2013
DOI: 10.4049/jimmunol.1300883
| View full text |Cite
|
Sign up to set email alerts
|

Abstract: Stomatococcus mucilaginosus is an oral commensal that has been occasionally reported to cause severe infections in immunocompromised patients. There is no information about the pathogenic role of S. mucilaginosus in airway infections. In a cohort of 182 subjects with bronchiectasis, we found that 9% were colonized with S. mucilaginosus in their lower airways by culture growth from bronchoalveolar lavage. To address the pathogenic potential of S.mucilaginosus, we developed a murine model of S. mucilaginosus lun… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
16
1

Year Published

2014
2014
2021
2021

Publication Types

Select...
7

Relationship

4
3

Authors

Journals

citations
Cited by 15 publications
(17 citation statements)
references
References 62 publications
0
16
1
Order By: Relevance
“…In a previous study, we demonstrated that activation of the signaling pathway of MyD88, an adaptor molecule of all TLRs, except TLR3, inhibited I/R injury in the small intestine via induction of COX-2 expression and PGE 2 synthesis [37] . Although some reports indicated involvement of the TLR2/MyD88-dependent signaling pathway in the induction of COX-2 [38] , [39] , [40] , we found that TLR2 deficiency did not affect COX-2 expression and PGE 2 synthesis in the small intestine during the development of intestinal I/R injury. Several lines of evidence demonstrated that the TLR4/MyD88-dependent pathway induced COX-2 expression, leading to prevention of damage and maintenance of mucosal integrity in the gastrointestinal tract [41] , [42] , [43] .…”
Section: Discussioncontrasting
confidence: 87%
“…In a previous study, we demonstrated that activation of the signaling pathway of MyD88, an adaptor molecule of all TLRs, except TLR3, inhibited I/R injury in the small intestine via induction of COX-2 expression and PGE 2 synthesis [37] . Although some reports indicated involvement of the TLR2/MyD88-dependent signaling pathway in the induction of COX-2 [38] , [39] , [40] , we found that TLR2 deficiency did not affect COX-2 expression and PGE 2 synthesis in the small intestine during the development of intestinal I/R injury. Several lines of evidence demonstrated that the TLR4/MyD88-dependent pathway induced COX-2 expression, leading to prevention of damage and maintenance of mucosal integrity in the gastrointestinal tract [41] , [42] , [43] .…”
Section: Discussioncontrasting
confidence: 87%
“…Samples were prepared in RIPA buffer containing proteinase and phosphatase inhibitors according to instructions (Sigma Aldrich, USA). Western blotting was performed as described previously 53 , appropriate primary antibodies and horseradish peroxidase-conjugated secondary antibodies were used prior to visualization via chemiluminescence (Amersham Biosciences, USA).…”
Section: Methodsmentioning
confidence: 99%
“…Lung samples were placed in 50 mmol/l K 2HPO4 buffer (pH 6.0) containing 0.5% hexadecyl trimethyl ammonium bromide and stored at Ϫ80°C until used. Myeloperoxidase (MPO) activity was measured as described previously (41,51).…”
Section: Methodsmentioning
confidence: 99%