A reduced diversity of the gastrointestinal commensal microbiota is associated with the development of several inflammatory diseases. Recent reports in humans and animal models have demonstrated the beneficial therapeutic effects of infections by parasitic worms (helminths) in some inflammatory disorders, such as inflammatory bowel disease (IBD) and coeliac disease (CeD). Interestingly, these studies have described how helminths may alter the intestinal microbiota, potentially representing a mechanism by which they regulate inflammation. However, for practical reasons, these reports have primarily analysed the faecal microbiota. In the present investigation, we have assessed, for the first time, the changes in the microbiota at the site of infection by a parasitic helminth (hookworm) and gluten-dependent inflammation in humans with CeD using biopsy tissue from the duodenum. Hookworm infection and gluten exposure were associated with an increased abundance of species within the Bacteroides phylum, as well as increases in the richness and diversity of the tissue-resident microbiota within the intestine, results that are consistent with previous reports using other helminth species in humans and animal models. Hence, this may represent a mechanism by which parasitic helminths may restore intestinal immune homeostasis and exert a therapeutic benefit in CeD, and potentially other inflammatory disorders.

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Recent studies suggest that notochordal cells (NCs) might be involved in intervertebral disc homeostasis, a role exploitable to counteract matrix degradation as observed during degeneration. This study aimed to evaluate the potential of NCs to promote matrix production by nucleus pulposus cells (NPCs) and to compare it to the currently proposed addition of bone marrow stromal cells (BMSCs). Using alginate beads, bovine NPCs were exposed for 28 d to porcine NC conditioned medium (NCCM); direct co-culture with porcine NCs or bovine BMSCs; or the combination of BMSCs and NCCM. Effects on cell proliferation, disc matrix production (proteoglycans, collagens) and disc matrix protein expression (aggrecan, collagen 1 and 2, SOX9) were determined and compared to TGFβ stimulation. NCCM strongly promoted NPC proliferation (x 2.2) and matrix production (x 3.9) to levels similar to that with TGFβ, whereas the direct addition of NCs had no effect. Co-culture of NPCs and BMSCs led to proteoglycan synthesis similar to NPCs alone, which was slightly improved by NCCM (x 1.5). Histological analysis confirmed biochemical data. Gene expression of analysed proteins remained stable for all groups and unaffected by medium conditions. NCs could substantially stimulate NPCs through factors secreted into conditioned medium and in levels similar to the addition of BMSCs. This study showed that molecular agents secreted by NCs constitute a promising alternative to the proposed "standard" injection of BMSCs for disc repair: their effects are similar, do not require the injection of a large number of cells and can be further amplified when the factors are identified.

The genome sequence described is that of strain BBH18, isolated from sputum, and not of strain RH4, which was isolated from blood. Consequently, the title should read "Genome Analysis of Moraxella catarrhalis Strain BBH18, a Human Respiratory Tract Pathogen," and the strain name RH4 should be replaced by BBH18 throughout the manuscript. Furthermore, in the abstract (page 3574, line 4), introduction (page 3574, column 2, line 27), and Materials and Methods (page 3575, column 1, lines 13 and 14), the phrase "isolated from blood of an infected patient (14)" should be changed to "isolated from sputum of a patient with COPD during an exacerbation (45)." The correct reference for strain BBH18 is reference 45 (A.