CTL2 is strongly upregulated during secondary wall formation in interfascicular fibers in A. thaliana. Reduction in LY 233053 crystalline cellulose content in ctl1 ctl2 mutants was demonstrated, leading to the to the suggestion that AtCTLs are involved in cellulose assembly. Furthermore, in P. trichocarpa, expression of chitinase genes related to AtCTL1, AtCTL2, and GhCTLVII are highly correlated with secondary wall formation of xylem. It has therefore been proposed that CTL1 and CTL2 work in conjunction with primary- and secondary-cell wall CESAs, respectively. One of the hypotheses for CTL1/2 function is regulation of cellulose assembly and of interL-798,106 action with hemicelluloses via binding to emerging cellulose microfibrils. However, the mechanism of CTL action in cell wall biosynthesis as well as substrates of catalytic activity remains unknown. It was suggested that the likely substrates of plant chitinases may be arabinogalactan proteins, chitooligosaccharides and other GlcNAc-containing glycoproteins or glycolipids and the mechanism by which CTLs act is more likely to involve binding of chitin oligosaccharides than catalysis. Also, it is assumed that chitinases may participate in the generation of such signal molecules that regulate the organogenesis process. The prevalence of community-acquired Staphylococcus aureus pneumonia is low, but the disease can be very severe, with lethality higher than 40% in children and young adults. Due to the spread of community-acquired methicillin-resistant S. aureus and the increased resistance of these strains to antibiotics, it is crucial to understand the pathophysiological mechanisms at play during severe CA-S. aureus pneumonia and to find novel therapeutic options. Panton Valentine Leukocidin is a bi-component leukotoxin composed of LukS-PV and LukF-PV. PVL is very cytotoxic to human neutrophils, monocytes and macrophages. Furthermore, PVL triggers the production of IL-8 by neutrophils and of IL- 1b by monocytes and macrophages. We have recently shown that IL-1b released by rPVL-intoxicated macrophages activates lung epithelial cells to release large amounts of IL-8. IL-1b and IL- 8 are key cytokines to recruit neutrophils. This inflammatory cascade could thus contribute to acute lung inflammation observed during infection. While inflammation is important to clear bacteria, it can be detrimental to the host by triggering tissue damage.