scholarly journals From the gut to the peripheral tissues: the multiple effects of butyrate

2010 ◽  
Vol 23 (2) ◽  
pp. 366-384 ◽  
Author(s):  
P. Guilloteau ◽  
L. Martin ◽  
V. Eeckhaut ◽  
R. Ducatelle ◽  
R. Zabielski ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Digestive Enzyme ◽  
Virulence Gene ◽  
Nutrient Digestibility ◽  
Host Cells ◽  
Feed Additive ◽  
Gut Health ◽  
Gastrointestinal Microbiota ◽  
Peripheral Tissues ◽  
Virulence Gene Expression

Butyrate is a natural substance present in biological liquids and tissues. The present paper aims to give an update on the biological role of butyrate in mammals, when it is naturally produced by the gastrointestinal microbiota or orally ingested as a feed additive. Recent data concerning butyrate production delivery as well as absorption by the colonocytes are reported. Butyrate cannot be detected in the peripheral blood, which indicates fast metabolism in the gut wall and/or in the liver. In physiological conditions, the increase in performance in animals could be explained by the increased nutrient digestibility, the stimulation of the digestive enzyme secretions, a modification of intestinal luminal microbiota and an improvement of the epithelial integrity and defence systems. In the digestive tract, butyrate can act directly (upper gastrointestinal tract or hindgut) or indirectly (small intestine) on tissue development and repair. Direct trophic effects have been demonstrated mainly by cell proliferation studies, indicating a faster renewal of necrotic areas. Indirect actions of butyrate are believed to involve the hormono–neuro–immuno system. Butyrate has also been implicated in down-regulation of bacteria virulence, both by direct effects on virulence gene expression and by acting on cell proliferation of the host cells. In animal production, butyrate is a helpful feed additive, especially when ingested soon after birth, as it enhances performance and controls gut health disorders caused by bacterial pathogens. Such effects could be considered for new applications in human nutrition.

scholarly journals 173 Lysed Corynebacterium glutamicum cell mass from lysine production as a novel feed additive to enhance gut health and growth of newly-weaned pigs

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 77-78
Author(s):  
Yi-Chi Cheng ◽  
Marcos E Duarte ◽  
Sung Woo Kim
Keyword(s):  
Growth Performance ◽  
Corynebacterium Glutamicum ◽  
Block Design ◽  
Cell Mass ◽  
Nutrient Digestibility ◽  
Feed Additive ◽  
Jejunal Mucosa ◽  
Gut Health ◽  
Weaned Pigs ◽  
Dietary Treatments

Abstract The objective was to determine the functional and nutritional values of Corynebacterium glutamicum Cell Mass (CGCM) on growth performance and gut health of newly-weaned pigs. Forty newly-weaned pigs (21 d of age; initial BW 7.1 ± 0.4 kg) were allotted to 5 dietary treatments based on randomized complete block design with sex and BW as blocks. The lysine broth of CGCM (CJ Bio, Fort Dodge, IA) was homogenized by using French press and dried to obtain lysed CGCM. Dietary treatments were: basal diet with lysed CGCM at 0, 0.7, 1.4, 2.1%, and with 1.4% intact CGCM. Experimental diets were formulated based on nutrient requirements (NRC, 2012) and pigs were fed based on 2 phases (10 and 11 d for each phase). Titanium dioxide (0.4%) was added to phase 2 diets as an indigestible external marker to calculate nutrient digestibility. Feed intake and BW were measured at d 0, 10, and 21. Pigs were euthanized on d 21 to collect proximal and distal jejunal mucosa to measure TNF-α, IL-8, MDA, IgA, and IgG concentrations. Diets and ileal digesta were collected to measure AID. Data were analyzed by SAS using MIXED, REG, and GLM procedures. Overall, increasing daily lysed CGCM intake increased (P < 0.05) ADG (211 to 296 g) and ADFI (432 to 501 g). Increasing levels of lysed CGCM decreased (P < 0.05) MDA and changed (quadratic, P < 0.05) IgA (max: 4.90 ng/mg at 1.13%) and IgG (max: 3.37 ng/mg at 1.04%) in the proximal jejunal mucosa. Increasing daily lysed CGCM intake had quadratic effect (P< 0.05) of protein carbonyl (max: 6.3 μmol/mg at 4.9 g/d). Lysed CGCM potentially benefits growth performance and gut health of newly-weaned pigs by reducing oxidative stress and increasing immune response.

scholarly journals Perforin-2 Protects Host Cells and Mice by Restricting the Vacuole to Cytosol Transitioning of a Bacterial Pathogen

2016 ◽  
Vol 84 (4) ◽  
pp. 1083-1091 ◽  
Author(s):  
Ryan McCormack ◽  
Wael Bahnan ◽  
Niraj Shrestha ◽  
Justin Boucher ◽  
Marcella Barreto ◽  
...  
Keyword(s):  
Bacterial Pathogen ◽  
Virulence Gene ◽  
Systemic Infection ◽  
Protective Role ◽  
Host Cells ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Membrane Bound ◽  
High Level ◽  
Macpf Domain

The host-encoded Perforin-2 (encoded by the macrophage-expressed gene 1,Mpeg1), which possesses a pore-forming MACPF domain, reduces the viability of bacterial pathogens that reside within membrane-bound compartments. Here, it is shown that Perforin-2 also restricts the proliferation of the intracytosolic pathogenListeria monocytogenes. Within a few hours of systemic infection, the massive proliferation ofL. monocytogenesinPerforin-2−/−mice leads to a rapid appearance of acute disease symptoms. We go on to show in culturedPerforin-2−/−cells that the vacuole-to-cytosol transitioning ofL. monocytogenesis greatly accelerated. Unexpectedly, we found that inPerforin-2−/−macrophages,Listeria-containing vacuoles quickly (≤15 min) acidify, and that this was coincident with greater virulence gene expression, likely accounting for the more rapid translocation ofL. monocytogenesto its replicative niche in the cytosol. This hypothesis was supported by our finding that aL. monocytogenesstrain expressing virulence factors at a constitutively high level replicated equally well inPerforin-2+/+andPerforin-2−/−macrophages. Our findings suggest that the protective role of Perforin-2 against listeriosis is based on it limiting the intracellular replication of the pathogen. This cellular activity of Perforin-2 may derive from it regulating the acidification ofListeria-containing vacuoles, thereby depriving the pathogen of favorable intracellular conditions that promote its virulence gene activity.

scholarly journals The Pseudomonas aeruginosa Periplasmic Protease CtpA Can Affect Systems That Impact Its Ability To Mount Both Acute and Chronic Infections

2013 ◽  
Vol 81 (12) ◽  
pp. 4561-4570 ◽  
Author(s):  
Jin Seo ◽  
Andrew J. Darwin
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Sigma Factor ◽  
Cell Envelope ◽  
Virulence Gene ◽  
Normal Function ◽  
Host Cells ◽  
Tissue Destruction ◽  
Chronic Infections ◽  
Content Type ◽  
Virulence Gene Expression

ABSTRACTProteases play important roles in the virulence ofPseudomonas aeruginosa. Some are exported to act on host targets and facilitate tissue destruction and bacterial dissemination. Others work within the bacterial cell to process virulence factors and regulate virulence gene expression. Relatively little is known about the role of one class of bacterial serine proteases known as the carboxyl-terminal processing proteases (CTPs). TheP. aeruginosagenome encodes two CTPs annotated as PA3257/Prc and PA5134/CtpA in strain PAO1. Prc degrades mutant forms of the anti-sigma factor MucA to promote mucoidy in some cystic fibrosis lung isolates. However, nothing is known about the role or importance of CtpA. We have now found that endogenous CtpA is a soluble periplasmic protein and that actpAnull mutant has specific phenotypes consistent with an altered cell envelope. Although actpAnull mutation has no major effect on bacterial growth in the laboratory, CtpA is essential for the normal function of the type 3 secretion system (T3SS), for cytotoxicity toward host cells, and for virulence in a mouse model of acute pneumonia. Conversely, increasing the amount of CtpA above its endogenous level induces an uncharacterized extracytoplasmic function sigma factor regulon, an event that has been reported to attenuateP. aeruginosain a rat model of chronic lung infection. Therefore, a normal level of CtpA activity is critical for T3SS function and acute virulence, whereas too much activity can trigger an apparent stress response that is detrimental to chronic virulence.

scholarly journals The Posttranslocation Chaperone PrsA2 Contributes to Multiple Facets of Listeria monocytogenes Pathogenesis

2009 ◽  
Vol 77 (7) ◽  
pp. 2612-2623 ◽  
Author(s):  
Francis Alonzo ◽  
Gary C. Port ◽  
Min Cao ◽  
Nancy E. Freitag
Keyword(s):  
Listeria Monocytogenes ◽  
Gene Product ◽  
Bacterial Pathogen ◽  
Virulence Gene ◽  
Host Cells ◽  
Listeriolysin O ◽  
Virulence Gene Expression ◽  
High Concentrations ◽  
Host Infection ◽  
Cell Spread

ABSTRACT Listeria monocytogenes is an intracellular bacterial pathogen whose virulence depends on the regulated expression of numerous secreted bacterial factors. As for other gram-positive bacteria, many proteins secreted by L. monocytogenes are translocated across the bacterial membrane in an unfolded state to the compartment existing between the membrane and the cell wall. This compartment presents a challenging environment for protein folding due to its high density of negative charge, high concentrations of cations, and low pH. We recently identified PrsA2 as a gene product required for L. monocytogenes virulence. PrsA2 was identified based on its increased secretion by strains containing a mutationally activated form of prfA, the key regulator of L. monocytogenes virulence gene expression. The prsA2 gene product is one of at least two predicted peptidyl-prolyl cis/trans-isomerases encoded by L. monocytogenes; these proteins function as posttranslocation protein chaperones and/or foldases. In this study, we demonstrate that PrsA2 plays a unique and important role in L. monocytogenes pathogenesis by promoting the activity and stability of at least two critical secreted virulence factors: listeriolysin O (LLO) and a broad-specificity phospholipase. Loss of PrsA2 activity severely attenuated virulence in mice and impaired bacterial cell-to-cell spread in host cells. In contrast, mutants lacking prsA1 resembled wild-type bacteria with respect to intracellular growth and cell-to-cell spread as well as virulence in mice. PrsA2 is thus distinct from PrsA1 in its unique requirement for the stability and full activity of L. monocytogenes-secreted factors that contribute to host infection.

scholarly journals Beyond homeostasis: potassium and pathogenesis during bacterial infections

2021 ◽  
Author(s):  
Elyza A. Do ◽  
Casey M. Gries
Keyword(s):  
Bacterial Infections ◽  
Pathogenic Bacteria ◽  
Virulence Gene ◽  
Potassium Transport ◽  
Host Cells ◽  
Mineral Nutrient ◽  
Inflammasome Activation ◽  
Bacterial Cells ◽  
Virulence Gene Expression ◽  
Neuronal Transmission

Potassium is an essential mineral nutrient required by all living cells for normal physiological function. Maintaining intracellular potassium homeostasis during bacterial infection is therefore a requirement for the survival of both host and pathogen. However, pathogenic bacteria require potassium transport not only to fulfill nutritional and chemiosmotic requirements, but potassium has been shown to directly modulate virulence gene expression, antimicrobial resistance, and biofilm formation. Host cells also require potassium to maintain fundamental biological processes as such as renal function, muscle contraction, and neuronal transmission, however, potassium flux also contributes to critical immunological and antimicrobial processes such as cytokine production and inflammasome activation. Here we review the role and regulation of potassium transport and signaling during infection in both mammalian and bacterial cells and highlight the importance of potassium to the success and survival of each organism.

Transcriptional Activator OvrA Encoded in O Island 19 Modulates Virulence Gene Expression in Enterohemorrhagic Escherichia coli O157:H7

2019 ◽  
Author(s):  
Bin Liu ◽  
Junyue Wang ◽  
Lu Wang ◽  
Peng Ding ◽  
Pan Yang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Gene Promoter ◽  
Virulence Gene ◽  
Coli Strain ◽  
Enterohemorrhagic Escherichia Coli ◽  
Bacterial Adherence ◽  
Host Cells ◽  
Virulence Gene Expression ◽  
E Coli

AbstractThe human intestinal pathogen enterohemorrhagic Escherichia coli (EHEC) O157:H7 causes bloody diarrhea, hemorrhagic colitis, and fatal hemolytic uremic syndrome. Its genome contains 177 unique O islands (OIs), which contribute largely to the high virulence and pathogenicity although most OI genes remain uncharacterized. In the current study, we demonstrated that OI-19 is required for EHEC O157:H7 adherence to host cells. Z0442 (OI-encoded virulence regulator A [OvrA]) encoded in OI-19 positively regulated bacterial adherence by activating locus of enterocyte effacement (LEE) gene expression through direct OvrA binding to the gene promoter region of the LEE gene master regulator Ler. Mouse colonization experiments revealed that OvrA promotes EHEC O157:H7 adherence in mouse intestine, preferentially the colon. Finally, OvrA also regulated virulence in other non-O157 pathogenic E. coli, including EHEC strains O145:H28 and O157:H16 and enteropathogenic E. coli strain O55:H7. Our work markedly enriches the understanding of bacterial adherence control and provides another example of laterally acquired regulators that mediate LEE gene expression.

scholarly journals Spatial Segregation of Virulence Gene Expression during Acute Enteric Infection with Salmonella enterica serovar Typhimurium

mBio ◽  
2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Richard C. Laughlin ◽  
Leigh A. Knodler ◽  
Roula Barhoumi ◽  
H. Ross Payne ◽  
Jing Wu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Salmonella Enterica ◽  
Virulence Gene ◽  
Bacterial Virulence ◽  
Natural Host ◽  
Host Cells ◽  
Enteric Infection ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Serovar Typhimurium

ABSTRACTTo establish a replicative niche during its infectious cycle between the intestinal lumen and tissue, the enteric pathogenSalmonella entericaserovar Typhimurium requires numerous virulence genes, including genes for two type III secretion systems (T3SS) and their cognate effectors. To better understand the host-pathogen relationship, including early infection dynamics and induction kinetics of the bacterial virulence program in the context of a natural host, we monitored the subcellular localization and temporal expression of T3SS-1 and T3SS-2 using fluorescent single-cell reporters in a bovine, ligated ileal loop model of infection. We observed that the majority of bacteria at 2 h postinfection are flagellated, express T3SS-1 but not T3SS-2, and are associated with the epithelium or with extruding enterocytes. In epithelial cells,S. Typhimurium cells were surrounded by intact vacuolar membranes or present within membrane-compromised vacuoles that typically contained numerous vesicular structures. By 8 h postinfection, T3SS-2-expressing bacteria were detected in the lamina propria and in the underlying mucosa, while T3SS-1-expressing bacteria were in the lumen. Our work identifies for the first time the temporal and spatial regulation of T3SS-1 and -2 expression during an enteric infection in a natural host and provides further support for the concept of cytosolicS. Typhimurium in extruding epithelium as a mechanism for reseeding the lumen.IMPORTANCEThe pathogenic bacteriumSalmonella entericaserovar Typhimurium invades and persists within host cells using distinct sets of virulence genes. Genes fromSalmonellapathogenicity island 1 (SPI-1) are used to initiate contact and facilitate uptake into nonphagocytic host cells, while genes within SPI-2 allow the pathogen to colonize host cells. While many studies have identified bacterial virulence determinants in animal models of infection, very few have focused on virulence gene expression at the single-cell level during anin vivoinfection. To better understand when and where bacterial virulence factors are expressed during an acute enteric infection of a natural host, we infected bovine jejunal-ileal loops withS. Typhimurium cells harboring fluorescent transcriptional reporters for SPI-1 and -2 (PinvFand PssaG, respectively). After a prescribed time of infection, tissue and luminal fluid were collected and analyzed by microscopy. During early infection (≤2 h), bacteria within both intact and compromised membrane-bound vacuoles were observed within the epithelium, with the majority expressing SPI-1. As the infection progressed,S. Typhimurium displayed differential expression of the SPI-1 and SPI-2 regulons, with the majority of tissue-associated bacteria expressing SPI-2 and the majority of lumen-associated bacteria expressing SPI-1. This underscores the finding thatSalmonellavirulence gene expression changes as the pathogen transitions from one anatomical location to the next.

scholarly journals Association and Virulence Gene Expression Vary among Serotype III Group B Streptococcus Isolates following Exposure to Decidual and Lung Epithelial Cells

2014 ◽  
Vol 82 (11) ◽  
pp. 4587-4595 ◽  
Author(s):  
Michelle L. Korir ◽  
David Knupp ◽  
Kathryn LeMerise ◽  
Erica Boldenow ◽  
Rita Loch-Caruso ◽  
...  
Keyword(s):  
Gene Expression ◽  
Epithelial Cells ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Lung Epithelial Cells ◽  
Host Cells ◽  
Virulence Gene Expression ◽  
Decidual Cells ◽  
Lung Epithelial ◽  
Group B

ABSTRACTGroup BStreptococcus(GBS) causes severe disease in neonates, the elderly, and immunocompromised individuals. GBS species are highly diverse and can be classified by serotype and multilocus sequence typing. Sequence type 17 (ST-17) strains cause invasive neonatal disease more frequently than strains of other STs. Attachment and invasion of host cells are key steps in GBS pathogenesis. We investigated whether four serotype III strains representing ST-17 (two strains), ST-19, and ST-23 differ in their abilities to attach to and invade both decidual cells and lung epithelial cells. Virulence gene expression following host cell association and exposure to amnion cells was also tested. The ST-17 strains differed in their abilities to attach to and invade decidual cells, whereas there were no differences with lung epithelial cells. The ST-19 and ST-23 strains, however, attached to and invaded decidual cells less than both ST-17 strains. Although the ST-23 strain attached to lung epithelial cells better than ST-17 and -19 strains, none of the strains effectively invaded the lung epithelial cells. Notably, the association with host cells resulted in the differential expression of several virulence genes relative to basal expression levels. Similar expression patterns of some genes were observed regardless of cell type used. Collectively, these results show that GBS strains differ in their abilities to attach to distinct host cell types and express key virulence genes that are relevant to the disease process. Enhancing our understanding of pathogenic mechanisms could aid in the identification of novel therapeutic targets or vaccine candidates that could potentially decrease morbidity and mortality associated with neonatal infections.

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