Activation of T cells in the intestinal mucosa in response to gluten exposure is thought to play a key role in the pathogenesis of coeliac disease. Moreover, the response of the rectal mucosa to gluten challenge has been considered a useful predictor of gluten sensitivity in coeliac disease. In the present study, we assessed early changes in the expression of proinflammatory cytokine genes and the T cell receptor (TCR) Vβ repertoire in the rectal mucosa of coeliac disease patients following experimental gluten challenge. Cytokine gene expression was assessed in rectal mucosal biopsies from coeliac disease subjects and controls before and after rectal gluten challenge using quantitative reverse transcription polymerase chain reaction analysis, and the TCR Vβ repertoire was characterized using a multiprobe RNase protection assay. Marked up‐regulation of expression of the C‐X‐C chemokine IL‐8, the proinflammatory cytokine IL‐1β, and the C‐C chemokine monocyte chemotactic protein‐1 occurred within 2–4 h of rectal gluten challenge in coeliac disease subjects, but not in controls. Furthermore, these changes occurred in the absence of parallel changes in the expressed repertoire of TCR Vβ genes in the rectal mucosa. Thus, an increased expression of proinflammatory cytokine genes precedes the expansion of antigen‐specific T cell populations in the early period following experimental exposure of the rectal mucosa of coeliac disease patients to gluten. These findings provide new insights into pathways that may be involved in the activation or reactivation of coeliac disease.

SUMMARYOne of the hallmarks of coeliac disease, both active and treated, is an increased number and proportion of°/± intraepithelial T lymphocytes in the small intestinal mucosa, and an increased number of°/± T cells in the small intestinal mucosa of coeliac disease patients has been associated with the inheritance of specific HLA class II DQ alleles. Nonetheless, the contribution of genetic factors to the development of the T cell receptor (TCR) ± repertoire in coeliac disease is not known. We have assessed the contribution of genetic factors to development of the TCR ± repertoire in coeliac disease, by characterizing the junctional diversity of TCR ± transcripts expressed in the intestine and peripheral blood of a pair of monozygotic (MZ) twins concordant for coeliac disease. TCR V±1, V±2 and V±3 transcripts from small intestinal and colon biopsies, and from peripheral blood mononuclear cells, were amplified by polymerase chain reaction (PCR) and the complementarity determining region (CDR)3 domains of TCR ± transcripts were analysed by denaturing PAGE and direct nucleotide sequencing. The repertoire of TCR ± transcripts and CDR3 amino acid motifs in the intestine and peripheral blood of MZ twins concordant for coeliac disease exhibited no overlap. The TCR ± repertoire in each twin was oligoclonal, and complexity of the junctional regions of their TCR ± transcripts was typical of the repertoire in healthy adults. Thus, genetically identical individuals with coeliac disease have distinct, non-overlapping TCR ± repertoires. Moreover, genetic factors that determine disease susceptibility do not appear to select for specific TCR ± sequences or CDR3 amino acid motifs. Keywords ±T cell receptor coeliac disease monozygotic twins T cell receptor repertoire°/

The Board of the Scandinavian Society of Anaesthesiology and Intensive Care Medicine (SSAI) recognises that the diversity of our members and of our professional and patient community must be reflected in all parts of our organisation. Diversity metrics include, but are not limited to, individual (e.g., age, gender, ethnicity, sexual orientation), cultural (e.g., religious affiliation) and geopolitical (e.g., nationality). These characteristics may cause individuals to feel naturally included in, or excluded from, a group 1 (Table 1).The purpose of this document is to outline a policy to ensure that the diversity of the Nordic community of anaesthesiologists, our workplace and our patients is explicitly addressed in the governance of SSAI, including the SSAI board and committees, clinical practice guidelines, conference speakers/chairs, meetings at local, national and international levels to (i) ensure representativeness, (ii) provide role models and (iii) foster a sense of community based on inclusion. This also applies to events that the SSAI may co-host or for which SSAI nominates a representative (e.g., a representative at meetings held by other networks/organisations or international meetings/ conferences).

Acute endotoxemia induces a prompt, marked and regionally differentiated pro-fibrinolytic response that cannot be discerned based on systemic levels of circulating tPA and that was normalized during volume resuscitation.

Plasma changes of tPA levels support a pulmonary release of tPA in early experimental ALI induced by acute ETX but not lavage, and are related to the inflammatory response. Despite increased vascular fibrinolytic capacity in ETX animals, pulmonary dysfunction was not different from BAL animals. The results demonstrate the close relation between inflammation and coagulation in early ALI.