 72,and 96 h later. Using Langendorff apparatus, haemodynamic differences during 25 min of global ischemia/30 min reperfusion were investigated. The concentration of $PGI_2$ in aliquots of the coronary effluent was determined by radioimmunoassay as its stable hydrolysis product $6-keto-PGF1_{\alpha}$ and lactate dehydrogenase release were measured as an indicative of cellular injury. LPS-induced cardiac protection against I/R injury appeared 4 h after LPS treatment and remained until 96 h after treatment. $PGI_2$ release increased 2-3 fold at the beginning of reperfusion compared to basal level except in hearts treated with LPS for 48 and 72 h. In hearts removed 48 and 72 h after LPS treatment, basal $PGI_2$ was increased. To determine the enzymatic step in relation to LPS-induced basal $PGI_2$ production, we examined prostaglandin H synthase (PGHS) protein expression, a rate limiting enzyme of prostaglandin production, by using Western blot analysis. LPS increased PGHS protein expression in hearts at 24, 48, 72, 96 h after LPS treatment. Induction of PGHS expression appeared in both isotypes of PGHS, a constitutive PGHS-1 and an inducible PGHS-2. To identify the correlationship between $PGI_2$ production and the cardioprotective effect against I/R injury, indomethacin was administered in vivo or in vitro. Indomethacin did not inhibit LPS-induced cardioprotection, which was not affected by the duration of LPS treatment. Taken together, our results suggest that $PGI_2$ might not be the major endogenous mediator of LPS-induced cardioprotection.

• Proceedings of the Korean Society for Applied Microbiology Conference
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• 2005.06a
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• pp.54-62
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• 2005

While genomics (the set of experimental and computational tools that allows the blueprints of life to be read) opens the doors to a more rational approach to the design and use of living cells to bring about desirable chemical transformations, genomics is, by itself, insufficient. We need tools that allow us to relate genomic and molecular information to cellular physiology and then to the response of a population of cells. We propose the development of hybrid computer cellular models. In such models genomics and chemical detail for a cellular subsystem (e.g. pathogenesis) is embedded in a coarse-grain cell model. Such a construct allows the quantitative and explicit linkage of genomic detail to cell physiology to the extracellular environment. To illustrate the principles involved we are constructing a model for a minimal cell. A minimal cell is a bacterial cell with the fewest number of genes necessary to sustain life as a free living microbe.

• Asian-Australasian Journal of Animal Sciences
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• v.2 no.4
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• pp.615-623
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• 1989

Three sheep fitted with rumen cannulae and abomasal cannulae were given daily 750 g (DM) of three diets consisting of straw-manure silage and barley mixture in the ratios of 75:25, 50:50 and 25:75. As the proportion of barley in the diet increased, there was an increase in the amount of OM apparently digested in the rumen and thole tract (P<.01). But ADF digestion was decreased. For the 25:75 diet the $NH_3-N$ content in the rumen showed the highest value, but the total VFA was the lowest. The rumen volume and dilution rate increased with increasing ratio of silage in diets. There were no significant differences between diets in abomasal NAN flow, and the bacterial-N for the 25:75 diet was 7.3 g N as compared with 9.2-9.6 g N for the other diets (P<.01). Rates of bacterial nitrogen synthesis in the rumen were 30.5, 24.1 and 14.9 g N per Kg OM apparently digested in the rumen for the 75:25, 50:50 and 25:75 diets, respectively.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.4
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• pp.229-238
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• 2022

Severe bacterial infections are frequently accompanied by depressed neutrophil functions. Thus, agents that increase the microbicidal activity of neutrophils could add to a direct antimicrobial therapy. Lysophosphatidylcholine augments neutrophil bactericidal activity via the glycine (Gly)/glycine receptor (GlyR) α2/TRPM2/p38 mitogen-activated protein kinase (MAPK) pathway. However, the direct effect of glycine on neutrophil bactericidal activity was not reported. In this study, the effect of glycine on neutrophil bactericidal activity was examined. Glycine augmented bactericidal activity of human neutrophils (EC₅₀ = 238 μM) in a strychnine (a GlyR antagonist)-sensitive manner. Glycine augmented bacterial clearance in mice, which was also blocked by strychnine (0.4 mg/kg, s.c.). Glycine enhanced NADPH oxidase-mediated reactive oxygen species (ROS) production and TRPM2-mediated [Ca²⁺]_i increase in neutrophils that had taken up E. coli. Glycine augmented Lucifer yellow uptake (fluid-phase pinocytosis) and azurophil granule-phagosome fusion in neutrophils that had taken up E. coli in an SB203580 (a p38 MAPK inhibitor)-sensitive manner. These findings indicate that glycine augments neutrophil microbicidal activity by enhancing azurophil granule-phagosome fusion via the GlyRα2/ROS/calcium/p38 MAPK pathway. We suggest that glycine could be a useful agent for increasing neutrophil bacterial clearance.

• Archives of Pharmacal Research
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• v.18 no.4
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• pp.262-266
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• 1995

Bacterial lipopolysaccharide (LPS) is one of the most potent inducers of various cytokines nad other proinflammatory mediators in macrophages. Although pathophysiological consequences of LPS-induced responses are well established, the mechanisms through which LPS-generated singals are transduced remain unclear. In the present study, we attempted to determine early intracellular events after LPS binding which transduced the signal for the induction of arachidonic acid metabolism in rat alveolar macrophages. While H-7, a protein kinase C(PKC) inhibitor, did not affect LPS-stimulated prostaglandin synthesis, staurosporine enhanced archidonic acid etabolism in macropahages treated with LPS. Phorbol-12-myristate-13 acetate snesitive to LPS compare with control group. PMA and H-7 did not alter the effect of flucose. Pertussis toxin did not show nay effect, thus pertussis toxin snesitive G-protein pathway appears not to play a role in this experimental system. Genistein and tyrphostin 25, protein tyrosine kinase 9PTK) inhibitors, markedly inhibited prostaglandin synthesis in macrophages nal transduction events leading to icnreased macrophage arachidonic acid metabolism.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.291-297
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• 2015

An oral environment is constantly exposed to environmental factors and microorganisms. The periodontal ligament (PDL) fibroblasts within this environment are subject to bacterial infection and allergic reaction. However, how these condition affect PDL fibroblasts has yet to be elucidated. PDL fibroblasts were isolated from healthy donors. We examined using reverse transcription-polymerase chain reaction and measuring the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$). This study investigated the receptors activated by exogenous bacterial pathogens (Lipopolysaccharide and peptidoglycan) and allergens (German cockroach extract and house dust mite) as well as these pathogenic mediators-induced effects on the intracellular $Ca^{2+}$ signaling in human PDL fibroblasts. Moreover, we evaluated the expression of pro-inflammatory cytokines (interleukin (IL)-$1{\beta}$, IL-6, and IL-8) and bone remodeling mediators (receptor activator of NF-${\kappa}B$ ligand and osteoprotegerin) and intracellular $Ca^{2+}$-involved effect. Bacterial pathogens and allergic mediators induced increased expression of pro-inflammatory cytokines, and these results are dependent on intracellular $Ca^{2+}$. However, bacterial pathogens and allergic mediators did not lead to increased expression of bone remodeling mediators, except lipopolysaccharide-induced effect on receptor activator of NF-${\kappa}B$ ligand expression. These experiments provide evidence that a pathogens and allergens-induced increase in $[Ca^{2+}]_i$ affects the inflammatory response in human PDL fibroblasts.

• Animal Bioscience
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• v.34 no.2
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• pp.243-255
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• 2021

Objective: Deoxynivalenol (DON) and zearalenone (ZEN) are mycotoxins that frequently contaminate maize and grain cereals, imposing risks to the health of both humans and animals and leading to economic losses. The gut microbiome has been shown to help combat the effects of such toxins, with certain microorganisms reported to contribute significantly to the detoxification process. Methods: We examined the cecum contents of three different dietary groups of pigs (control, as well as diets contaminated with 8 mg DON/kg feed or 0.8 mg ZEN/kg feed). Bacterial 16S rRNA gene amplicons were acquired from the cecum contents and evaluated by next-generation sequencing. Results: A total of 2,539,288 sequences were generated with ~500 nucleotide read lengths. Firmicutes, Bacteroidetes, and Proteobacteria were the dominant phyla, occupying more than 96% of all three groups. Lactobacillus, Bacteroides, Megasphaera, and Campylobacter showed potential as biomarkers for each group. Particularly, Lactobacillus and Bacteroides were more abundant in the DON and ZEN groups than in the control. Additionally, 52,414 operational taxonomic units were detected in the three groups; those of Bacteroides, Lactobacillus, Campylobacter, and Prevotella were most dominant and significantly varied between groups. Hence, contamination of feed by DON and ZEN affected the cecum microbiota, while Lactobacillus and Bacteroides were highly abundant and positively influenced the host physiology. Conclusion: Lactobacillus and Bacteroides play key roles in the process of detoxification and improving the immune response. We, therefore, believe that these results may be useful for determining whether disturbances in the intestinal microflora, such as the toxic effects of DON and ZEN, can be treated by modulating the intestinal bacterial flora.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.151-152
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• 2002

Bacterial infection is a very complex process in which both pathogenic microorganisms and host cells play crucial roles, and it is the outcome of interactions between the two participants. To elucidate the bacterial pathogenesis mechanisms, therefore, it is essential to understand the cellular and systemic responses of the host as well as the virulence factors of the pathogen. Infection of a host by pathogenic bacteria causes drastic changes in the physiology of host cells, leading to activation of a program of various gene expression. (omitted)

• Asian-Australasian Journal of Animal Sciences
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• v.9 no.1
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• pp.45-49
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• 1996

A series of in vitro experiments was conducted to investigate response of rumen bacterial deamination to the ionophore salinomycin. Addition of salinomycin to the inoculum, strained rumen fluid, depressed ammonia production from casein, while increased accumulation of ${\alpha}$-amino acids. This suggests an inhibitory effect of salinomycin on ruminal deamination. When the effect in washed bacterial suspension was monitored with individual amino acid, aspartic acid degradation was markedly inhibited by salinomycin. This inhibition was not observed when the mixed rumen bacteria were ultrasonically disrupted and used as the enzyme source. Extent of the inhibition tended to be higher in the bacteria source from sheep on a high roughage diet. From these results it was speculated that the inhibition of deamination with salinomycin is caused by a decreased transport of amino acid into the bacterial cells as well as a decreased proportion of deaminating bacteria in the rumen.