155 Introduction Inflammatory bowel diseases (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), are chronic ulcerative inflammatory diseases of the gastrointestinal (GI) tract, which are characterized by an inappropriate and uncontrolled immune response against microbiota in genetically susceptible individuals.1 The etiology of IBD remains incompletely understood, although it is believed that a complex interplay between genetic and environmental factors, the gut microbiota and host immunity is driving disease pathogenesis.2,3 Gut microbiota alterations are commonly observed in patients with IBD, which are characterized by decreased microbial diversity, increased proportions of potentially pathogenic bacteria, and decreased proportions of commensal, butyrate-producing bacteria.4-6 Gut bacteria closely interact with the intestinal barrier, where a prodigious passage of luminal antigens occurs, which are continuously sampled by the underlying mucosal immune system as an immune surveillance mechanism.7 A compromised mucosal barrier is a hallmark of IBD, which results in excessive translocation of luminal antigens, eliciting both mucosal and systemic immune responses, which may in turn trigger and/or aggravate intestinal inflammation.8,9 Antimicrobial antibody responses are frequently observed in patients with IBD, particularly in CD.10,11 Circulating IgG may leak into the intestinal lumen when mucosal barrier integrity is compromised by, for example, ulcerative inflammation.12,13 This may result in increased IgGcoating of fecal bacteria. Indeed, we previously observed that IgG-coated fecal bacteria were overrepresented in CD compared with healthy controls, which may also associate with disease activity.13-15 Notably, patients with CD demonstrated elevated binding of IgG derived from autologous serum to fecal bacteria, suggesting earlier exposure to these bacterial antigens, perhaps during disease flares when mucosal barrier function was impaired.13 However, the exact antigenic nature of these IgG immune responses is largely unknown, as well as the exact bacteria that are targeted by autologous serum IgG. In this study, we aimed to investigate to which bacterial genera the humoral IgG response is directed to in patients with IBD and in healthy individuals. To do so, we leveraged magneticactivated cell sorting (MACS) and flow cytometry (FC) procedures to quantify the fractions of different IgG-coated bacteria after incubating fecal samples from patients and healthy individuals with their own (autologous) serum. Furthermore, we characterized the fecal microbial composition of both untreated and autologous serum-incubated fecal samples using 16S rRNA gene sequencing. Antimicrobial IgG immune responses in IBD
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