Molecular characterization of phosphorylcholine expression on the lipooligosaccharide of Histophilus somni

Elswaifi, Shaadi F.; Michael, Frank St.; Sreenivas, Avula; Cox, Andrew D.; Carman, George M.; Inzana, Thomas J.

doi:10.1016/j.micpath.2009.08.001

Cited by 18 publications

(16 citation statements)

References 48 publications

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“…H. influenzae [44e46] and H. somni [47e49] both undergo random phase and antigenic variation of the LOS in vitro or in response to the specific host immune response leading to changes in the composition or structure of the LOS [50e52]. H. somni LOS can also be modified by the addition of phosphorylcholine, which has been demonstrated to be important for colonization of the bacteria to bovine upper respiratory tract [32] and platelet aggregation [39]. Here, we did not observe NET formation in response to LOS purified from H. somni 649, which produces LOS with phosphorylcholine modifications.…”

Section: Discussionmentioning

confidence: 99%

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Histophilus somni causes extracellular trap formation by bovine neutrophils and macrophages

Hellenbrand

Forsythe

Rivera-Rivas

et al. 2013

Microbial Pathogenesis

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Histophilus somni (formerly Haemophilus somnus) is a Gram-negative pleomorphic coccobacillus that causes respiratory, reproductive, cardiac and neuronal diseases in cattle. H. somni is a member of the bovine respiratory disease complex that causes severe bronchopneumonia in cattle. Previously, it has been reported that bovine neutrophils and macrophages have limited ability to phagocytose and kill H. somni. Recently, it was discovered that bovine neutrophils and macrophages produce extracellular traps in response to Mannheimia haemolytica, another member of the bovine respiratory disease complex. In this study, we demonstrate that H. somni also causes extracellular trap production by bovine neutrophils in a dose- and time-dependent manner, which did not coincide with the release of lactate dehydrogenase, a marker for necrosis. Neutrophil extracellular traps were produced in response to outer membrane vesicles, but not lipooligosacchride alone. Using scanning electron microscopy and confocal microscopy, we observed H. somni cells trapped within a web-like structure. Further analyses demonstrated that bovine neutrophils trapped and killed H. somni in a DNA-dependent manner. Treatment of DNA extracellular traps with DNase I freed H. somni cells and diminished bacterial death. Treatment of bovine monocyte-derived macrophages with H. somni cells also caused macrophage extracellular trap formation. These findings suggest that extracellular traps may play a role in the host response to H. somni infection in cattle.

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Section: Discussionmentioning

confidence: 99%

“…DNase I (source: bovine pancreas), PMA, Escherichia coli lipopolysaccharide (LPS) and cytochalasin D were purchased from SigmaeAldrich. H. somni LOS was kindly provided by Dr. Tom Inzana (Blacksburg, VA) [32]. MPER was purchased from Pierce (Rockford, IL) and used to make bPMN lysates.…”

Section: Reagentsmentioning

confidence: 99%

Histophilus somni causes extracellular trap formation by bovine neutrophils and macrophages

Hellenbrand

Forsythe

Rivera-Rivas

et al. 2013

Microbial Pathogenesis

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“…Changes in the RU number of this SSR can introduce frame shifts in the protein coded by the predicted transcript, potentially affecting function. Choline kinases have been reported to be an important virulence factor in H. somni and other species 19,20 thus, the modulation of SSR length could conceivably impact virulence.…”

Section: Resultsmentioning

confidence: 99%

A Computational Method to Quantify the Effects of Slipped Strand Mispairing on Bacterial Tetranucleotide Repeats

Harhay

Bono

et al. 2019

Sci Rep

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The virulence and pathogenicity of bacterial pathogens are related to their adaptability to changing environments. One process enabling adaptation is based on minor changes in genome sequence, as small as a few base pairs, within segments of genome called simple sequence repeats (SSRs) that consist of multiple copies of a short sequence (from one to several nucleotides), repeated in series. SSRs are found in eukaryotes as well as prokaryotes, and length variation in them occurs at frequencies up to a million-fold higher than bacterial point mutations through the process of slipped strand mispairing (SSM) by DNA polymerase during replication. The characterization of SSR length by standard sequencing methods is complicated by the appearance of length variation introduced during the sequencing process that obscures the lower abundance repeat number variants in a population. Here we report a computational approach to correct for sequencing process-induced artifacts, validated for tetranucleotide repeats by use of synthetic constructs of fixed, known length. We apply this method to a laboratory culture of Histophilus somni, prepared from a single colony, and demonstrate that the culture consists of populations of distinct sequence phase and length variants at individual tetranucleotide SSR loci.

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“…Choline (Cho) is essential for the cell wall [64]. Phosphorylcholine (ChoP) is synthesized from Cho by ChoK [65,66]. ChoP involvement in the production of teichoic acids (TA) in the form of lipoteichoic acid (LTA) attached to the membrane and cell wall teichoic acid (CTA) indicates that ChoP is also essential [65,67,68].…”

Section: Bacterial Membrane Lipidsmentioning

confidence: 99%

ChoK-ing the Pathogenic Bacteria: Potential of Human Choline Kinase Inhibitors as Antimicrobial Agents

Khalifa

Few

Too

2020

BioMed Research International

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Novel antimicrobial agents are crucial to combat antibiotic resistance in pathogenic bacteria. Choline kinase (ChoK) in bacteria catalyzes the synthesis of phosphorylcholine, which is subsequently incorporated into the cell wall or outer membrane. In certain species of bacteria, phosphorylcholine is also used to synthesize membrane phosphatidylcholine. Numerous human ChoK inhibitors (ChoKIs) have been synthesized and tested for anticancer properties. Inhibition of S. pneumoniae ChoK by human ChoKIs showed a promising effect by distorting the cell wall and retarded the growth of this pathogen. Comparison of amino acid sequences at the catalytic sites of putative choline kinases from pathogenic bacteria and human enzymes revealed striking sequence conservation that supports the potential application of currently available ChoKIs for inhibiting bacterial enzymes. We also propose the combined use of ChoKIs and nanoparticles for targeted delivery to the pathogen while shielding the human host from any possible side effects of the inhibitors. More research should focus on the verification of putative bacterial ChoK activities and the characterization of ChoKIs with active enzymes. In conclusion, the presence of ChoK in a wide range of pathogenic bacteria and the distinct function of this enzyme has made it an attractive drug target. This review highlighted the possibility of “choking” bacterial ChoKs by using human ChoKIs.

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Molecular characterization of phosphorylcholine expression on the lipooligosaccharide of Histophilus somni

Cited by 18 publications

References 48 publications

Histophilus somni causes extracellular trap formation by bovine neutrophils and macrophages

Histophilus somni causes extracellular trap formation by bovine neutrophils and macrophages

A Computational Method to Quantify the Effects of Slipped Strand Mispairing on Bacterial Tetranucleotide Repeats

ChoK-ing the Pathogenic Bacteria: Potential of Human Choline Kinase Inhibitors as Antimicrobial Agents

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