Bugging inflammation: role of the gut microbiota

Shen, Sj; Wong, Connie Hoi Yee

doi:10.1038/cti.2016.12

Cited by 59 publications

(45 citation statements)

References 143 publications

(290 reference statements)

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“…Inflammasome activation does not always correlate with disease. There is extensive evidence indicating beneficial and immunomodulatory effects of a high‐fiber diet on inflammation and inflammatory diseases 2,10,11,38 . However, high‐fiber diet feeding in mice resulted in increased protein levels of cleaved caspase‐1 and IL‐18 in colonic epithelial cells, and G protein‐coupled receptor (GPR)43‐ and GPR109A‐dependent increases in serum IL‐18 levels 2 .…”

Section: Microbiome‐mediated Effects On Nlrp3 Inflammasome Responsesmentioning

confidence: 99%

The role of the microbiome and the NLRP3 inflammasome in the gut and lung

Donovan

Liu

Shen

et al. 2020

Journal of Leukocyte Biology

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The nucleotide‐binding oligomerization domain (NOD)‐like receptor (NLR) family, pyrin domain‐containing protein 3 (NLRP3) inflammasome, is one of the most well‐characterized inflammasomes, activated by pathogen‐associated molecular patterns and damage‐associated molecular patterns, including from commensal or pathogenic bacterial and viral infections. The NLRP3 inflammasome promotes inflammatory cell recruitment and regulates immune responses in tissues such as the gastrointestinal tract and the lung, and is involved in many diseases that affect the gut and lung. Recently, the microbiome in the gut and the lung, and the crosstalk between these organs (gut–lung axis), has been identified as a potential mechanism that may influence disease in a bidirectional manner. In this review, we focus on themes presented in this area at the 2019 World Congress on Inflammation. We discuss recent evidence on how the microbiome can affect NLRP3 inflammasome responses in the gut and lung, the role of this inflammasome in regulating gut and lung inflammation in disease, and its potential role in the gut–lung axis. We highlight the exponential increase in our understanding of the NLRP3 inflammasome due to the synthesis of the NLRP3 inflammasome inhibitor, MCC950, and propose future studies that may further elucidate the roles of the NLRP3 inflammasome in gut and lung diseases.

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Section: Microbiome‐mediated Effects On Nlrp3 Inflammasome Responsesmentioning

confidence: 99%

The role of the microbiome and the NLRP3 inflammasome in the gut and lung

Donovan

Liu

Shen

et al. 2020

Journal of Leukocyte Biology

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“…Human gut microbiota is determined by genetic, epigenetic, and dietary factors (6). When diets and overall health change, the composition of human intestinal microbiota also changes over time (7,8).…”

Section: Introductionmentioning

confidence: 99%

Gut microbiota differences between psoriatic arthritis and undifferentiated arthritis patients

Hsu¹,

Kuo²,

Su³

2020

Preprint

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Introduction Psoriatic arthritis (PSA) is a form of immune-mediated inflammatory arthritis. Studying the gut microbiota of PSA patients may offer new insights into the pathophysiology of this inflammatory joint disease. We designed a prospective study to examine gut microbiome from patients with PSA, primarily with enthesitis and dactylitis, and compared the data with undifferentiated arthritis patients (NO PSA), without enthesitis or dactylitis.Methods We enrolled nine PSA patients and 10 NO PSA patients in this study. The fecal samples were investigated by using 16S rRNA amplicon sequencing, followed by bioinformatics and statistical analyses. Results None of the available objective clinical laboratory data could differentiate PSA from the NO PSA subgroup. The microbiota result shows that Family: XIII_AD3011 is significantly higher in NO PSA patients than PSA patients’ stool samples (p=0.039). Megasphaera elsdenii in the PSA was 10000 times higher than in the NO PSA group.Conclusion Our results demonstrated high intra-group homogeneous and high inter-group heterogeneous microbiota. The clinical symptoms of either enthesitis or dactylitis link to the specific microbiota in the current study. In the future, a larger cohort and thorough biochemical study is needed for confirmation.

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“…The gut epithelium represents the largest barrier in the body, and its continuous cross-talk with gut microbiota is critical for health. 1 Mucosal homeostasis depends on the interplay between epithelia and the immune system. 2 These finely balanced pro-inflammatory and tolerogenic mechanisms are vital for preventing pathogenic infections and fine tuning the microbiome.…”

Section: Introductionmentioning

confidence: 99%

HIV-2 infection is associated with preserved GALT homeostasis and epithelial integrity despite ongoing mucosal viral replication

et al. 2018

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The mechanisms that enable preservation of gut mucosal integrity during persistent viral replication and inherent inflammation remain unclear. Here, we investigated, for the first time, gut homeostasis in HIV-2 infection, a naturally occurring form of attenuated HIV disease. We found viral replication in both sigmoid and ileum of asymptomatic HIV-2+ patients (range: 240-851 circulating CD4+T-cells per μl) despite their undetectable viremia, accompanied by interferon-γ-producing CD8 T-cell expansion, irrespective of antiretroviral treatment. Nevertheless, there was no CD4 T-cell depletion, and Foxp3+ and IL-17- or IL-22-producing CD4 T-cell numbers were unaffected. Moreover, IL-22-producing innate lymphoid cells and IL-22-induced antimicrobial peptides and mucins were maintained. In agreement, the epithelium histology was preserved, including tight junction protein zonula occludens (ZO-1) levels. Furthermore, in vitro infection of colon epithelia with primary isolates revealed no HIV-2 impact on ZO-1 expression. Notably, sigmoid transcriptional levels of CCL20 and CCL28 were significantly increased, in direct correlation with GM-CSF, indicating a local response able to enhance CD4 T-cell recruitment. In conclusion, maintenance of mucosal integrity in HIV-2 infection was associated with T-cell recruitment responses, potentially counteracting CD4 T-cell depletion due to HIV-2 replication. These data have unique implications for the design of therapies targeting gut homeostasis in HIV-1 infection and other chronic inflammatory settings.

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Bugging inflammation: role of the gut microbiota

Cited by 59 publications

References 143 publications

The role of the microbiome and the NLRP3 inflammasome in the gut and lung

The role of the microbiome and the NLRP3 inflammasome in the gut and lung

Gut microbiota differences between psoriatic arthritis and undifferentiated arthritis patients

HIV-2 infection is associated with preserved GALT homeostasis and epithelial integrity despite ongoing mucosal viral replication

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