Review Article

Collaborative Action of Toll-Like and Nod-Like Receptors as Modulators of the Inflammatory Response to Pathogenic Bacteria

Table 3

Analysis of the collaborative action of TLRs and NRLs in response to pathogenic bacteria.

Organism/Cell typePathogen bacteriaReceptors involvedCellular response evaluated

Human homozygotic macrophages (3020insC mutation) and macrophages from TLR2−/− or WT miceMycobacterium tuberculosis NOD2 and TLR2Production of TNF-, IL-1 and IL-6

Human homozygotic macrophages (3020insC mutation) and macrophages from TLR2−/−, TLR4−/−, MyD88−/− or WT miceMycobacterium paratuberculosis NOD2, TLR2 and TLR4Production of TNF-, IL-1, IL-6 and IL-10

Bone marrow-derived macrophages from TLR2−/−, NOD2−/− or WT miceStreptococcus pneumoniae cell wall (PnCW)NOD2 and TLR2Production of IL-10

Mesothelial cells from RICK−/−, NOD1−/− or WT miceListeria monocytogenes NOD1 and TLR2Production of CXCL1 and CCL2

NOD1−/−, NOD2−/−, RIP2−/− or WT miceChlamydophila pneumoniae NOD1, NOD2, TLR2 and TLR4Expression of iNOS, production of NO, IL-6, IL12p40 and IFN-, and bacterial clearance

NLRC4−/−/TLR5−/− or WT miceLegionella pneumophila NLRC4 and TLR5Bacterial clearance, recruitment of neutrophils

MyD88−/−, RIP2−/−, WT mice or with nonfunctional Naip5 geneLegionella pneumophila NLRC4, TLR2, TLR5 and TLR9Replication and dissemination of bacteria, rates of mortality and production of IL-6

NOD1−/−, NOD2−/−, NLRP3−/−, NLRC4−/−, Casp1−/−, Asc−/−, TLR2−/− or WT miceHelicobacter pylori NOD2, TLR2 and NLRP3Production of IL-1 and NLRP3 activation

BALB/c mice and human monocyitic leukemia THP-1Salmonella enterica serovar TyphimuriumNOD1 and TLR5Bacterial clearance and production of IL-5, IL-6, IL-13, IL-21, IL-22, TNF- and -defensin 3

Dendritic cell
Keratinocytes from oral epithelium
Staphylococcus aureus NOD2 and TLR2Production of IL-6 and IL-1

Mice double deficient in Myd−/−Trif−/− Vibrio vulnificus and Vibrio  cholerae TLRs and NLRP3Activation of NF-B

Mice and primary monocytes Pseudomonas aeruginosa TLR5 and NLRC4Autophagy and production of IL-17, IL-18 and Type I IFN