Chronic hepatitis D (CHD) is a severe viral hepatitis characterized by a rapid progression towards advanced chronic liver disease (ACLD). This study aimed to characterize the Austrian CHD epidemiology with respect to disease severity, systemic inflammation and genetic markers. Patients attending one of six participating hospitals from 2020 onwards were included and assessed regarding laboratory data, liver stiffness measurement (LSM) and biopsy, hepatic venous pressure gradient (HVPG) measurement, endoscopy and imaging. In a subset, single nucleotide polymorphisms (SNPs) in genes of interest (IL28B, PNPLA3, SERPINA1, NTCP) were assessed. Biomarkers of liver disease severity were compared to an age-matched cohort of treatment-eligible and treatment-naïve chronic hepatitis B (CHB) patients. A total of 59 CHD patients (median age: 44.0 years, 59.3

BACKGROUND & AIMS:Chronic hepatitis D (CHD) often progresses to advanced chronic liver disease (ACLD). Bulevirtide (BLV) is approved for CHD, yet treatment duration, management of suboptimal response, and the potential for finite treatment remain unclear. METHODS:Patients receiving BLV at 10 Austrian centers were included. Virological, biochemical, and combined response (VR/BR/CR) were assessed every 6 months (M6-M24). Pegylated interferon alfa-2a (PegIFN) was offered to suboptimal responders. RESULTS:Sixty-one patients (median age: 45 years, 60.7% men, ACLD: 68.9%) receiving BLV for a median of 29.0 months were included. VR (Month [M]6: 36.4%, M12: 64.2%, M24: 61.9%), BR (M6: 56.4%, M12: 69.8%, M24: 66.7%), and CR (M6: 25.5%, M12: 47.2%, M24: 42.9%) were maintained for 2 years. Liver stiffness and systemic inflammation (i.e. C-reactive protein [CRP] and procalcitonin [PCT]) decreased under BLV treatment (all p <0.01). Nineteen patients (31.1%) received add-on PegIFN to BLV monotherapy after a median of 10.5 months, inducing a further HDV-RNA decline by 1.65 (IQR 0.81-2.11) log10 copies/ml and reductions in HBsAg levels by 0.08 (IQR 0.02-0.12) log10 IU/L after 24 weeks of combined therapy (both p <0.01). Overall, 32.8% (20/61 patients) achieved HDV-RNA target not detected (TND). Ten (seven BLV mono and three BLV + PegIFN) stopped treatment after 23.0 (IQR 12.0-29.0) months. Seven patients maintained HDV-RNA TND through the last follow-up (median 36.0 months), whereas three patients relapsed but achieved TND again following BLV retreatment. CONCLUSIONS:High response rates to BLV were observed in this nationwide cohort. In suboptimal BLV responders, PegIFN add-on was associated with a significant and partly sustained decline in HDV-RNA and HBsAg, indicating a relevant contribution to long-term viral infection control. Sustained negative HDV-RNA could help identify candidates for finite BLV treatment. IMPACT AND IMPLICATIONS:CHD is a severe form of viral hepatitis with rapid progression to cirrhosis and hepatocellular carcinoma, highlighting the need for effective treatments. In this real-world cohort of 61 Austrian patients, BLV significantly reduced HDV-RNA, alanine aminotransferase, and liver stiffness (p <0.001). Add-on PegIFN resulted in a further decline of HDV-RNA and HBsAg by 24 weeks of combined treatment (p <0.01) in 19 patients with suboptimal response to BLV treatment, and long-term HDV-RNA TND allowed elective treatment discontinuation in 10 patients under close surveillance.

Short bowel syndrome is a rare complex disease that mainly develops due to extensive bowel resections and can lead to chronic intestinal failure. Due to the decreased intestinal surface absorption of macronutrient, micronutrient and/or fluids is reduced. Correspondingly manifold symptoms arise as diarrhoea, weight loss, vitamin deficiencies, chronic kidney disease, hepatopathy and others with great impact on quality of life of patients. Therapy is complex and needs interdisciplinary collaboration between dieticians, gastroenterologists, surgeons and also a dense monitoring of general practitioners. Commonly patients need permanent home-parenteral support. Therapies have to be decided individually and have to be reviewed regularly for effectivity and side effects. Furthermore, periodic monitoring of several clinical and laboratory tests should be performed. Morbidity and mortality of this disease complex is high and lead by appearance and management of complications. This practical guide should give an overview about the disease, diagnostics and management and should enable the best possible care of these complex patients.

Inflammatory bowel disease (IBD) is not only associated with an increased risk of malnutrition, but obesity has also recently emerged, complicating the nutritional management of patients with IBD. Obesity in IBD increases the risk of complications, especially in surgical procedures, and may reduce the response to immunosuppressive treatment. In addition, diet is also likely to play a role in the development of IBD, and highly processed foods in particular may be important. These and other aspects are addressed in the thoroughly revised guideline "Clinical nutrition in inflammatory bowel disease" in 62 evidence- and expert-based recommendations. The guideline is based on the previous DGEM guideline from 2014 and in particular on the current European guideline "ESPEN guideline on Clinical Nutrition in inflammatory bowel disease" from 2023. The guideline was prepared according to the "SIGN methodology", based on an updated literature search from Dec. 2021 to Nov. 2023. For the first time, the new "Crohn's disease exclusion diet" is also discussed in addition to oral nutrition and enteral and parenteral nutrition. The guideline makes clear that professional nutritional diagnostics, nutritional counseling and weight control as well as oral nutrition supplements and oral/enteral formulas play an important role in the treatment of IBD. This can improve the course of the disease and quality of life in IBD patients.

Extending human healthspan requires understanding how lifestyle interventions impact molecular systems across tissues and time. Here, we present the TirolGESUND Lifestyle Atlas (ClinicalTrials.gov: [NCT05678426][1]), a longitudinal, multi-modal resource profiling 156 healthy women (aged 30-60 years) undergoing 6-month intermittent fasting (n=114) or smoking cessation (n=42) interventions. Participants were sampled up to four times across seven tissues and fluids, generating >3,450 biospecimens with harmonised DNA methylation, metabolomics, microbiome, and immune profiling, alongside skin histology, barrier measurements, and rich clinical metadata. We demonstrate the utility of this dataset through: (i) multi-omics-wide association studies linking traits to molecular features; (ii) integrative factor modelling revealing coordinated cross-tissue signatures; (iii) epigenetic-biomarker cross-omic associations, and (iv) CpG-level variance decomposition mapping stable, individual-specific, tissue-restricted, and intervention-responsive methylation patterns. We further show that ageing-linked features are selectively malleable: highly compliant intermittent fasting participants exhibited attenuated or even age-opposing molecular trajectories within six months. The atlas enables unprecedented within-cohort comparisons across omic layers and tissues, supporting discovery of context-dependent biomarkers, cross-system coordination, and intervention responsiveness. Data are available via an interactive portal, with sensitive data under controlled access (). This resource provides a foundation for exploring biomarker association and multi-tissue epigenetics, enabling hypothesis generation and benchmarking for systems biology and human healthspan research. ![Figure][2] Graphical abstract Highlights ### Competing Interest Statement The authors have declared no competing interest. European Union, 874662 Land Tirol Standortagentur Tirol GmbH [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT05678426&atom=%2Fbiorxiv%2Fearly%2F2025%2F09%2F05%2F2025.08.30.673115.atom [2]: pending:yes

While intermittent fasting (IF) promotes longevity in animal models, its systemic effects in humans remain poorly understood. Here, we present a six-month longitudinal IF intervention in 114 women (BMI 25-35) with deep clinical, molecular, and microbiome profiling across >3,400 biospecimens from six tissues. Analyses spanning >2,200 multi-omic features and 11,000 microbial function predictions demonstrate coordinated clinical benefits, including improvements in body composition and cardiorespiratory fitness, and reveal coordinated molecular responses across tissues. Iron metabolism emerged as a central axis: transferrin increased while ferritin, haemoglobin, and erythrocytes decreased, changes that opposed ageing trajectories yet remained within physiological limits. Epithelial DNA methylation biomarkers (cervical, buccal) of cancer risk reduced, while blood clocks were largely unresponsive, underscoring tissue-specificity of the epigenome. Immune profiling uncovered dynamic, partially reversible shifts. Notably, we derived a new immunophenotyping-based ImmuneAge score that increased during fasting and tracked with inflammatory function, while the pro-inflammatory cytokine IL-17A declined selectively in postmenopausal women. Oral microbiota showed rapid restructuring, whereas gut microbiota shifted more subtly toward enhanced metabolic capacity. Together, these data provide unprecedented insight into the systemic and tissue-specific responses to IF in humans and identify iron homeostasis and immune remodelling as candidate mechanisms. Our findings are available through the Lifestyle Atlas (). Highlights ### Competing Interest Statement The authors have declared no competing interest. European Union, 874662 Land Tirol Standortagentur Tirol GmbH

Smoking is one of the single most important preventable risk factors for cancer and other adverse health outcomes [1][1],[2][2]. Smoking cessation represents a key public health intervention with the potential to reduce its negative health outcomes [2][2]–[4][3]. While epidemiological, cross-sectional, and individual longitudinal ‘omic’ or biomarker studies have evaluated the impact of smoking cessation, no study to date has systematically profiled molecular and clinical changes in several organ systems or tissues longitudinally over the course of smoking cessation that could allow for more detailed assessment of response biomarkers and the identification of interindividual differences in the recovery of physiological functions. Here, we report the first human longitudinal multi-omic study of smoking cessation, evaluating 2,501 unique single or composite features from 1,094 longitudinal samples. Our comprehensive analysis, leveraging over half a million longitudinal data points, revealed a profound effect of smoking cessation on epigenetic biomarkers and microbiome features across multiple organ systems within 6 months of smoking cessation, alongside shifts in the immune and blood oxygenation system. Moreover, our multi-omic analysis provided unprecedented granularity that allows for identification of new cross-ome associations for mechanistic discovery. We anticipate that data and an interactive app from the Tyrol Lifestyle Atlas ([eutops.github.io/lifestyle-atlas][4]), comprising the current study and a parallel study arm evaluating the impact of diet on biomarkers of health and disease, will provide the basis for future discovery, biomarker benchmarking in their responsiveness to health-promoting interventions, and study of individualised response group, representing a major advance for personalised health monitoring using biomarkers. ### Competing Interest Statement The authors have declared no competing interest. European Union, https://ror.org/019w4f821, 874662 Land Tirol Standortagentur Tirol GmbH [1]: #ref-1 [2]: #ref-2 [3]: #ref-4 [4]: https://eutops.github.io/lifestyle-atlas

Abstract Background Therapeutic options for patients with IBD have increased substantially over the last decades. Nevertheless, there is still an unmet need for optimization and more targeted allocation of therapies. Treatment with the anti-integrin-a4b7-antibody vedolizumab (VDZ) achieves clinical remission at week 6 in about 50 % of patients with CD and UC . Clinical decision support tools have been developed to help identify patients with a higher likelihood of responding to VDZ. Furthermore, exploratory studies reported associations of response to VDZ with differences in baseline multi-omics measurements. However, personalized selection of biologic therapies in IBD is not yet feasible in clinical practice. Methods IBD patients scheduled for therapy with VDZ (n=70, both biologic-naive and -experienced) were recruited and biosamples were obtained before initiating therapy. Response was assessed at week 20 using a multimodal definition incorporating clinical (Harvey-Bradshaw Index < 5 or partial Mayo Score < 2; no need for steroids after week 12) and biochemical criteria (faecal calprotectin < 250 µg/g). Metabolic assessment of baseline plasma samples was performed using a mass-spectrometry-based commercially available technique (Biocrates MxP Quant 500). Differences in absolute concentrations of 630 metabolites were measured and compared between patients responding and not responding to therapy using multivariate statistical approaches accounting for IBD subtype and patient sex. Results Significant differences between responders and non-responders to VDZ in the baseline concentrations of three metabolites were detected. These included acylcarnitine (HMDB00062) and a ceramide species (HMDB0004950) which were lower in patients who would respond to VDZ. Conversely, N-methylglycine (HMDB00271) was elevated in responders to VDZ. Additionally, dimensionality reduction using partial least-squares discriminant analysis (PLS-DA) revealed associations between the baseline abundance of certain primary and secondary bile acids and response to VDZ. Conclusion In this cohort of IBD patients undergoing therapy with VDZ, baseline host metabolomic variation was associated with response to therapy. Differences in metabolomic profiles are linked to established pathophysiologic processes in the intestine and IBD and represent intriguing possibilities for application in the context of a predictive biomarker signature for response to VDZ.

Background Corticosteroids are used for induction of remission in patients with moderately to severely active ulcerative colitis. However, up to one-third of patients fail to this therapy. We investigated if fecal microbial composition or its metabolic capacity are associated with response to systemic corticosteroids. Methods In this prospective, multicenter study, patients with active ulcerative colitis (Lichtiger score ≥4) receiving systemic corticosteroids were eligible. Data were assessed and fecal samples collected before and after 4 weeks of treatment. Patients were divided into responders (decrease of Lichtiger Score ≥50%) and nonresponders. The fecal microbiome was assessed by the 16S rRNA gene marker and analyzed with QIIME 2. Microbial metabolic pathways were predicted using parsimonious flux balance analysis. Results Among 93 included patients, 69 (74%) patients responded to corticosteroids after 4 weeks. At baseline, responders could not be distinguished from nonresponders by microbial diversity and composition, except for a subgroup of biologic-naïve patients. Within 4 weeks of treatment, responders experienced changes in beta diversity with enrichment of ascribed beneficial taxa, including Blautia, Anaerostipes, and Bifidobacterium, as well as an increase in predicted butyrate synthesis. Nonresponders had only minor longitudinal taxonomic changes with a significant increase of Streptococcus salivarius and a microbial composition shifting away from responders. Conclusion Baseline microbial diversity and composition seem to be of limited use to predict response to systemic corticosteroids in active ulcerative colitis. Response is longitudinally associated with restoration of microbial composition and its metabolic capacity.

Colitis ulcerosa ist eine chronisch entzündliche Darmerkrankung mit Befall des Kolons. Die häufigsten Symptome sind blutige und schleimige Durchfälle, Stuhldrang sowie abdominelle Schmerzen. Diese Symptome stellen für die Betroffenen oft eine wesentliche gesundheitliche Beeinträchtigung dar. Filgotinib ist ein Medikament, das in oraler Form zur Behandlung der moderat bis schwer aktiven Colitis ulcerosa angewendet wird. Es zählt zur Klasse der Januskinase-Inhibitoren und blockiert bevorzugt das Enzym Januskinase 1, das zytokinvermittelte Inflammationsprozesse bei Colitis ulcerosa aufrechterhält. Die Wirksamkeit und Sicherheit von Filgotinib im Vergleich zu Placebo zur Behandlung der moderat bis schwer aktiven Colitis ulcerosa wurden in der SELECTION-Studie über 58 Wochen untersucht. Filgotinib 200 mg führte im Vergleich zu Placebo bei signifikant mehr Patienten zu einer schnellen Verbesserung klinischer Symptome innerhalb der ersten 3–4 Tage der Anwendung. Es führte weiters zu einer höheren Rate an klinischer, endoskopischer und histologischer Remission sowohl nach 10 als auch nach 58 Wochen. Das Sicherheitsprofil der Substanz wurde in einer Langzeitstudie evaluiert. Dabei wurden am häufigsten Übelkeit, Infektionen der oberen Atemwege und der Harnwege, Schwindelgefühl und Lymphopenie berichtet. Die Häufigkeiten von schwerwiegenden Infektionen, Thrombosen und schweren kardialen Nebenwirkungen waren gering und vergleichbar zwischen Filgotinib und Placebo. Besondere Merkmale von Filgotinib sind die einmal tägliche orale Anwendung, die gute Steuerbarkeit aufgrund der kurzen Halbwertzeit sowie die nicht vorhandene Immunogenität im Gegensatz zu den Biologika.

The humanized monoclonal anti-alpha 4 beta 7-integrin-antibody vedolizumab is one of several biologic therapeutic options in moderate-to-severe ulcerative colitis and Crohn's disease. Within the VISIBLE trial program, a novel subcutaneous application route was evaluated in addition to the already established intravenous form. In this position statement, the working group "Inflammatory Bowel Diseases" of the Austrian Society for Gastroenterology and Hepatology (OEGGH) summarizes the evidence regarding the subcutaneous application of vedolizumab. This work supplements a position paper on the value of vedolizumab as a first-line biologic that has already been published and offers useful recommendations for clinical practice.

SummaryIBD is characterized by altered immune reactions and infections are thought to trigger the chronic inflammatory response in IBD. The gut represents a productive reservoir for SARS-CoV-2 and the aforementioned factors together with immunosuppression used to treat IBD are likely influencing the outcomes of IBD patients in COVID-19. We used large and small intestinal organoids from IBD patients and controls to comparatively assess the transcriptional response of the gut epithelium during SARS- CoV-2 infection. Our analysis showed that IBD epithelia exhibit reduced viral loads compared to controls associated with a reduced expression of SARS-CoV-2 entry factors including the host receptor ACE2. Moreover, several genes implicated in the epithelial response to viral infection are intrinsically altered in IBD likely counteracting viral propagation. Notably, differences between IBD phenotypes exist wherein ulcerative colitis represents with induced cell death pathways and an induction of IL-1β despite overall lower viral loads suggestive of increased epithelial stress in this IBD phenotype. Altogether our analysis shows that IBD epithelia are not more prone to SARS-CoV-2 infection but epithelia from ulcerative colitis and Crohn’s disease exhibit specific differences which might explain the differing COVID-19 outcomes between IBD phenotypes.

ZusammenfassungDer humanisierte monoklonale anti-α4β7-Integrin-Antikörper Vedolizumab ist eine von mehreren biologischen Therapieoptionen bei moderaten und schweren Verläufen von Colitis ulcerosa und Morbus Crohn. Im Zuge des VISIBLE-Studienprogramms wurde zusätzlich zur etablierten intravenösen Verabreichung eine subkutane Administrationsform von Vedolizumab erprobt. Die Arbeitsgruppe CED der Österreichischen Gesellschaft für Gastroenterologie und Hepatologie (ÖGGH) fasst in diesem Positionspapier die Datenlage zur subkutanen Applikation von Vedolizumab zusammen, ergänzt ein bestehendes Positionspapier zum Stellenwert von Vedolizumab als Erstlinientherapie bei chronisch entzündlichen Darmerkrankungen und bietet praxisnahe Empfehlungen zur praktischen Anwendung.

Background: Among patients with ulcerative colitis, 30–50% receive corticosteroids within the first five years after diagnosis. We aimed to reconsider their effectiveness in the context of the biologic era. Methods: In this prospective, multicenter study, patients with active ulcerative colitis (Lichtiger score ≥ 4) were eligible if initiating systemic corticosteroids. The primary endpoint was clinical response (decrease in the Lichtiger score of ≥50%) at week 4. Secondary endpoints included combined response defined as clinical response and any reduction in elevated biomarkers (CRP and/or calprotectin). Steroid dependence was assessed after three months. Results: A total of 103 patients were included. Clinical response was achieved by 73% of patients, and combined response by 68%. A total of 15% of patients were steroid-dependent. Activity of colitis did not influence short-term response to treatment but increased the risk for steroid dependence. Biologic-naïve patients responded better than biologic-experienced patients. Past smoking history (OR 5.38 [1.71, 20.1], p = 0.003), hemoglobin levels (OR 0.76 [0.57, 0.99] for higher levels, p = 0.045), and biologic experience (OR 3.30 [1.08, 10.6], p = 0.036) were independently associated with nonresponse. Conclusion: Disease activity was not associated with short-term response to systemic corticosteroids but was associated with steroid dependence in patients with active ulcerative colitis. Exposure to biologics negatively affects response rates.

Hintergrund Unter Kurzdarmsyndrom versteht man einen Symptomenkomplex, der durch eingeschränkte resorptive Kapazität des Darms nach chirurgischer Resektion und damit einhergehender mangelnder Fähigkeit ausreichend Nährstoffe sowie Flüssigkeit zu absorbieren, gekennzeichnet ist. Üblicherweise spricht man hiervon bei einer verbleibenden Darmlänge von 150-200cm. In Abhängigkeit der Länge sowie der Art des verbleibenden Darms kommt es in unterschiedlicher Ausprägung zu Durchfällen, Malabsorption und Malnutrition. So stellt sich beim Kurzdarmsyndrom auch die Frage nach adäquater Resorbierbarkeit notwendiger Medikamente. Sogenannte „direct acting agents“ (DAA) sind eine etablierte und gut tolerierbare Therapie der chronischen Hepatitis C Infektion . Zur Wirksamkeit von DAAs bei Kurzdarmsyndrom liegen aber nur spärlich Fallberichte vor. Bei unserem 39-jährigen polytoxikomanischen Patienten lag neben einem Kurzdarmsyndrom aufgrund einer mesenteriellen Luftembolie mit einer residuellen Darmlänge von 145cm auch eine chronische Hepatitis C Infektion mit hoher Virämie (5 500000 IE/ml) und elevierten Transaminasen vor.

Das Kurzdarmsyndrom ist eine Form von chronisch intestinalem Versagen, ein sehr seltenes und komplexes Krankheitsbild mit großer Auswirkung auf andere Organe und stark eingeschränkter Lebensqualität. Während andere Organversagen wie Leberversagen oder Herzinsuffizienz weithin bekannt sind, ist das Versagen des Dünndarmes ein unterschätztes und unterdiagnostiziertes Krankheitsbild. Es tritt als Folge von ausgeprägten Darmresektionen (Dünndarmrestlänge <2m) auf, seltener aufgrund angeborener Darmatresie oder hoher Fistulierung, und ist gekennzeichnet durch die Notwendigkeit von parenterale Unterstützung. Der Mangel an Mikro-, Makro-Nährstoffen und/oder Flüssigkeit führt zu vielfältigen Symptomen und Problemen und bedarf individueller Therapiekonzepte in enger Zusammenarbeit mit Diätolog*innen und Chirurg*innen. Aufgrund der Seltenheit dieser Erkrankung (Inzidenz von ca 20-40/Million Einwohner) sollten die Patienten an Zentren mit Expertise in Kooperation mit dem Hausärzte-Netzwerk betreut werden. Dieser Leitfaden zielt darauf ab, Hausärzt*innen und anderen Ärzt*innen sowie Patient*innen einen Anhalt zur Diagnostik und Therapie zu geben. Dies ist insbesondere wichtig, da die Mortalität und Morbidität durch die Beherrschung der Komplikationen stark reduziert werden kann ([Table 1]).

The humanized monoclonal anti-α4β7-integrin-antibody vedolizumab is one of several biologic therapeutic options in moderate-to-severe ulcerative colitis and Crohn's disease. Within the VISIBLE trial program, a novel subcutaneous application route was evaluated in addition to the already established intravenous form. In this position statement, the working group "Inflammatory Bowel Diseases" of the Austrian Society for Gastroenterology and Hepatology (OEGGH) summarizes the evidence regarding the subcutaneous application of vedolizumab. This work supplements a position paper on the value of vedolizumab as a first-line biologic that has already been published and offers useful recommendations for clinical practice.

Abstract Background The complement system is a central humoral part of innate immunity and provides essential pattern recognition capabilities as well as effector functions such as opsonisation and target cell lysis. Its prominent role in infection and immunity is undisputed but its involvement in the pathogenesis of inflammatory bowel diseases remains less clear. Published data point to a role of complement within the intestinal lumen supporting clearance of pathogens1. Methods Expression of complement proteins within the intestinal epithelium was quantified by real-time qPCR on lesional and non-lesional biopsy samples from patients with IBD and healthy controls. The concentration of complement proteins was measured in fecal supernatants using ELISA. Flow cytometry of fecal bacterial single cell suspensions was used to assess complement (C3) and antibody (IgA) opsonisation status. Finally, cytometrically distinct populations were isolated by fluorescence-assisted cell sorting (FACS) and microbial community composition was investigated using 16S rDNA sequencing. Prediction of functional profiles from amplicon data was performed using Tax4Fun2. Results Complement expression in intestinal tissue was increased during active inflammation but certain targets were significantly less expressed in lesional mucosal sites (e.g. C6, C7). Free complement proteins in fecal supernatants were mostly undetectable by ELISA. In contrast, complement opsonisation was verified on fecal bacteria using flow cytometry. The degree of complement deposited on bacterial surfaces was significantly correlated with fecal calprotectin (p < 0.01). The percentage of complement-opsonized bacteria ranged from 0 to 5.3 % and did not correlate with intestinal inflammation while percentages of IgA opsonisation were generally higher (0.4 - 90.1%) and increased with fecal calprotectin (p < 0.01). FACS followed by 16S amplicon sequencing detected differences in bacterial taxa abundance between complement-opsonized, IgA-opsonized and non-opsonized fractions. Functional in-silico profiling revealed associations of complement-opsonization with bacterial virulence factors. Conclusion Luminal and mucosal complement expression and activity is evident in patients with IBD. Complement opsonisation profiles are distinct from IgA opsonisation and show features of specificity regarding recognition of microbial features. References: 1 K.P. Aßhauer, B. Wemheuer, R. Daniel, P. Meinicke (2015) Tax4Fun: predicting functional profiles from metagenomic 16S rRNA dataBioinformatics (2015) 31 (17): 2882-2884. 2 Sorbara, M. T., et al. (2018). Complement C3 Drives Autophagy-Dependent Restriction of Cyto-invasive Bacteria. Cell Host Microbe 23(5): 644-652 e645.