Injury to the cerebellum is becoming increasingly recognized in preterm infants. Also in animal models, reduced number of neurons in cerebellum has been reported in the postnatal guinea-pig and fetal sheep following intrauterine growthrestriction. Moreover, a recent study found a diffuse pattern of cerebellar white matter damage in animals exposed to LPS while there was no obvious injury to the cerebellar cortex or of Purkinje cells. In the present study, we found a significant decrease in the volume of the molecular layer after Pam3CSK4 treatment while there were no differences in the granule cell layer or number of Purkinje cells between groups. These observations suggest that TLR effects on the cerebellum may be region specific. We found a significant increase in the number of microglia in Pam3CSK4 treated mice, but we saw no such increase in LPS treated animals. It is generally accepted that microglia are responsible for the innate immune response and that microglia express all TLRs, including TLR2 and TLR4, at readily detectable levels. Thus, direct TLR2 stimulation could lead to the activation of microglia and release of pro-inflammatory cytokines, chemokines and free radicals, which could cause toxicity to neurons or oligodendrocytes. Indeed, levels of IL-1ß, IL-6, KC and MCP-1 significantly increased at 6 hours after the first Pam3CSK4 injection at PND3, indicating that the observed gray/white matter changes in the neonatal brain might be at least partly due to cytokine/chemokine toxicity to neurons/oligodendrocytes. Similar levels of most cytokines were seen after both Pam3CSK4 and LPS treatment, except for IL-1ß and IL-6, which was only significantly elevated following TLR2 agonist stimulation but not LPS stimulation. Of note, such observations may be consistent with the polarization of neonatal mononuclear cells towards relatively high TLR2-mediated IL-6 production. Whether such differences in cytokine responses between Pam3CSK4 and LPS treatment contributed to the differences in microglia activation between these two treatments will be the subject of future investigation. Interestingly, IL-1ß is known to sensitize excitotoxic neonatal brain injury and blocking of the IL-1ß receptor protects the immature brain from hypoxic-ischemic brain damage. We did not observe differences in markers of Bortezomib proliferation or apoptosis at least not at PND 12 and 53, but decreased mature neuronal number suggests that effects of Pam3CSK4 on cell survival may have occurred at a time point prior to that examined. The liver and spleen play a central role in immune responses and the liver is crucial in metabolizing microbial constituents such as Pam3CSK4. Thus the transient enlargement of the spleen and liver in Pam3CSK4 treated mice may indicate an acute reaction of the adaptive immune system and attempts to remove Pam3CSK4 in the blood. Although our study demonstrates that repeated, high-dose, systemic administration of a TLR2 agonist can lead to CNS injury, it is important to note that these effects are likely contextdependent. Indeed, vaccines containing TLR2 agonists, including intradermal bacille Calmette-Guerin and certain formulations of the intramuscular Haemophilus influenzae type b vaccine, have been safely and effectively administered to millions of infants. This underscores the importance of context, including route, frequency, and dose of administration when considering the impact of TLR agonists in injury models. In conclusion, we found that systemic administration of a TLR2 agonist to neonatal mice caused transient gray and white matter injury in both the cerebrum and cerebellum. This suggests that engagement of the TLR2 pathway can have detrimental effects on the developing brain, and may play a role in neonatal brain injury associated with bacterial sepsis. However, neonatal brain injury is often multifactorial, and TLR2 agonist effects may interact with other exposures such as hypoxia/ischemia and/or be involved in a broader inflammatory response following Gram-positive bacterial exposure. Accordingly, it is possible that during Gram-positive bacterial infection, combined insults, including those driven via TLR2, may cause long-lasting functional or structural deficits. Flax phloem fibers are a valuable industrial feedstock and are also a convenient model system for studying secondary cell wall formation. The mechanical properties of bast fibers are largely dependent on the composition of their secondary walls. Bast fibers have gelatinous-type walls, which are rich in cellulose and lack detectable xylan and lignin. Gelatinous fibers are widespread in various land plant taxa, but have been studied primarily in angiosperms. Depending on the species, either phloem or xylem can produce gelatinous fibers in various organs including stems, roots, tendrils, vines, and peduncles. The mechanisms of gelatinous cell wall development in these fibers remain largely unclear. However, some genes implicated in gelatinous cell wall development have been identified. The list includes fasciclin-like arabinogalactan proteins, b-galactosidases, and lipid transfer proteins. A role for b-galactosidases in G-type wall development has been demonstrated functionally. Transcripts of genes encoding chitinase-like proteins are reportedly enriched in fibers, particularly during the cell wall thickening stage of flax phloem cellulosic fiber development. Expression of CTLs during primary or secondary cell wall deposition has also been reported in species other than flax. Plant chitinase-like proteins have been identified in a wide range of organelles and tissues, including the apoplast and vacuole. Chitinase-like proteins belong to a large gene family that includes genuine chitinases and other homologous proteins, which may not have chitinase activity.