About: The Gut Microbiota-Host Partnership as a Potential Driver of Kawasaki Syndrome

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About: The Gut Microbiota-Host Partnership as a Potential Driver of Kawasaki Syndrome Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The Gut Microbiota-Host Partnership as a Potential Driver of Kawasaki Syndrome
Creator	Esposito, Susanna Rigante, Donato Polinori, Ilaria Lee, Kyung-Yil Iebba, Valerio Jeong, Italy Pasteur Italia, Istituto Yu, Jin
Source	Medline; PMC
abstract	Kawasaki syndrome (KS) is a necrotizing vasculitis of small- and medium-sized vessels mostly affecting children under 5 years of age; a host of clinical and epidemiological data supports the notion that KS might result from an infectious disease. However, many efforts have failed to identify a potentially universal trigger of KS. The contribution of the intestinal microbial community—called the “microbiota”—to KS has been evaluated by an increasing number of studies, though limited to small cohorts of patients. Differences in the microbiota composition were found in children with KS, both its acute and non-acute phase, with abnormal colonization by Streptococcus species in the intestinal tract and a wider presence of Gram-positive cocci in jejunal biopsies. In particular, a higher number of Gram-positive cocci (of the genera Streptococcus and Staphylococcus), Eubacterium, Peptostreptococcus, and HSP60-producing Gram-negative microbes have been found in the stools of KS children, and their effects on the antigenic repertoire of specific T cells and Vβ2 T cell expansion have been assessed. Conversely, Lactobacilli were lacking in most children with KS compared with other febrile illnesses and healthy controls. All studies available to date have confirmed that an imbalance in the gut microbiota might indirectly interfere with the normal function of innate and adaptive immunity, and that variable microbiota interactions with environmental factors, mainly infectious agents, might selectively drive the development of KS in genetically susceptible children. Further investigations of the intestinal microflora in larger cohorts of KS patients will provide clues to disentangle the pathogenesis of this disease and probably indicate disease-modifying agents or more rational KS-specific therapies.
has issue date	2019-04-05(xsd:dateTime)
bibo:doi	10.3389/fped.2019.00124
bibo:pmid	31024869
has license	cc-by
sha1sum (hex)	c0713cd16ef0d30221483b314837bcf9e642a884
schema:url	https://doi.org/10.3389/fped.2019.00124
resource representing a document's title	The Gut Microbiota-Host Partnership as a Potential Driver of Kawasaki Syndrome
has PubMed Central identifier	PMC6460951
has PubMed identifier	31024869
schema:publication	Front Pediatr
resource representing a document's body	covid:c0713cd16ef0d30221483b314837bcf9e642a884#body_text
is schema:about of	named entity 'Partnership' named entity 'GUT MICROBIOTA' named entity 'THE GUT' named entity 'HOST' named entity 'POTENTIAL' named entity 'KAWASAKI SYNDROME' named entity 'DRIVER' named entity 'PARTNERSHIP' named entity 'cytomegalovirus' named entity 'intestinal tract' named entity 'Roseburia' named entity 'biopsies' named entity 'antibiotics' named entity 'Veillonella' named entity 'systemic vasculitis' named entity 'acute phase' named entity 'non-infectious diseases' named entity 'gut microbiota' named entity 'human bocavirus' named entity 'Clostridium' named entity 'gut microbiota' named entity 'Korea' named entity 'acute phase' named entity 'acute phase' named entity 'culture methods' named entity 'microbiota' named entity 'Staphylococcus aureus' named entity 'simple sugars' named entity 'anti-inflammatory' named entity 'visfatin' named entity 'autoinflammatory' named entity 'Staphylococcus' named entity 'cesarean delivery' named entity 'non-alcoholic steatohepatitis' named entity 'Enterococcus' named entity 'class II' named entity 'pathogenesis' named entity 'non-infectious' named entity 'necrotizing' named entity 'epithelia' named entity 'anaerobes' named entity 'San Diego' named entity 'infusion' named entity 'heart disease' named entity 'intestinal microbiota' named entity 'ischemic cardiomyopathy' named entity 'vasculitis' named entity 'monogenic' named entity 'IgA' named entity 'herpesvirus 6' named entity 'polymerase chain reaction' named entity 'microbiota' named entity 'Crohn's disease' named entity 'atherosclerosis' named entity 'etiology' named entity 'immune response' named entity 'fat' named entity 'Bifidobacterium' named entity 'febrile' named entity 'innate immunity' named entity 'small subunit ribosomal RNA gene' named entity 'rheumatoid arthritis' named entity 'evidence-based' named entity 'immune cells' named entity '2, 3' named entity 'Gram-negative' named entity 'microbiota' named entity 'β-glucan' named entity 'IVIG' named entity 'microbes' named entity 'anti-inflammatory' named entity 'TNF-α' named entity 'angiogenesis' named entity 'inflammatory reaction'

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