The inherent properties of chitosan, being nontoxic, biodegradable and antimicrobial have attracted many scientists developing products for humans use in the fields of biomaterials and pharmaceuticals. Examples of such uses are as a carrier for vaccines and drugs, and as a scaffold for living cells. Many projects have failed due to unwanted side reactions, failure to meet technical specifications or to comply with the regulatory standards set by the medical authorities. There are several contradictions in the literature regarding the role chitosan plays in inducing inflammatory reactions. One common view is that chitosan possess anti-inflammatory properties but there are also examples indicating the opposite, that chitosan promotes inflammation. The origin of an inflammatory reaction is often difficult to tell, is it an effect of the chitosan itself or could it be attributed to remaining impurities in it, like endotoxins or protein residues? Purity and consistency in manufacturing are certainly two issues that need to be overcome. The role of chitosan in inflammatory processes is still not fully understood and further experiments with well characterized preparations are needed to reveal the underlying mechanisms.

Technically chitosan can be divided in two categories based on their acetylation pattern, heterogeneously and homogeneously deacetylated chitosans.  Their different acetylation pattern follows on the processes used for their manufacturing. This means that depending on the manufacturing process two chitosans could have the same degree of deacetylation and molecular weight, be indistinguishable by ¹H-NMR and still be structurally different.

With a set of well characterized samples, representing heterogeneously and homogeneously deacetylated chitosans, we have investigated the effects of six different chitosans with respect to their impact on different inflammatory markers and cell toxicity. Our results show large differences between the two categories. The homogenously deacetylated chitosans are all poor inducers of inflammatory reactions and show very low toxicity whereas their heterogeneously deacetyleted cousins are significantly more toxic and seems to promote inflammatory reactions.