TABLE 3.

Studies revealing the activation of TLRs in response to bacterial presence/perturbation in various tumors.

Tumors	Bacterial signals	Activated TLRs	Effects	References
Lower gastrointestinal tumor	Helicobacter pylori	TLR2 upregulation	Proliferation of intestinal epithelial cells	Huang et al., 2007
	Fusobacterium nucleatum	TLR2/TLR4	Proliferation of cancer cells Resistance to chemotherapy in CRC	Yu et al., 2017; Sun et al., 2019
	LPS	TLR4	M2 macrophages switch and secretion of cytokines in CRC	Li et al., 2019
Esophageal adenocarcinoma	Gram negative bacteria	TLR4	Inflammation, apoptosis blockage, innate, and adaptive immune responses	Neto et al., 2016
Oral squamous cell carcinoma	LPS	TLR4	Cancer progression and migration Tumor escape	Huang et al., 2005; Kurago et al., 2008; He et al., 2015; Zhang et al., 2019
Pancreatic cancer	Distal microbial dysbiosis	TLR2 and TLR5 upregulation	Immunosuppressive phenotype, T cells anergy and increased tumor growth	Pushalkar et al., 2018
Liver cancer	LPS	TLR4	Hepatocellular carcinoma promotion, proliferation and prevention of apoptosis	Dapito et al., 2012
Lung cancer	Pneumotype supraglottic predominant taxa (SPT)	TLR2/4	Attenuated immune responses of alveolar macrophages	Segal et al., 2016
	Lactobacillus, Streptococcus, and Staphylococcus	TLR-MyD88 dependent pathways	Expansion of IL-17-producing γδ T cells	Jin et al., 2019
	Staphylococcus aureus	TLR2	Recruitment and polarization of CCR2 + CD11B + monocytes into M2 alveolar macrophages	Wang et al., 2013
Breast cancer	Lower number of bacteria	TLR2, 5 and 9	Lower pro-inflammatory cytokines as IL-12A	Xuan et al., 2014
	LPS	TLR4	Metastasis	Beutler, 2000
	Pseudomonas aeruginosa	TLR4	Metastasis	Li et al., 2017

The table shows TLRs activated in different tumors (lower and upper gastrointestinal, pancreas, liver, lungs, and breast) by different bacterial signals, derived from microbial changes at the tumor site (dysbiosis). On the right, references are reported.