Aberrant expansion of segmented filamentous bacteria in IgA-deficient gut

By Keiichiro Suzuki, B. Meek, Yasuko Doi, M. Muramatsu, T. Chiba, Tasuku Honjo, S. Fagarasan. Proceedings of the National Academy of Sciences of the United States of America, 2004

742 citations recorded by the source corpus.

Subfields: Biotechnology, Food Science, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/8ebb062718a26e3343cd1c0508078895e5bc6a20

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biotechnology

In Food Science

In Molecular Biology

Citations in the corpus

Paneth cells, antimicrobial peptides and maintenance of intestinal homeostasis (2011, background): “In addition, the absence of IgA results in notable changes in microbial colonizatio”
Worlds within worlds: evolution of the vertebrate gut microbiota (2008, background): “Furthermore, the adaptive immune system is known to shape community composition in the gut: for example, IgA deficiency leads to altered gut communities in mic”
Immune adaptations that maintain homeostasis with the intestinal microbiota (2010, background): “Secreted IgA limits bacterial association with the intestinal epithelial cell surfac”
Ecological and evolutionary forces shaping microbial diversity in the human intestine. (2006, positive): “…the gut microbial communities of immunodeficient mice has failed to demonstrate marked changes in species composition compared to normal controls (Suzuki et al., 2004), suggesting that the adaptive immune system is not effective in eliminating a single species but rather modulates the relative…”
The human gut microbiome: ecology and recent evolutionary changes. (2011, background): “Although the mechanism involved is not well understood, IgA may also shape the diversity of the normal gut microbiota and reduce the amount of bacteria in the proximal SI (90).”
NLRP6 inflammasome is a regulator of colonic microbial ecology and risk for colitis (2011, positive): “To identify whether increased colitis severity is driven by bacterial components, we first treated ASC À/À mice with a combination of antibiotics known to reduce the proportional representation of a broad range of bacterial phylotypes in the gut (Suzuki et al., 2004; Rakoff-Nahoum et al., 2004).”
Induction of intestinal Th17 cells by segmented filamentous bacteria (2009, background): “Mice lacking the activation-induced cytidine deaminase (AID) required for antibody diversification had outgrowth of SFB in their small intestine (Suzuki et al., 2004).”
Communicable ulcerative colitis induced by T-bet deficiency in the innate immune system. (2007, positive): “A genomic survey of mouse intestinal microbiota showed an anaerobic expansion of the microbiota in RAG2-/- mice (Suzuki et al., 2004).”
How bacterial pathogens colonize their hosts and invade deeper tissues. (2015, background): “IgA, produced by B cells in the lamina propria and secreted into 99 the mucus via epithelial cells, are also involved in limiting bacterial association with the 100 intestinal epithelium and intestinal barrier crossing [13],[14].”
Gut microbiota in health and disease. (2010, background): “Interestingly, although Gm bacteria or their structural components were able to stimulate IgA production, the absence of intestinal IgA resulted in overgrowth of SFB, a group of Gm bacteria (300), suggesting that induction of sIgA might also be a form of competition between different microbiota memb”
IgA response to symbiotic bacteria as a mediator of gut homeostasis. (2007, background): “Changes in gut microbial ecology have been docu- mented in mice with immune deficiencies (Fagarasan et al., 2002; Suzuki et al., 2004).”