Enzymatic treatments can be used to modify biopolymers and their interaction, however, so far the entire cell wall of solid bulk wood samples have barely be modified by enzymes. Lignin significantly inhibits enzymatic activity which is due to the fact that lignin adsorbs enzyme physically and restricts the physical contact between enzyme and polysaccharides to a large extent . On the contrary, the cell walls of pulped fibres can be rather easily accessed , therefore it was speculated that the lignin incrustation predominately inhibits the enzyme activity on cellulose and hemicelluloses .
We succeeded in modifying the entirely lignified cell wall of individual fibres by adding a swelling procedure prior to enzyme treatment  and by using a high enzyme concentration. Swelling enhanced penetration of enzymes by loosening of polymers or possibly breaking some bonds between hemicelluloses and lignin. The data indicate that the swelling agent itself did not change the mechanical performance of the load-bearing network under tensile loads.
Being a hydrolase, cellulase enzyme was expected to act on β-1-4-glycosidic linkage of pure cellulose . However, the mode of action might be different in case of native tissues and in pure cellulose. This is due to the higher complexity in the cell wall and presence of other macromolecules like lignin . The mechanisms of enzymatic hydrolysis on crystalline cellulose are not fully clear yet, but hydrogen bond breaking due to action of cellulase on crystalline cellulose was proposed [25, 26]. In agreement with this interpretation, previously Simon and Cosgrove  observed that some hydrogen bond breaking within cellulose enhances the enzyme activity.
As FT-IR measurements before and after the enzymatic treatment were done exactly on the same fibre, the observed diminishing of the bands is due to enzymatic treatment. Hence, the reduction of all the bands might be explained by a thinning of the fibre, where all components were partly “excised” as reported by White and Brown  for the thinning of bacterial cellulose due to cellulase treatment. Recently, similar thinning of cellulose films due to cellulase activity was reported . Though enzymes are substrate specific, our FT-IR results show some degree of removal of glucomannan and lignin after enzyme treatment. This might be explained by the close association between lignin and xylan and between glucomannan and cellulose .
Due to enzyme treatment, mechanical behaviour of isolated fibres differed from unmodified fibres and from simply swollen fibres. A reduced ultimate stress level in enzymatic treated fibres revealed the expected mechanical function of the cellulose reinforcement in the entire cell wall. However, only 20% of the fibres showed the targeted increase in deformability, whereas 80% of the fibres revealed brittle fracture after the same enzyme treatment. In the mechanical response to the enzyme treated fibres two fracture processes may coexist, due to heterogeneity within the fibre or different enzymatic permeability along the fibre. On one hand, a high number of cellulose fibril bundles are disrupted perpendicular to the cellulose chain direction resulting in a brittle failure event before a gliding of fibrils may occur. On the other hand, even though cellulose fibril bundles are partly disrupted, fibrils start gliding due to a pronounced reduction in cross-linking between cellulose fibrils and matrix. This large deformability of fibres up to 20% indicates that a partial degradation of cellulose may enable cellulose fibril gliding in normal wood cells, so far only known for wood with high cellulose microfibril angle.
In contrast to the compression wood fibre (Fig. 1), the enzymatically treated normal wood fibres showed severe damage before the plastic deformation indicating different types of deformation mechanisms. The high cellulose microfibril angle in compression wood fibres allows for a gliding of the cellulose fibrils after the shear strength of the matrix is exceeded. Unloading and reloading of the fibres results in a stiffness recovery indicating that the plastic deformation is mainly mediated by the opening of hydrogen bonds, which does not result in a substantial damage . On the contrary, in terms of the enzymatically modified normal wood fibres, the interface between cellulose fibrils and matrix is pre-damaged, which results in high plastic deformation without stiffness recovery most likely due to gliding of fibrils after severe fracture events at the fibril/matrix interface.
In terms of veneer utilization, the significant reduction of strength and stiffness would be tolerable, since mainly optical properties and a high plastic deformability are important for the covering layer. However, for processing of the veneers, the damage occurring before plastic deformation has to be diminished to avoid too severe or fatal fracture. This problem might be solved by preferential degradation of hemicelluloses, which tether the cellulose fibrils . Another important factor for a transfer of the findings in single fibre tests to veneer processing is related to cell–cell interactions in the veneer. Adjacent cells might reduce the plastic deformability to some extent. However, under wet condition, a higher deformability of individual cells is still preserved in thin tissue sheets ( compression wood behaviour) so that cell–cell interactions do not necessarily reduce deformability drastically. Alternatively, the cell–cell interactions might compensate for the fatal fracture of some individual cell members helping to maintain the structural integrity of the veneer.