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Article ; Online: Case Report-Secondary Antibody Deficiency Due to Endogenous Hypercortisolism.

Sarcevic, Jelena / Cavelti-Weder, Claudia / Berger, Christoph T / Trendelenburg, Marten

2020 Volume 11, Page(s) 1435

Abstract: Therapeutic corticosteroids have an immunosuppressive function involving several pathways, including lymphocytopenia and hypogammaglobulinemia. While these effects have been well-described in patients that received corticosteroids for therapeutic reasons, ...

Abstract	Therapeutic corticosteroids have an immunosuppressive function involving several pathways, including lymphocytopenia and hypogammaglobulinemia. While these effects have been well-described in patients that received corticosteroids for therapeutic reasons, the effects of endogenous corticosteroids on the immune system are less well-understood. Here, we describe a 21-year old patient with hypercortisolism due to an ACTH producing thymic tumor. In this patient, we observed a decrease in some of the immunoglobulin classes, and in specific B and T cell populations that resembled effects caused by corticosteroid treatment. IgG levels were restored following treatment and normalization of the hypercortisolism.
MeSH term(s)	Adrenocorticotropic Hormone/metabolism ; Agammaglobulinemia/diagnosis ; Agammaglobulinemia/etiology ; B-Lymphocytes/physiology ; Cushing Syndrome/complications ; Cushing Syndrome/diagnosis ; Humans ; Lymphopenia ; Male ; T-Lymphocytes/physiology ; Thymectomy ; Thymus Neoplasms/diagnosis ; Thymus Neoplasms/etiology
Chemical Substances	Adrenocorticotropic Hormone (9002-60-2)
Language	English
Publishing date	2020-07-07
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01435
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Article ; Online: Metabolic outcomes in obese mice undergoing one-anastomosis gastric bypass (OAGB) with a long or a short biliopancreatic limb.

Lazaridis, Ioannis I / Bosch, Angela J T / Keller, Lena / Low, Andy J Y / Tamarelle, Jeanne / Moser, Seraina O / Winter, Denise V / Gómez, Cristina / Peterson, Caspar J / Schneider, Romano / Kraljević, Marko / Odermatt, Alex / Vonaesch, Pascale / Peterli, Ralph / Delko, Tarik / Cavelti-Weder, Claudia

American journal of physiology. Endocrinology and metabolism

2024

Abstract: One-anastomosis gastric bypass (OAGB) has gained importance as a safe and effective operation to treat morbid obesity. It is not known whether a long biliopancreatic limb (BPL) in OAGB surgery compared to a short BPL results in beneficial metabolic ... ...

Abstract	One-anastomosis gastric bypass (OAGB) has gained importance as a safe and effective operation to treat morbid obesity. It is not known whether a long biliopancreatic limb (BPL) in OAGB surgery compared to a short BPL results in beneficial metabolic outcomes. 5-week-old male C57BL/6J mice fed a high-fat diet for 8 weeks underwent OAGB surgery with defined short and long BPL lengths, or sham surgery combined with caloric restriction. Weight loss, glucose tolerance, obesity-related comorbidities, endocrine effects, gut microbiota and bile acids were assessed. Total weight loss was independent of the length of the BPL after OAGB surgery. However, a long BPL was associated with lower glucose-stimulated insulin on day 14, and an improved glucose tolerance on day 35 after surgery. A long BPL resulted in reduced total cholesterol. There were no differences in the resolution of metabolic dysfunction-associated steatotic liver disease and adipose tissue inflammation. Tendencies of an attenuated hypothalamic-pituitary-adrenal axis and aldosterone were present in the long BPL group. In OAGB-operated mice, we found an increase in primary conjugated bile acids (pronounced in long BPL) along with a loss in bacterial
Language	English
Publishing date	2024-04-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00327.2023
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Book ; Online: Generating Personalized Insulin Treatments Strategies with Deep Conditional Generative Time Series Models

Schürch, Manuel / Li, Xiang / Allam, Ahmed / Rathmes, Giulia / Mollaysa, Amina / Cavelti-Weder, Claudia / Krauthammer, Michael

2023

Abstract: We propose a novel framework that combines deep generative time series models with decision theory for generating personalized treatment strategies. It leverages historical patient trajectory data to jointly learn the generation of realistic personalized ...

Abstract	We propose a novel framework that combines deep generative time series models with decision theory for generating personalized treatment strategies. It leverages historical patient trajectory data to jointly learn the generation of realistic personalized treatment and future outcome trajectories through deep generative time series models. In particular, our framework enables the generation of novel multivariate treatment strategies tailored to the personalized patient history and trained for optimal expected future outcomes based on conditional expected utility maximization. We demonstrate our framework by generating personalized insulin treatment strategies and blood glucose predictions for hospitalized diabetes patients, showcasing the potential of our approach for generating improved personalized treatment strategies. Keywords: deep generative model, probabilistic decision support, personalized treatment generation, insulin and blood glucose prediction Comment: Extended Abstract presented at Machine Learning for Health (ML4H) symposium 2023, December 10th, 2023, New Orleans, United States, 17 pages
Keywords	Statistics - Machine Learning ; Computer Science - Machine Learning
Subject code	670
Publishing date	2023-09-28
Publishing country	us
Document type	Book ; Online
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Article ; Online: Diesel Exhaust Particle (DEP)-induced glucose intolerance is driven by an intestinal innate immune response and NLRP3 activation in mice.

Bosch, Angela J T / Rohm, Theresa V / AlAsfoor, Shefaa / Low, Andy J Y / Baumann, Zora / Parayil, Neena / Noreen, Faiza / Roux, Julien / Meier, Daniel T / Cavelti-Weder, Claudia

Particle and fibre toxicology

2023 Volume 20, Issue 1, Page(s) 25

Abstract: Background: We previously found that air pollution particles reaching the gastrointestinal tract elicit gut inflammation as shown by up-regulated gene expression of pro-inflammatory cytokines and monocyte/macrophage markers. This inflammatory response ... ...

Abstract	Background: We previously found that air pollution particles reaching the gastrointestinal tract elicit gut inflammation as shown by up-regulated gene expression of pro-inflammatory cytokines and monocyte/macrophage markers. This inflammatory response was associated with beta-cell dysfunction and glucose intolerance. So far, it remains unclear whether gut inflammatory changes upon oral air pollution exposure are causally linked to the development of diabetes. Hence, our aim was to assess the role of immune cells in mediating glucose intolerance instigated by orally administered air pollutants. Methods: To assess immune-mediated mechanisms underlying air pollution-induced glucose intolerance, we administered diesel exhaust particles (DEP; NIST 1650b, 12 µg five days/week) or phosphate-buffered saline (PBS) via gavage for up to 10 months to wild-type mice and mice with genetic or pharmacological depletion of innate or adaptive immune cells. We performed unbiased RNA-sequencing of intestinal macrophages to elucidate signaling pathways that could be pharmacologically targeted and applied an in vitro approach to confirm these pathways. Results: Oral exposure to air pollution particles induced an interferon and inflammatory signature in colon macrophages together with a decrease of CCR2 Conclusion: In mice, oral exposure to air pollution particles triggers an immune-mediated response in intestinal macrophages that contributes to the development of a diabetes-like phenotype. These findings point towards new pharmacologic targets in diabetes instigated by air pollution particles.
MeSH term(s)	Mice ; Animals ; Vehicle Emissions/toxicity ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Glucose Intolerance/chemically induced ; Inflammation ; Immunity, Innate
Chemical Substances	Vehicle Emissions ; NLR Family, Pyrin Domain-Containing 3 Protein
Language	English
Publishing date	2023-07-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2170936-1
ISSN	1743-8977 ; 1743-8977
ISSN (online)	1743-8977
ISSN	1743-8977
DOI	10.1186/s12989-023-00536-8
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Article ; Online: Lung versus gut exposure to air pollution particles differentially affect metabolic health in mice.

Bosch, Angela J T / Rohm, Theresa V / AlAsfoor, Shefaa / Low, Andy J Y / Keller, Lena / Baumann, Zora / Parayil, Neena / Stawiski, Marc / Rachid, Leila / Dervos, Thomas / Mitrovic, Sandra / Meier, Daniel T / Cavelti-Weder, Claudia

Particle and fibre toxicology

2023 Volume 20, Issue 1, Page(s) 7

Abstract: Background: Air pollution has emerged as an unexpected risk factor for diabetes. However, the mechanism behind remains ill-defined. So far, the lung has been considered as the main target organ of air pollution. In contrast, the gut has received little ... ...

Abstract	Background: Air pollution has emerged as an unexpected risk factor for diabetes. However, the mechanism behind remains ill-defined. So far, the lung has been considered as the main target organ of air pollution. In contrast, the gut has received little scientific attention. Since air pollution particles can reach the gut after mucociliary clearance from the lungs and through contaminated food, our aim was to assess whether exposure deposition of air pollution particles in the lung or the gut drive metabolic dysfunction in mice. Methods: To study the effects of gut versus lung exposure, we exposed mice on standard diet to diesel exhaust particles (DEP; NIST 1650b), particulate matter (PM; NIST 1649b) or phosphate-buffered saline by either intratracheal instillation (30 µg 2 days/week) or gavage (12 µg 5 days/week) over at least 3 months (total dose of 60 µg/week for both administration routes, equivalent to a daily inhalation exposure in humans of 160 µg/m Results: Mice on standard diet exposed to particulate air pollutants by intratracheal instillation developed lung inflammation. While both lung and gut exposure resulted in increased liver lipids, glucose intolerance and impaired insulin secretion was only observed in mice exposed to particles by gavage. Gavage with DEP created an inflammatory milieu in the gut as shown by up-regulated gene expression of pro-inflammatory cytokines and monocyte/macrophage markers. In contrast, liver and adipose inflammation markers were not increased. Beta-cell secretory capacity was impaired on a functional level, most likely induced by the inflammatory milieu in the gut, and not due to beta-cell loss. The differential metabolic effects of lung and gut exposures were confirmed in a "prestressed" HFD/STZ model. Conclusions: We conclude that separate lung and gut exposures to air pollution particles lead to distinct metabolic outcomes in mice. Both exposure routes elevate liver lipids, while gut exposure to particulate air pollutants specifically impairs beta-cell secretory capacity, potentially instigated by an inflammatory milieu in the gut.
MeSH term(s)	Humans ; Mice ; Animals ; Air Pollutants/toxicity ; Air Pollutants/analysis ; Lung ; Air Pollution ; Particulate Matter/toxicity ; Vehicle Emissions/toxicity ; Lipids
Chemical Substances	Air Pollutants ; Particulate Matter ; Vehicle Emissions ; Lipids
Language	English
Publishing date	2023-03-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2170936-1
ISSN	1743-8977 ; 1743-8977
ISSN (online)	1743-8977
ISSN	1743-8977
DOI	10.1186/s12989-023-00518-w
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Article ; Online: CSF1R inhibition with PLX5622 affects multiple immune cell compartments and induces tissue-specific metabolic effects in lean mice.

Bosch, Angela J T / Keller, Lena / Steiger, Laura / Rohm, Theresa V / Wiedemann, Sophia J / Low, Andy J Y / Stawiski, Marc / Rachid, Leila / Roux, Julien / Konrad, Daniel / Wueest, Stephan / Tugues, Sonia / Greter, Melanie / Böni-Schnetzler, Marianne / Meier, Daniel T / Cavelti-Weder, Claudia

Diabetologia

2023 Volume 66, Issue 12, Page(s) 2292–2306

Abstract: Aims/hypothesis: Colony stimulating factor 1 (CSF1) promotes the proliferation, differentiation and survival of macrophages, which have been implicated in both beneficial and detrimental effects on glucose metabolism. However, the physiological role of ... ...

Abstract	Aims/hypothesis: Colony stimulating factor 1 (CSF1) promotes the proliferation, differentiation and survival of macrophages, which have been implicated in both beneficial and detrimental effects on glucose metabolism. However, the physiological role of CSF1 signalling in glucose homeostasis and the potential therapeutic implications of modulating this pathway are not known. We aimed to study the composition of tissue macrophages (and other immune cells) following CSF1 receptor (CSF1R) inhibition and elucidate the metabolic consequences of CSF1R inhibition. Methods: We assessed immune cell populations in various organs by flow cytometry, and tissue-specific metabolic effects by hyperinsulinaemic-euglycaemic clamps and insulin secretion assays in mice fed a chow diet containing PLX5622 (a CSF1R inhibitor) or a control diet. Results: CSF1R inhibition depleted macrophages in multiple tissues while simultaneously increasing eosinophils and group 2 innate lymphoid cells. These immunological changes were consistent across different organs and were sex independent and reversible after cessation of the PLX5622. CSF1R inhibition improved hepatic insulin sensitivity but concomitantly impaired insulin secretion. In healthy islets, we found a high frequency of IL-1β Conclusions/interpretation: Macrophages and macrophage-derived factors, such as IL-1β, play an important role in physiological insulin secretion. A better understanding of the tissue-specific effects of CSF1R inhibition on immune cells and glucose homeostasis is crucial for the development of targeted immune-modulatory treatments in metabolic disease. Data availability: The RNA-Seq dataset is available in the Gene Expression Omnibus (GEO) under the accession number GSE189434 ( http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE189434 ).
MeSH term(s)	Mice ; Animals ; Immunity, Innate ; Lymphocytes ; Macrophages/metabolism ; Glucose/metabolism
Chemical Substances	PLX5622 ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-10-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-023-06007-1
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Article ; Online: Liver, NAFLD and COVID-19.

Hoffmann, Carlotta / Gerber, Philipp A / Cavelti-Weder, Claudia / Licht, Louisa / Kotb, Reham / Al Dweik, Rania / Cherfane, Michele / Bornstein, Stefan R / Perakakis, Nikolaos

Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme

2022 Volume 54, Issue 8, Page(s) 522–531

Abstract: Coronavirus disease 2019 (COVID-19) is characterized by a wide clinical spectrum that includes abnormalities in liver function indicative of liver damage. Conversely, people with liver diseases are at higher risk of severe COVID-19. In the current review, ...

Abstract	Coronavirus disease 2019 (COVID-19) is characterized by a wide clinical spectrum that includes abnormalities in liver function indicative of liver damage. Conversely, people with liver diseases are at higher risk of severe COVID-19. In the current review, we summarize first the epidemiologic evidence describing the bidirectional relationship between COVID-19 and liver function/liver diseases. Additionally, we present the most frequent histologic findings as well as the most important direct and indirect mechanisms supporting a COVID-19 mediated liver injury. Furthermore, we focus on the most frequent liver disease in the general population, non-alcoholic or metabolic-associated fatty liver disease (NAFLD/MAFLD), and describe how COVID-19 may affect NAFLD/MAFLD development and progression and conversely how NAFLD/MAFLD may further aggravate a COVID-19 infection. Finally, we present the long-term consequences of the pandemic on the development and management of NAFLD.
MeSH term(s)	COVID-19 ; Humans ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/epidemiology ; Pandemics ; Risk Factors
Language	English
Publishing date	2022-04-25
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	80125-2
ISSN	1439-4286 ; 0018-5043
ISSN (online)	1439-4286
ISSN	0018-5043
DOI	10.1055/a-1834-9008
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Article ; Online: GLP-1 Analogues as a Complementary Therapy in Patients after Metabolic Surgery: a Systematic Review and Qualitative Synthesis.

Schneider, Romano / Kraljević, Marko / Peterli, Ralph / Rohm, Theresa V / Klasen, Jennifer M / Cavelti-Weder, Claudia / Delko, Tarik

Obesity surgery

2020 Volume 30, Issue 9, Page(s) 3561–3569

Abstract: The evidence is strong that bariatric surgery is superior to medical treatment in terms of weight loss and comorbidities in patients with severe obesity. However, a considerable part of patients presents with unsatisfactory response in the long term. It ... ...

Abstract	The evidence is strong that bariatric surgery is superior to medical treatment in terms of weight loss and comorbidities in patients with severe obesity. However, a considerable part of patients presents with unsatisfactory response in the long term. It remains unclear whether postoperative administration of glucagon-like peptide-1 analogues can promote additional benefits. Therefore, a systematic review of the current literature on the management of postoperative GLP-1 analogue usage after metabolic surgery was performed. From 4663 identified articles, 6 met the inclusion criteria, but only one was a randomized controlled trial. The papers reviewed revealed that GLP-1 analogues may have beneficial effects on additional weight loss and T2D remission postoperatively. Thus, the use of GLP-1 analogues in addition to surgery promises good results concerning weight loss and improvements of comorbidities and can be used in patients with unsatisfactory results after bariatric surgery.
MeSH term(s)	Bariatric Surgery ; Complementary Therapies ; Diabetes Mellitus, Type 2/drug therapy ; Glucagon-Like Peptide 1 ; Humans ; Obesity, Morbid/surgery ; Randomized Controlled Trials as Topic
Chemical Substances	Glucagon-Like Peptide 1 (89750-14-1)
Language	English
Publishing date	2020-06-05
Publishing country	United States
Document type	Journal Article ; Review ; Systematic Review
ZDB-ID	1070827-3
ISSN	1708-0428 ; 0960-8923
ISSN (online)	1708-0428
ISSN	0960-8923
DOI	10.1007/s11695-020-04750-7
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Article ; Online: Roux-en-Y gastric bypass with a long versus a short biliopancreatic limb improves weight loss and glycemic control in obese mice.

Schneider, Romano / Kraljević, Marko / Peterli, Ralph / Rohm, Theresa V / Bosch, Angela J T / Low, Andy J Y / Keller, Lena / AlAsfoor, Shefaa / Häfliger, Simon / Yilmaz, Bahtiyar / Peterson, Caspar J / Lazaridis, Ioannis I / Vonaesch, Pascale / Delko, Tarik / Cavelti-Weder, Claudia

Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery

2022 Volume 18, Issue 11, Page(s) 1286–1297

Abstract: Background: Roux-en-Y gastric bypass (RYGB) results in long-term weight loss and reduced obesity related co-morbidities. However, little is known about how the lengths of the biliopancreatic limb (BPL), the alimentary limb (AL), and the common limb (CL) ...

Abstract	Background: Roux-en-Y gastric bypass (RYGB) results in long-term weight loss and reduced obesity related co-morbidities. However, little is known about how the lengths of the biliopancreatic limb (BPL), the alimentary limb (AL), and the common limb (CL) affect weight loss and glucose metabolism. Objectives: Our aim was to establish a RYGB obese mouse model with defined proportions of the AL and BPL and a constant CL to assess the effects on weight loss,glucose metabolism, and obesity-related co-morbidities. Setting: In vivo mouse study. Methods: Six-week-old male C57BL/6J mice fed with a high-fat diet (HFD) underwent bariatric surgery with defined BPL lengths: a very long, long, and short BPL (35%, 25%, and 15% of total bowel length), or sham surgery. The length of the AL was adjusted to achieve the same CL length. Mice were analyzed for weight loss, glycemic control, and obesity-related co-morbidities. Results: Mice undergoing RYGB surgery with a very long BPL had excessive weight loss and mortality and were therefore not further analyzed. Mice with a long BPL showed a significantly increased total weight loss when compared with mice with a short BPL. In addition, a long BPL improved glucose tolerance, particularly early after surgery. A long BPL was also associated with lower triglyceride levels. Resolution of hepatic steatosis and adipose tissue inflammation was, however, not statistically significant. Of note, bariatric surgery dramatically changed gut microbiota, regardless of limb length. Conclusion: In obese mice, a long BPL results in enhanced weight loss and improved glucose tolerance. These findings could potentially be translated to humans by tailoring the BPL length according to body weight, obesity-related co-morbidities, and total bowel length of an individual patient.
MeSH term(s)	Male ; Humans ; Mice ; Animals ; Gastric Bypass/methods ; Mice, Obese ; Obesity, Morbid/surgery ; Glycemic Control ; Mice, Inbred C57BL ; Weight Loss ; Obesity/surgery ; Glucose
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-06-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2274243-8
ISSN	1878-7533 ; 1550-7289
ISSN (online)	1878-7533
ISSN	1550-7289
DOI	10.1016/j.soard.2022.06.286
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Article ; Online: Epithelial GPR35 protects from Citrobacter rodentium infection by preserving goblet cells and mucosal barrier integrity.

Melhem, Hassan / Kaya, Berna / Kaymak, Tanay / Wuggenig, Philipp / Flint, Emilio / Roux, Julien / Oost, Koen C / Cavelti-Weder, Claudia / Balmer, Maria L / Walser, Jean-Claude / Morales, Rodrigo A / Riedel, Christian U / Liberali, Prisca / Villablanca, Eduardo J / Niess, Jan Hendrik

Mucosal immunology

2022 Volume 15, Issue 3, Page(s) 443–458

Abstract: Goblet cells secrete mucin to create a protective mucus layer against invasive bacterial infection and are therefore essential for maintaining intestinal health. However, the molecular pathways that regulate goblet cell function remain largely unknown. ... ...

Abstract	Goblet cells secrete mucin to create a protective mucus layer against invasive bacterial infection and are therefore essential for maintaining intestinal health. However, the molecular pathways that regulate goblet cell function remain largely unknown. Although GPR35 is highly expressed in colonic epithelial cells, its importance in promoting the epithelial barrier is unclear. In this study, we show that epithelial Gpr35 plays a critical role in goblet cell function. In mice, cell-type-specific deletion of Gpr35 in epithelial cells but not in macrophages results in goblet cell depletion and dysbiosis, rendering these animals more susceptible to Citrobacter rodentium infection. Mechanistically, scRNA-seq analysis indicates that signaling of epithelial Gpr35 is essential to maintain normal pyroptosis levels in goblet cells. Our work shows that the epithelial presence of Gpr35 is a critical element for the function of goblet cell-mediated symbiosis between host and microbiota.
MeSH term(s)	Animals ; Citrobacter rodentium ; Colon/microbiology ; Enterobacteriaceae Infections/metabolism ; Goblet Cells/physiology ; Intestinal Mucosa/metabolism ; Mice ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism
Chemical Substances	GPR35 protein, mouse ; Receptors, G-Protein-Coupled
Language	English
Publishing date	2022-03-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2411370-0
ISSN	1935-3456 ; 1933-0219
ISSN (online)	1935-3456
ISSN	1933-0219
DOI	10.1038/s41385-022-00494-y
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