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dc.contributor.authorKarmarkar, Dipti
dc.contributor.authorRock, Kenneth L.
dc.date2022-08-11T08:08:30.000
dc.date.accessioned2022-08-23T15:57:46Z
dc.date.available2022-08-23T15:57:46Z
dc.date.issued2013-12-01
dc.date.submitted2015-01-15
dc.identifier.citationImmunology. 2013 Dec;140(4):483-92. doi: 10.1111/imm.12159. <a href="http://dx.doi.org/10.1111/imm.12159">Link to article on publisher's site</a>
dc.identifier.issn0019-2805 (Linking)
dc.identifier.doi10.1111/imm.12159
dc.identifier.pmid23909393
dc.identifier.urihttp://hdl.handle.net/20.500.14038/30277
dc.description.abstractIn the present study, we have found that intestinal flora strongly influence peritoneal neutrophilic inflammatory responses to diverse stimuli, including pathogen-derived particles like zymosan and sterile irritant particles like crystals. When germ-free and flora-deficient (antibiotic-treated) mice are challenged with zymosan intraperitoneally, neutrophils are markedly impaired in their ability to extravasate from blood into the peritoneum. In contrast, in these animals, neutrophils can extravasate in response to an intraperitoneal injection of the chemokine, macrophage inflammatory protein 2. Neutrophil recruitment upon inflammatory challenge requires stimulation by microbiota through a myeloid differentiation primary response gene (88) (MyD88) -dependent pathway. MyD88 signalling is crucial during the development of the immune system but depending upon the ligand it may be dispensable at the time of the actual inflammatory challenge. Furthermore, pre-treatment of flora-deficient mice with a purified MyD88-pathway agonist is sufficient to restore neutrophil migration. In summary, this study provides insight into the role of gut microbiota in influencing acute inflammation at sites outside the gastrointestinal tract.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23909393&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1111/imm.12159
dc.subjectAnimals
dc.subjectBacteria
dc.subjectChemokines
dc.subjectDisease Models, Animal
dc.subjectInflammation Mediators
dc.subjectIntestines
dc.subjectLipopolysaccharides
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMyeloid Differentiation Factor 88
dc.subject*Neutrophil Infiltration
dc.subjectNeutrophils
dc.subjectPeritonitis
dc.subjectReceptors, Interleukin-1
dc.subject*Signal Transduction
dc.subjectToll-Like Receptors
dc.subjectZymosan
dc.subjectImmunopathology
dc.subjectPathology
dc.titleMicrobiota signalling through MyD88 is necessary for a systemic neutrophilic inflammatory response
dc.typeJournal Article
dc.source.journaltitleImmunology
dc.source.volume140
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/530
dc.identifier.contextkey6532257
html.description.abstract<p>In the present study, we have found that intestinal flora strongly influence peritoneal neutrophilic inflammatory responses to diverse stimuli, including pathogen-derived particles like zymosan and sterile irritant particles like crystals. When germ-free and flora-deficient (antibiotic-treated) mice are challenged with zymosan intraperitoneally, neutrophils are markedly impaired in their ability to extravasate from blood into the peritoneum. In contrast, in these animals, neutrophils can extravasate in response to an intraperitoneal injection of the chemokine, macrophage inflammatory protein 2. Neutrophil recruitment upon inflammatory challenge requires stimulation by microbiota through a myeloid differentiation primary response gene (88) (MyD88) -dependent pathway. MyD88 signalling is crucial during the development of the immune system but depending upon the ligand it may be dispensable at the time of the actual inflammatory challenge. Furthermore, pre-treatment of flora-deficient mice with a purified MyD88-pathway agonist is sufficient to restore neutrophil migration. In summary, this study provides insight into the role of gut microbiota in influencing acute inflammation at sites outside the gastrointestinal tract.</p>
dc.identifier.submissionpathfaculty_pubs/530
dc.contributor.departmentDepartment of Pathology
dc.source.pages483-92


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