. 2015 Jan 1;4(1):24–37. doi: 10.1089/wound.2014.0546

Table 2.

Members of the microbiome modulate the host immune response via toll-like receptors

Bacteria	Interactions with TLRs
S. epidermidis	Modulates TLR3-dependent inflammation by initiating a TLR2-mediated crosstalk mechanism to suppress inflammation.^20,34
	Induces keratinocytes to express endogenous AMPs through a TLR2-dependent mechanism.^20,34
S. aureus	Induction of hBD3 gene expression is TLR2 dependent.^20,34
	Bacterial lipoproteins and lipoteichoic acid serve as TLR2/6 or TLR2/2 agonists.⁵³
Propionibacterium acnes	Colonizes sebaceous glands and stimulates keratinocytes to release inflammatory cytokines via TLR2 activation.⁴⁹
Escherichia coli	Flagellin from the bacteria triggers TLR5 in keratinocytes and induces expression of psoriasin (S100A7c).¹⁵
Listeria monocytogenes	TLR2 is required for rapid inflammasome activation in response to infection.⁶⁴
Mycobacterium leprae	PAMPs from Mycobacteria are capable of altering the expression levels of TLR2 and TLR1.⁶⁵

These interactions are crucial for maintaining tissue homeostasis and limiting pathologic inflammation. TLR recognition of specific microbial targets allows the host to differentiate between normal inhabitants of the microbiome and invasive pathogens.

PAMPs, pathogen-associated molecular patterns.