Fusobacterium nucleatum is a gram-negative anaerobic; within the Fusobacterium genus, most human infections are caused mainly by two species, F. necrophorum, and F. nucleatum.
Numerous studies have reported an association between Fusobacterium nucleatum and CRC. The bacterium has been consistently detected at higher levels in CRC tissues than in adjacent normal tissues. Its presence in CRC has been observed across different geographical regions and populations.
The prevalence of F. nucleatum in CRC tumors varies among studies. Detection rates can range from approximately 20% to over 80%, depending on the population, methods of detection, and other factors. Some studies have guided that the prevalence of Fusobacterium nucleatum may be higher in specific subtypes of CRC, such as microsatellite instability-high (MSI-H) tumors.
Recent research reveals that F. nucleatum may play a role in forming colorectal cancer. F. nucleatum was detected in significantly higher levels in adenoma cells with high-grade dysplasia in 52 Irish people suffering from colorectal adenoma (CRA) than in comparable normal tissues. F. nucleatum was found in tumor and normal tissue from 122 individuals having colorectal cancer (CRC) in three European cohorts, including Germany, the Czech Republic, & Iceland.
F. nucleatum is a type of oral Gram-negative anaerobic bacterium that is non-motile and does not produce spores.
Sizes range from 0.5 to 5 m long and 0.2 to 0.5 m wide.
F. nucleatum cells occurs as fusiform rods with a wide range of lengths. The organism is described as a tiny spindle-shaped rod in the name.
The cell envelope of Fusobacterium nucleatum is complicated structure, with an inner cytoplasmic barrier, an outer membrane, and a thin peptidoglycan layer.
Lipopolysaccharides (LPS) are the basic structures in the outer membrane; the lipid A component of lipopolysaccharides contains beta-1′,6-linked D glucosamine disaccharides and has two phosphatase groups: one in ester linkage and one in glycosidic linkage. D-3-hydroxy hexadecanoic acid substitutes the amino groups of glucosamine disaccharides.
The O-antigen: The lipopolysaccharide (LPS) of Fusobacterium nucleatum comprises three major components: lipid A, core oligosaccharide, and O-antigen. The O-antigen, also known as the O-specific polysaccharide, is the outermost portion of the LPS and is responsible for the antigenic diversity among different strains of F. nucleatum. By using NMR classification, O-antigens were determined in the structure of F. nucleatum‘s strain ATCC 51191, in which the repetitive unit is made up of three distinct monosaccharide residues: β-d-GlcpNAcA, β-d-FucpNAc4NAc, and β-d-GlcpNAc3NAlaA.
Fap2 protein:F nucleatum produces the protein known as Fap2 (Fusobacterium adhesin proteins 2). There is high heterogeneity in the Fap2 protein between strains and subspecies. It participates in the interactions between host epithelial cells and F. nucleatum, especially in the mouth and gastrointestinal tract.
F. nucleatum may also cling to and destroy basement membranes in vivo and it can also link to type 4 collagens. This bacterium has a very high chance of being pathogenic because of its high frequency in periodontal lesions, its production of irritants that affect the tissue, and its ability to form numerous aggregates with other suspected pathogens in periodontal disease (therefore, it functions as a bridge between early and late colonizers on surfaces of teeth).
The bacterium F. nucleatum produces toxic substances that kill or inhibit the proliferation of normal periodontal cells (fibroblasts). F. nucleatum’s ability to produce sulfides may assist the bacterium in eluding detection by the human immune system. Propionate, butyric acid, and ammonium ions are produced.
F. nucleatum can coaggregate and form mutual synergisms with other bacteria in mixed infections. They can adhere to colorectal cancer cells, and this interaction has been shown to enhance the invasion and proliferation of Epstein-Barr Virus (EBV)-infected cells. The combination of F. nucleatum and EBV has been suggested to synergistically promote tumor development and progression in colorectal cancer.
Fusobacterium nucleatum can adhere to the oral mucosa, and this adherence has been shown to enhance the persistence of Human Papillomavirus (HPV) infection and the formation of oral squamous cell carcinoma (OSCC).
Host-derived extracellular tsRNAs are typically encapsulated in extracellular vesicles or associated with proteins to confer tsRNAs stability in human saliva.Host mucosal barriers possess an arsenal of defense molecules to maintain host-microbe homeostases, such as antimicrobial peptides and immunoglobulins like IgA and IgG.
Small RNAs (sRNAs)-mediated interactions between human oral keratinocytes and Fusobacterium nucleatum (Fn) have been reported recently.
Anti-Fn-IgA antibodies: Immunoglobulin A (IgA) is a class of antibodies predominantly found in mucosal secretions, such as saliva, tears, and respiratory and gastrointestinal tracts. IgA plays a crucial role in defending against F. nucleatum—anti-Fn-IgA antibodies. Assessing the levels of anti-Fn-IgA antibodies can provide insights into the immune response to F. nucleatum in the oral cavity.
Human Colorectal Cancer (CRC): F. nucleatum has been linked to CRC tumor characteristics such as advanced stage, greater tumor dimension, and lymph node metastasis. F. nucleatum can build complex microbial communities inside CRC tumors by interacting with other bacterial species found in the gut microbiome.
Acute and Chronic Periodontal Lesions:
In acute lesions, the breakdown of periodontal ligaments, alveolar bone loss, and Fusobacterium nucleatum may cause systemic consequences. Bacteremia, the liberation of bacteria in the bloodstream, can transmit the infection to other body parts or exacerbate systemic conditions in susceptible individuals.
Chronic periodontal lesions develop over an extended period, often because of untreated or inadequately managed periodontal disease progression. Chronic lesions involving F. nucleatum lead to persistent Inflammation, biofilm Formation, and the gradual destruction of the periodontal ligament and alveolar bone. It leads to the formation of deep periodontal pockets, gingival recession, tooth mobility, and eventual tooth loss if left untreated.
Lemierre’s Syndrome: Lemierre’s syndrome, also known as post-anginal sepsis, is a rare but serious condition caused by a Fusobacterium nucleatum infection. It typically starts with a severe sore throat (pharyngitis/tonsillitis) and progresses to the formation of an abscess in the throat, followed by septicemia (bloodstream infection). This syndrome can lead to the formation of septic emboli in distant organs, such as the lungs or joints.
Intra-abdominal Infections:Fusobacterium nucleatum can cause intra-abdominal infections, including peritonitis, appendicitis, and abscesses in the abdominal cavity. These infections often occur due to the spread of bacteria from the gastrointestinal tract or secondary to bowel perforation.
Culture method: The cultures can be grown anaerobically in brain heart infusion media supplemented with 0.5% cysteine and 0.5% haemin.
TaqMan probe-based qPCR examination: Clinical samples, such as oral swabs, saliva, or tissue biopsies, are collected from the patient. The samples are processed to extract DNA, isolating the genetic material of Fusobacterium nucleatum. It utilizes fluorescently labeled probes that bind to the target DNA during amplification. The TaqMan probe is designed with a quencher at the 3′ end and a fluorescent dye at the 5′ end. As the DNA amplification progresses, the probe binds to the target DNA and is degraded by the DNA polymerase enzyme, causing the fluorescence signal to be released. The instrument captures the fluorescence signals generated during the qPCR reaction, and the cycle threshold (Ct) values are determined.
16S rRNA gene V4 region amplification: Tumor samples are collected from patients, typically through biopsy or surgical resection. The samples are processed to extract DNA, isolating the genetic material from the tumor cells and the associated Fusobacterium nucleatum. The amplicons obtained after amplification are purified and then quantified to determine their concentration. The sequencing library containing the V4 amplicons is subjected to high-throughput sequencing using a platform such as Illumina. It generates millions of short reads, each representing a sequence from the V4 region of the 16S rRNA gene.
Control:
Maintaining good oral hygiene is crucial in controlling F. nucleatum in the oral cavity. It includes regular and proper teeth brushing, flossing, and antibacterial mouthwash.
If periodontal disease is present, appropriate treatment should be sought to control F. nucleatum and prevent its progression. It may be scaling, root planing, periodontal surgery, or antibiotic therapy prescribed by a dentist or periodontist.
Structure of the O‐Antigen and the Lipid A from the Lipopolysaccharide of Fusobacterium nucleatum ATCC 51191 – Garcia‐Vello – 2021 – ChemBioChem – Wiley Online Library
Fusobacterium nucleatum is a gram-negative anaerobic; within the Fusobacterium genus, most human infections are caused mainly by two species, F. necrophorum, and F. nucleatum.
Numerous studies have reported an association between Fusobacterium nucleatum and CRC. The bacterium has been consistently detected at higher levels in CRC tissues than in adjacent normal tissues. Its presence in CRC has been observed across different geographical regions and populations.
The prevalence of F. nucleatum in CRC tumors varies among studies. Detection rates can range from approximately 20% to over 80%, depending on the population, methods of detection, and other factors. Some studies have guided that the prevalence of Fusobacterium nucleatum may be higher in specific subtypes of CRC, such as microsatellite instability-high (MSI-H) tumors.
Recent research reveals that F. nucleatum may play a role in forming colorectal cancer. F. nucleatum was detected in significantly higher levels in adenoma cells with high-grade dysplasia in 52 Irish people suffering from colorectal adenoma (CRA) than in comparable normal tissues. F. nucleatum was found in tumor and normal tissue from 122 individuals having colorectal cancer (CRC) in three European cohorts, including Germany, the Czech Republic, & Iceland.
F. nucleatum is a type of oral Gram-negative anaerobic bacterium that is non-motile and does not produce spores.
Sizes range from 0.5 to 5 m long and 0.2 to 0.5 m wide.
F. nucleatum cells occurs as fusiform rods with a wide range of lengths. The organism is described as a tiny spindle-shaped rod in the name.
The cell envelope of Fusobacterium nucleatum is complicated structure, with an inner cytoplasmic barrier, an outer membrane, and a thin peptidoglycan layer.
Lipopolysaccharides (LPS) are the basic structures in the outer membrane; the lipid A component of lipopolysaccharides contains beta-1′,6-linked D glucosamine disaccharides and has two phosphatase groups: one in ester linkage and one in glycosidic linkage. D-3-hydroxy hexadecanoic acid substitutes the amino groups of glucosamine disaccharides.
The O-antigen: The lipopolysaccharide (LPS) of Fusobacterium nucleatum comprises three major components: lipid A, core oligosaccharide, and O-antigen. The O-antigen, also known as the O-specific polysaccharide, is the outermost portion of the LPS and is responsible for the antigenic diversity among different strains of F. nucleatum. By using NMR classification, O-antigens were determined in the structure of F. nucleatum‘s strain ATCC 51191, in which the repetitive unit is made up of three distinct monosaccharide residues: β-d-GlcpNAcA, β-d-FucpNAc4NAc, and β-d-GlcpNAc3NAlaA.
Fap2 protein:F nucleatum produces the protein known as Fap2 (Fusobacterium adhesin proteins 2). There is high heterogeneity in the Fap2 protein between strains and subspecies. It participates in the interactions between host epithelial cells and F. nucleatum, especially in the mouth and gastrointestinal tract.
F. nucleatum may also cling to and destroy basement membranes in vivo and it can also link to type 4 collagens. This bacterium has a very high chance of being pathogenic because of its high frequency in periodontal lesions, its production of irritants that affect the tissue, and its ability to form numerous aggregates with other suspected pathogens in periodontal disease (therefore, it functions as a bridge between early and late colonizers on surfaces of teeth).
The bacterium F. nucleatum produces toxic substances that kill or inhibit the proliferation of normal periodontal cells (fibroblasts). F. nucleatum’s ability to produce sulfides may assist the bacterium in eluding detection by the human immune system. Propionate, butyric acid, and ammonium ions are produced.
F. nucleatum can coaggregate and form mutual synergisms with other bacteria in mixed infections. They can adhere to colorectal cancer cells, and this interaction has been shown to enhance the invasion and proliferation of Epstein-Barr Virus (EBV)-infected cells. The combination of F. nucleatum and EBV has been suggested to synergistically promote tumor development and progression in colorectal cancer.
Fusobacterium nucleatum can adhere to the oral mucosa, and this adherence has been shown to enhance the persistence of Human Papillomavirus (HPV) infection and the formation of oral squamous cell carcinoma (OSCC).
Host-derived extracellular tsRNAs are typically encapsulated in extracellular vesicles or associated with proteins to confer tsRNAs stability in human saliva.Host mucosal barriers possess an arsenal of defense molecules to maintain host-microbe homeostases, such as antimicrobial peptides and immunoglobulins like IgA and IgG.
Small RNAs (sRNAs)-mediated interactions between human oral keratinocytes and Fusobacterium nucleatum (Fn) have been reported recently.
Anti-Fn-IgA antibodies: Immunoglobulin A (IgA) is a class of antibodies predominantly found in mucosal secretions, such as saliva, tears, and respiratory and gastrointestinal tracts. IgA plays a crucial role in defending against F. nucleatum—anti-Fn-IgA antibodies. Assessing the levels of anti-Fn-IgA antibodies can provide insights into the immune response to F. nucleatum in the oral cavity.
Human Colorectal Cancer (CRC): F. nucleatum has been linked to CRC tumor characteristics such as advanced stage, greater tumor dimension, and lymph node metastasis. F. nucleatum can build complex microbial communities inside CRC tumors by interacting with other bacterial species found in the gut microbiome.
Acute and Chronic Periodontal Lesions:
In acute lesions, the breakdown of periodontal ligaments, alveolar bone loss, and Fusobacterium nucleatum may cause systemic consequences. Bacteremia, the liberation of bacteria in the bloodstream, can transmit the infection to other body parts or exacerbate systemic conditions in susceptible individuals.
Chronic periodontal lesions develop over an extended period, often because of untreated or inadequately managed periodontal disease progression. Chronic lesions involving F. nucleatum lead to persistent Inflammation, biofilm Formation, and the gradual destruction of the periodontal ligament and alveolar bone. It leads to the formation of deep periodontal pockets, gingival recession, tooth mobility, and eventual tooth loss if left untreated.
Lemierre’s Syndrome: Lemierre’s syndrome, also known as post-anginal sepsis, is a rare but serious condition caused by a Fusobacterium nucleatum infection. It typically starts with a severe sore throat (pharyngitis/tonsillitis) and progresses to the formation of an abscess in the throat, followed by septicemia (bloodstream infection). This syndrome can lead to the formation of septic emboli in distant organs, such as the lungs or joints.
Intra-abdominal Infections:Fusobacterium nucleatum can cause intra-abdominal infections, including peritonitis, appendicitis, and abscesses in the abdominal cavity. These infections often occur due to the spread of bacteria from the gastrointestinal tract or secondary to bowel perforation.
Culture method: The cultures can be grown anaerobically in brain heart infusion media supplemented with 0.5% cysteine and 0.5% haemin.
TaqMan probe-based qPCR examination: Clinical samples, such as oral swabs, saliva, or tissue biopsies, are collected from the patient. The samples are processed to extract DNA, isolating the genetic material of Fusobacterium nucleatum. It utilizes fluorescently labeled probes that bind to the target DNA during amplification. The TaqMan probe is designed with a quencher at the 3′ end and a fluorescent dye at the 5′ end. As the DNA amplification progresses, the probe binds to the target DNA and is degraded by the DNA polymerase enzyme, causing the fluorescence signal to be released. The instrument captures the fluorescence signals generated during the qPCR reaction, and the cycle threshold (Ct) values are determined.
16S rRNA gene V4 region amplification: Tumor samples are collected from patients, typically through biopsy or surgical resection. The samples are processed to extract DNA, isolating the genetic material from the tumor cells and the associated Fusobacterium nucleatum. The amplicons obtained after amplification are purified and then quantified to determine their concentration. The sequencing library containing the V4 amplicons is subjected to high-throughput sequencing using a platform such as Illumina. It generates millions of short reads, each representing a sequence from the V4 region of the 16S rRNA gene.
Control:
Maintaining good oral hygiene is crucial in controlling F. nucleatum in the oral cavity. It includes regular and proper teeth brushing, flossing, and antibacterial mouthwash.
If periodontal disease is present, appropriate treatment should be sought to control F. nucleatum and prevent its progression. It may be scaling, root planing, periodontal surgery, or antibiotic therapy prescribed by a dentist or periodontist.
Structure of the O‐Antigen and the Lipid A from the Lipopolysaccharide of Fusobacterium nucleatum ATCC 51191 – Garcia‐Vello – 2021 – ChemBioChem – Wiley Online Library
Fusobacterium nucleatum is a gram-negative anaerobic; within the Fusobacterium genus, most human infections are caused mainly by two species, F. necrophorum, and F. nucleatum.
Numerous studies have reported an association between Fusobacterium nucleatum and CRC. The bacterium has been consistently detected at higher levels in CRC tissues than in adjacent normal tissues. Its presence in CRC has been observed across different geographical regions and populations.
The prevalence of F. nucleatum in CRC tumors varies among studies. Detection rates can range from approximately 20% to over 80%, depending on the population, methods of detection, and other factors. Some studies have guided that the prevalence of Fusobacterium nucleatum may be higher in specific subtypes of CRC, such as microsatellite instability-high (MSI-H) tumors.
Recent research reveals that F. nucleatum may play a role in forming colorectal cancer. F. nucleatum was detected in significantly higher levels in adenoma cells with high-grade dysplasia in 52 Irish people suffering from colorectal adenoma (CRA) than in comparable normal tissues. F. nucleatum was found in tumor and normal tissue from 122 individuals having colorectal cancer (CRC) in three European cohorts, including Germany, the Czech Republic, & Iceland.
F. nucleatum is a type of oral Gram-negative anaerobic bacterium that is non-motile and does not produce spores.
Sizes range from 0.5 to 5 m long and 0.2 to 0.5 m wide.
F. nucleatum cells occurs as fusiform rods with a wide range of lengths. The organism is described as a tiny spindle-shaped rod in the name.
The cell envelope of Fusobacterium nucleatum is complicated structure, with an inner cytoplasmic barrier, an outer membrane, and a thin peptidoglycan layer.
Lipopolysaccharides (LPS) are the basic structures in the outer membrane; the lipid A component of lipopolysaccharides contains beta-1′,6-linked D glucosamine disaccharides and has two phosphatase groups: one in ester linkage and one in glycosidic linkage. D-3-hydroxy hexadecanoic acid substitutes the amino groups of glucosamine disaccharides.
The O-antigen: The lipopolysaccharide (LPS) of Fusobacterium nucleatum comprises three major components: lipid A, core oligosaccharide, and O-antigen. The O-antigen, also known as the O-specific polysaccharide, is the outermost portion of the LPS and is responsible for the antigenic diversity among different strains of F. nucleatum. By using NMR classification, O-antigens were determined in the structure of F. nucleatum‘s strain ATCC 51191, in which the repetitive unit is made up of three distinct monosaccharide residues: β-d-GlcpNAcA, β-d-FucpNAc4NAc, and β-d-GlcpNAc3NAlaA.
Fap2 protein:F nucleatum produces the protein known as Fap2 (Fusobacterium adhesin proteins 2). There is high heterogeneity in the Fap2 protein between strains and subspecies. It participates in the interactions between host epithelial cells and F. nucleatum, especially in the mouth and gastrointestinal tract.
F. nucleatum may also cling to and destroy basement membranes in vivo and it can also link to type 4 collagens. This bacterium has a very high chance of being pathogenic because of its high frequency in periodontal lesions, its production of irritants that affect the tissue, and its ability to form numerous aggregates with other suspected pathogens in periodontal disease (therefore, it functions as a bridge between early and late colonizers on surfaces of teeth).
The bacterium F. nucleatum produces toxic substances that kill or inhibit the proliferation of normal periodontal cells (fibroblasts). F. nucleatum’s ability to produce sulfides may assist the bacterium in eluding detection by the human immune system. Propionate, butyric acid, and ammonium ions are produced.
F. nucleatum can coaggregate and form mutual synergisms with other bacteria in mixed infections. They can adhere to colorectal cancer cells, and this interaction has been shown to enhance the invasion and proliferation of Epstein-Barr Virus (EBV)-infected cells. The combination of F. nucleatum and EBV has been suggested to synergistically promote tumor development and progression in colorectal cancer.
Fusobacterium nucleatum can adhere to the oral mucosa, and this adherence has been shown to enhance the persistence of Human Papillomavirus (HPV) infection and the formation of oral squamous cell carcinoma (OSCC).
Host-derived extracellular tsRNAs are typically encapsulated in extracellular vesicles or associated with proteins to confer tsRNAs stability in human saliva.Host mucosal barriers possess an arsenal of defense molecules to maintain host-microbe homeostases, such as antimicrobial peptides and immunoglobulins like IgA and IgG.
Small RNAs (sRNAs)-mediated interactions between human oral keratinocytes and Fusobacterium nucleatum (Fn) have been reported recently.
Anti-Fn-IgA antibodies: Immunoglobulin A (IgA) is a class of antibodies predominantly found in mucosal secretions, such as saliva, tears, and respiratory and gastrointestinal tracts. IgA plays a crucial role in defending against F. nucleatum—anti-Fn-IgA antibodies. Assessing the levels of anti-Fn-IgA antibodies can provide insights into the immune response to F. nucleatum in the oral cavity.
Human Colorectal Cancer (CRC): F. nucleatum has been linked to CRC tumor characteristics such as advanced stage, greater tumor dimension, and lymph node metastasis. F. nucleatum can build complex microbial communities inside CRC tumors by interacting with other bacterial species found in the gut microbiome.
Acute and Chronic Periodontal Lesions:
In acute lesions, the breakdown of periodontal ligaments, alveolar bone loss, and Fusobacterium nucleatum may cause systemic consequences. Bacteremia, the liberation of bacteria in the bloodstream, can transmit the infection to other body parts or exacerbate systemic conditions in susceptible individuals.
Chronic periodontal lesions develop over an extended period, often because of untreated or inadequately managed periodontal disease progression. Chronic lesions involving F. nucleatum lead to persistent Inflammation, biofilm Formation, and the gradual destruction of the periodontal ligament and alveolar bone. It leads to the formation of deep periodontal pockets, gingival recession, tooth mobility, and eventual tooth loss if left untreated.
Lemierre’s Syndrome: Lemierre’s syndrome, also known as post-anginal sepsis, is a rare but serious condition caused by a Fusobacterium nucleatum infection. It typically starts with a severe sore throat (pharyngitis/tonsillitis) and progresses to the formation of an abscess in the throat, followed by septicemia (bloodstream infection). This syndrome can lead to the formation of septic emboli in distant organs, such as the lungs or joints.
Intra-abdominal Infections:Fusobacterium nucleatum can cause intra-abdominal infections, including peritonitis, appendicitis, and abscesses in the abdominal cavity. These infections often occur due to the spread of bacteria from the gastrointestinal tract or secondary to bowel perforation.
Culture method: The cultures can be grown anaerobically in brain heart infusion media supplemented with 0.5% cysteine and 0.5% haemin.
TaqMan probe-based qPCR examination: Clinical samples, such as oral swabs, saliva, or tissue biopsies, are collected from the patient. The samples are processed to extract DNA, isolating the genetic material of Fusobacterium nucleatum. It utilizes fluorescently labeled probes that bind to the target DNA during amplification. The TaqMan probe is designed with a quencher at the 3′ end and a fluorescent dye at the 5′ end. As the DNA amplification progresses, the probe binds to the target DNA and is degraded by the DNA polymerase enzyme, causing the fluorescence signal to be released. The instrument captures the fluorescence signals generated during the qPCR reaction, and the cycle threshold (Ct) values are determined.
16S rRNA gene V4 region amplification: Tumor samples are collected from patients, typically through biopsy or surgical resection. The samples are processed to extract DNA, isolating the genetic material from the tumor cells and the associated Fusobacterium nucleatum. The amplicons obtained after amplification are purified and then quantified to determine their concentration. The sequencing library containing the V4 amplicons is subjected to high-throughput sequencing using a platform such as Illumina. It generates millions of short reads, each representing a sequence from the V4 region of the 16S rRNA gene.
Control:
Maintaining good oral hygiene is crucial in controlling F. nucleatum in the oral cavity. It includes regular and proper teeth brushing, flossing, and antibacterial mouthwash.
If periodontal disease is present, appropriate treatment should be sought to control F. nucleatum and prevent its progression. It may be scaling, root planing, periodontal surgery, or antibiotic therapy prescribed by a dentist or periodontist.
Structure of the O‐Antigen and the Lipid A from the Lipopolysaccharide of Fusobacterium nucleatum ATCC 51191 – Garcia‐Vello – 2021 – ChemBioChem – Wiley Online Library
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