Table 1.
Wnt signaling and host-pathogen interaction.
| S.no. | Pathogen | Disease | Associated Wnt homolog | Host-pathogen interaction | References |
|---|---|---|---|---|---|
| 1. | Pseudomonas sp., Streptococcus sp. | Respiratory diseases (e.g., COPD, sepsis etc.) | Wnt5a, Wnt3A | Wnt5a-RAC1-Disheveled mediated cytoskeletal actin rearrangement facilitates autophagy and containment of infection. | (3) |
| Wnt3A mediated increase in antimicrobial peptides causes killing of Pseudomonas. | (46) | ||||
| 2. | Salmonella sp. | Inflammatory bowel disease (IBD), Typhoid | Wnt11 | Wnt11 signaling protects the host from bacterial infection and inhibits apoptosis in intestinal cells. | (43) |
| 3. | Ehrlichia chaffeensis | Human monocytotropic ehrlichiosis (HME) | Wnt5a, Wnt10, Wnt6 | Wnt ligands and associated signaling pathway (β-catenin mediated, NFAT-C1 mediated and others) promotes survival of the pathogen inside the host. | (8) |
| 4. | Mycobacterium tuberculosis | Tuberculosis | Wnt5a, Wnt3A, Wnt6 | Mycobacterium infection promotes Wnt5A expression in human PBMC and blockade of Wnt5A signaling results in inhibition of IL-12p40 and IFNγ secretion. Mycobacterium infection downregulates Wnt5A expression in mouse lungs. | (47, 50) |
| Enhanced IL36γ secretion during infection induces Wnt5A expression which aids in controlling infection through COX-2 mediated autophagy. | (54) | ||||
| Wnt3A promotes an anti-inflammatory effect in murine macrophages during infection in lungs. | (49, 52, 53) | ||||
| Mycobacterium infection induces Wnt6 expression and promotes anti-inflammatory phenotype of macrophages through Arginase-1 expression. | (47) | ||||
| 5. | Leishmania donovani | Visceral leishmaniasis (Kala azar) | Wnt5a | Wnt5A-Rac1-Rho mediated cytoskeletal alteration promotes enhanced fusion of parasitophorous vacuole with lysosome which helps in restraining infection. | (4) |
| 6. | Trypanosoma cruzi | Chagas disease | Wnt3a, Wnt5a | T. cruzi early infection increases expression of Wnt5A, 3A, several Frizzled receptors, and Wnt signaling intermediates. | (7) |
| Activation of β-catenin promotes inhibition of inflammatory cytokine secretion and replication of parasite. | |||||
| 7. | Aspergillus fumigatus | Fungal keratitis | Wnt5a | Host PRR activates Wnt5A expression through ERK and JNK pathway. Wnt5A attracts neutrophils for clearance of Aspergillus fumigatus. | (65) |