**2. Conclusion(s)**

*Advances in Rehabilitation of Hearing Loss*

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**Figure 2.**

**Figure 3.**

*the repair of primary auditory cortex.*

[44–46]. In both humans and animals, this rapid pulmonary entrapment is followed by clearance from the lungs and accumulation in the liver and spleen over subsequent hours to days [43–45]. The MSCs, while entrapped, cause a marked change in circulating cytokines and immune system phenotype [47]. Notably, human MSCs have been shown to be capable of migrating to an area of injury and recruiting tissue specific progenitor cells and regulating the immune response through the secretion of immunomodulatory cytokines and microvesicles (exosomes) containing a variety of bioactive molecules including enzymes, coding and non-coding RNAs, and growth factors [48]. MSCs are also known to secrete molecules that modulate both innate and adaptive immune responses [49]. These secreted molecules act to inhibit the maturation of monocytes into antigen presenting dendritic cells [50], promote a shift in macrophage phenotype from M1 to M2 [51], inhibit the

*Graphical representation of mean fractional anisotropy between responding (blue) and non-responding (orange) subjects at region of interest sites in Heschl's gyrus following cord blood mononuclear treatment for SHNL in children. The data suggest an increase in fractional anisotropy in responding subjects, but not in nonresponders. An increase in the fractional anisotropy suggests improved white matter tract integrity and possibly* 

*Raw axial DTI image with the ROI of the right sided Heschl's gyrus used for FA analysis, outlined in red.*

SNHL is a permanent sensory disorder and a significant worldwide public health problem. Untreated sound deprivation causes permanent reorganization of the auditory pathways that first interferes with and then prevents the development of spoken language. Current treatments augment the function of a damaged cochlea and no reparative treatments currently exist. Both preclinical and clinical data suggest that treatment with progenitor cells may result in cochlear repair in mammals. In addition, very limited data suggest that the repair process may extend beyond the cochlea to the auditory pathways and auditory cortex. This evolving area of research may allow the development of a reparative treatment for non-genetic SNHL.

## **Acknowledgements**

The cord blood phase one trial [3] was supported by a research grant from cord blood registry (CBR®).

## **Conflict of interest**

The authors have no relevant conflicts of interest to report related to this chapter.
