AMCase is induced during TH2 inflammation through an interleukin (IL)-13 dependent mechanism
and has been demonstrated to be heavily over-expressed in human asthmatic tissue [10,12]. Inhibition
of the AMCase with the well known chitinase inhibitor allosamidin reduced the inflammation [12].
The fact that chitinases are a factor in host antiparasite responses and in asthmatic TH2 inflammation
led to the hypothesis that asthma may be a parasite-independent antiparasite response [10], which
again suggests that inhibition of AMCase is a potential target for asthma therapy [9–12]. It has been
shown that partially deacetylated CHOS can function as inhibitors of family 18 chitinases [103–105].
There is therefore a great potential for CHOS as an anti-inflammatory drug in patients with asthma.
For a more detailed description of this and related topics, see the review by Muzzarelli in this special
issue of Marine Drugs [143].