Human Choriogonadotropin-like Material in Bacteria of Different Species: Electron Microscopy and Immunocytochemical Studies with Monoclonal and Polyclonal Antibodies

Acevedo, Hernan F.; Pardo, Matias; Campbell-Acevedo, E A; Domingue, Gerald J.

doi:10.1099/00221287-133-3-783

Cited by 14 publications

(9 citation statements)

References 19 publications

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“…This ability of intact GC to adsorb anti-hCG antibodies is consistent with previous studies on prokaryote hCG-like molecules which used immunocytochemical protocols to demonstrate production of hCG-like material on the surface of bacteria (1)(2)(3). In addition, studies have determined that this hCG-like material was associated with the bacterial membranes as well as in the soluble protein fraction (19).…”

Section: Discussionsupporting

confidence: 77%

Role of Ribosomal Protein L12 in Gonococcal Invasion of Hec1B Cells

Spence

Clark

2000

Infect Immun

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Previous studies led to the development of a model of contact-induced enhanced gonococcal invasion of human reproductive cells that utilizes the lutropin receptor (LHr) as both the induction signal for conversion to this enhanced-gonococcal-invasion phenotype (Inv ؉ GC) and as the specific Inv ؉ GC uptake mechanism. This model proposes that gonococci express a surface feature that mimics human chorionic gonadotropin (hCG), the cognate ligand for LHr, and that this structure is responsible for the specific and productive interaction of GC with LHr. In this report, we identify a 13-kDa gonococcal protein with immunological similarities to hCG. The antiserum reactivity is specific since interaction with the 13-kDa gonococcal protein can be blocked by the addition of highly purified hCG. This gonococcal "hCG-like" protein, purified from two-dimensional gels and by immunoprecipitation, was determined by N-terminal sequencing to be the ribosomal protein L12. We present evidence that gonococcal L12 is membrane associated and surface exposed in gonococci, as shown by immunoblot analysis of soluble and insoluble gonococcal protein and antibody adsorption studies with fixed GC. Using highly purified recombinant gonococcal L12, we show that preincubation of Inv ؊ GC with micromolar amounts of rL12 leads to a subsequent five-to eightfold increase in invasion of the human endometrial cell line, Hec1B. In addition, nanomolar concentrations of exogenous L12 inhibits gonococcal invasion to approximately 70% of the level in controls. Thus, we propose a novel cellular location for the gonococcal ribosomal protein L12 and concomitant function in LHr-mediated gonococcal invasion of human reproductive cells.

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Section: Discussionsupporting

confidence: 77%

Role of Ribosomal Protein L12 in Gonococcal Invasion of Hec1B Cells

Spence

Clark

2000

Infect Immun

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“…Vaccines prepared with chemically killed SB containing this human choriogonadotropin-like material on the cell surface have immunogenic properties and elicited antibody responses in rabbits. These antibodies also reacted with the human trophoblastic hormone and were similar to antibodies produced by human choriogonadotropin (Domingue et al, 1986 ; Acevedo et al, 1987 ). Furthermore, capsule and cell wall may contribute to the antigenicity of SB .…”

Section: Clinical Infections and Host-immune Response Due To Sbsec Inmentioning

confidence: 53%

The Road to Infection: Host-Microbe Interactions Defining the Pathogenicity of Streptococcus bovis/Streptococcus equinus Complex Members

Jans¹,

Boleij²

2018

Front. Microbiol.

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The Streptococcus bovis/Streptococcus equinus complex (SBSEC) comprises several species inhabiting the animal and human gastrointestinal tract (GIT). They match the pathobiont description, are potential zoonotic agents and technological organisms in fermented foods. SBSEC members are associated with multiple diseases in humans and animals including ruminal acidosis, infective endocarditis (IE) and colorectal cancer (CRC). Therefore, this review aims to re-evaluate adhesion and colonization abilities of SBSEC members of animal, human and food origin paired with genomic and functional host-microbe interaction data on their road from colonization to infection. SBSEC seem to be a marginal population during GIT symbiosis that can proliferate as opportunistic pathogens. Risk factors for human colonization are considered living in rural areas and animal-feces contact. Niche adaptation plays a pivotal role where Streptococcus gallolyticus subsp. gallolyticus (SGG) retained the ability to proliferate in various environments. Other SBSEC members have undergone genome reduction and niche-specific gene gain to yield important commensal, pathobiont and technological species. Selective colonization of CRC tissue is suggested for SGG, possibly related to increased adhesion to cancerous cell types featuring enhanced collagen IV accessibility. SGG can colonize, proliferate and may shape the tumor microenvironment to their benefit by tumor promotion upon initial neoplasia development. Bacteria cell surface structures including lipotheichoic acids, capsular polysaccharides and pilus loci (pil1, pil2, and pil3) govern adhesion. Only human blood-derived SGG contain complete pilus loci and other disease-associated surface proteins. Rumen or feces-derived SGG and other SBSEC members lack or harbor mutated pili. Pili also contribute to binding to fibrinogen upon invasion and translocation of cells from the GIT into the blood system, subsequent immune evasion, human contact system activation and collagen-I-binding on damaged heart valves. Only SGG carrying complete pilus loci seem to have highest IE potential in humans with significant links between SGG bacteremia/IE and underlying diseases including CRC. Other SBSEC host-microbe combinations might rely on currently unknown mechanisms. Comparative genome data of blood, commensal and food isolates are limited but required to elucidate the role of pili and other virulence factors, understand pathogenicity mechanisms, host specificity and estimate health risks for animals, humans and food alike.

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“…"Seven of these were isolated from patients with cancer and were definitely identified as Streptococcus faecalis (three strains), Staphylococcus haemolyticus (two strains) and Staphylococcus epidermidis and Escherichia coli (single strains). The other two strains were cell-wall-deficient (CWD) variants, one identified as Streptococcus bovis, isolated from the blood of a patient with a fever of unknown origin and a possible brain abscess (Acevedo et al, 1987)." • Coatings of proteins, glycoproteins and glycolipids encapsulate many viruses.…”

Section: Biologically Closed Electric Circuitsmentioning

confidence: 99%

Cancer: The ultimate plan

Hague¹

2019

Gen Med Open

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Introduction 2. Electricity, charge carriers and electrical properties of cells. 3. Cellular electrical properties and electromagnetic fields (EMF). 4. Attunement. 5. More details about the electrical roles of membranes and mitochondria. 6. What structures are involved in cancerous transformation? 7. Electronic roles of the cell membrane and the electrical charge of cell surface coats. 8. Cells actually have a number of discrete electrical zones. 9. The electrical properties of cancer cells part 1. 10. The electrical properties of cancer cells part 2. 11. Anatomical concepts • The intravascular space and its components • The cell membrane covering of cells and the attached glycocalyx: Chemical and anatomical roles of the cell membrane. • The extracellular space and the components of the extracellular matrix (ECM) connect to the cytoskeleton of the cells: The electronic functions of the cells and the ECM are involved in healing and tissue regeneration. • The ECM-glycocalyx-membrane interface • The intracellular space 12. Signaling mechanisms may be either chemically or resonantly mediated. 13. Resonance communication mechanisms. 14. The Bioelectrical control system. 15. Electrical properties of the ECM 16. Pathology of the ECM. 17. Mineral and water abnormalities in cancerous and injured tissues: sodium, potassium, magnesium and calcium: their effect on cell membrane potential. 18. Tumor cell differentiation, tumor hypoxia and low cellular pH can affect: gene expression, genetic stability, genetic repair, protein structures, protein activity, intracellular mineral concentrations, and types of metabolic pathways used for energy production. 19. Tumor cells express several adaptations in order to sustain their sugar addiction and metabolic strategies to address this issue. 20. Tumor acidification versus tumor alkalization. 21. The pH of the intracellular and extracellular compartments will also affect the intracellular potassium concentration. 22. Tumor cell coats contain human chorionic gonadotropin and sialic acid as well as negatively charged residues of RNA, which give tumor cells a strong negative charge on their cell surface. 23. Biologically Closed Electric Circuits. 24. Bacteria and viruses in cancer. 25. Treatment devices. 26. Polychromatic states and health: a unifying theory? 27. Treatment Section: Topics to be covered on the electrical properties of cancer cells pH changes Mineral changes Structural membrane changes Membrane potential changes Extracellular matrix changes Protein changes Gene changes Sialic acid-tumor coats-negative charge Sialic acid in viral coats and role of drugs, blood electricfication, nutrients to change infectivity

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Human Choriogonadotropin-like Material in Bacteria of Different Species: Electron Microscopy and Immunocytochemical Studies with Monoclonal and Polyclonal Antibodies

Cited by 14 publications

References 19 publications

Role of Ribosomal Protein L12 in Gonococcal Invasion of Hec1B Cells

Role of Ribosomal Protein L12 in Gonococcal Invasion of Hec1B Cells

The Road to Infection: Host-Microbe Interactions Defining the Pathogenicity of Streptococcus bovis/Streptococcus equinus Complex Members

Cancer: The ultimate plan

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