**5. Conclusion**

Wnt5A signaling maintains immune homeostasis [40]. If Wnt5A signaling is not sufficient a disturbed immune homeostasis could lead to adverse effects during *L. donovani* infection. Recently, it has been suggested that *L. donovani* infection associated with a skewed hematopoiesis program promotes the visceral disease [60]. Since Wnt5A signaling is involved in hematopoiesis [61], it is important to have a clear understanding of the role of Wnt5A directed hematopoiesis during *L. donovani* infection.

*L. donovani* through its evolution has undergone various changes to accommodate itself efficiently in its ever-changing environment. Often drugs have been rendered useless by the emergence of drug resistant strains. Therefore, it would be an efficient strategy to identify host cell factors, which act against these infections and revamp them. Our results indicate that host Wnt5A signaling restricts infection by both antimony drug sensitive and resistant *L. donovani* strains at least partly by prohibiting parasite niche formation within host macrophages. Interestingly, in a follow up study we found a similar kind of result with *Pseudomonas aeruginosa* or *Streptococcus pneumoniae*. These pathogenic bacteria degrade Wnt5A from the system and when Wnt5A is added exogenously the macrophages efficiently lower the bacterial load. The clearance of bacteria was found to happen through cytoskeletal reorganization and efficient formation of LC3B containing phagosome [43]. Recently high serum levels of the Wnt antagonist Dkk1 has been correlated with a predominantly Th2 phenotype during the onset of experimental cutaneous leishmaniasis [62]. Since Wnt5A supports a pro-inflammatory cytokine signature its potential for protection against parasite infection may also involve prevention of the predominantly Th2 signature that sustains infection. Thus Wnt5A signaling plays an important role in maintaining an innate immune readiness within macrophages for pathogenic onslaught.

**111**

**Author details**

Arijit Chakraborty, Shreyasi Maity and Malini Sen\*

\*Address all correspondence to: msen648@gmail.com

Chemical Biology, Kolkata, India

provided the original work is properly cited.

Division of Cancer Biology and Inflammatory Disorder, CSIR-Indian Institute of

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

*Wnt5A Signaling Antagonizes* Leishmania donovani *Infection*

This work was supported by ICMR, Govt. of India (2016-0222/CMB/ADHOC-

BMS dated 04/12/2018), Institutional funding (BSC0114, BSC0116). SM was

supported by Research Scholar Fellowship from UGC, Govt. of India.

The authors declare that there is no conflict of interest.

*DOI: http://dx.doi.org/10.5772/intechopen.87928*

**Acknowledgements**

**Conflict of interest**
