Streptococcus anginosus in the development and treatment of precancerous lesions of gastric cancer

Table 1 Microorganisms associated with precancerous lesions of gastric cancer

Microorganisms	Primary site	Potential mechanism	Ref.
Helicobacter pylori	Gastrointestinal tract, oral	Cytotoxin-associated gene A and vacuolar cytotoxin A cause DNA damage. increased genetic instability leads to mutations	Salvatori et al[71]
			Malfertheiner et al[72]
Streptococcus Anginosus	Oral, nasopharyngeal, gastrointestinal tract, vaginal	The streptococcal surface protein TMPC interacts with ANXA2-mediated attachment and colonization. Spontaneously induces progressive chronic gastritis, atrophy, heterotrophic hyperplasia	Fu et al[73]
			Stasiewicz and Karpiński[74]
EBV	Oropharynx, blood, lymphatic system and other tissues and organs	Viral proteins inducing methylation, regulating host gene expression and malignant transformation	Yang et al[75]
		EBV driving DNA hypermethylation, frequent PIK3CA mutations, and the overexpression of JAK2, PD-L1, and PD-L2	Iizasa et al[47]
Candida albicans	Skin, oral, gastrointestinal tract	Reduces the diversity and abundance of fungi in the stomach; destroys the mucosal epithelium, produces carcinogens, triggers chronic inflammation, induces Th17 immune responses, among other mechanisms	Yu and Liu[49]
			Zhong et al[50]
Others	Gastrointestinal tract, oral, etc.	Homogeneity and diversity of the gastric microbiota; the inflammatory response; dysbiosis of the gastric microbiota favors invasion and growth of pathogens and disrupts the mucosal barrier	Stewart et al[37]
			Liao et al[76]

EBV: Epstein-Barr virus.

Table 2 Studies on various systems of Streptococcus anginosus

Primary site	Developing diseases	Mechanism of action	Subsequent effect	Ref.
Oral	Periodontal abscess	Production of bacteriocins enhances membrane permeability, inhibits the growth of associated species, promotes the development of chronic inflammation and abscesses	Dental periapical abscesses	Fisher and Russell[77]
			OIs	Furuholm et al[78]
Respiratory tract	Lung abscess	Inhalation of oral secretions, direct trauma or surgical bedding, adjacent extension, and hematogenous dissemination	Parapneumonic empyema	Gonzalez et al[79]
Esophagus	Esophageal cancer	Correlated with GrzB+ and CD8+T-cell infiltration in tumor tissues	Esophageal squamous cell carcinoma; Barrett's esophagus	Lv et al[80]
				Wu et al[81]
Stomach	Gastric cancer	Spontaneously induced chronic inflammation, atrophy, mucus chemotaxis, and heterogeneous hyperplasia of the gastric mucosa	PLGC	Yang[7]
				Zhou et al[82]
Intestinal tract	Colorectal cancer	Loss of integrity of the blood mucosal barrier forms pus-filled and infected	Adenocarcinoma of the colon	Rawla et al[83]
Liver	Liver abscess	Causes localized suppurative inflammation destroying hepatocytes and surrounding tissues	PLA	Pilarczyk-Zurek et al[55]
				Morii et al[84]
Genitourinary tract	Genitourinary infections	Invades the bloodstream following urinary tract infections; causes lysis of vaginal epithelial cells	Urinary tract infection	Wu and Zheng[85]
			Aerobic vaginitis	Tao et al[86]
Hearts	Pericarditis, endocarditis	Hematogenous dissemination from distant organs	Bacterial pericarditis; infective endocarditis	Finn et al[87]
Cerebrum	Brain abscess, meningitis	Continuous venous dissemination or hematogenous dissemination from a distant site; invasive pyogenic infection	Subdural hemorrhage	Esplin et al[88]
			Intracranial subdural abscess; hydrocephalus	Sakurai et al[89]

OIs: Odontogenic infections; PLGC: Precancerous lesions of gastric cancer; PLA: Pyogenic liver abscess.