2012
DOI: 10.1113/expphysiol.2012.065854
|View full text |Cite
|
Sign up to set email alerts
|

Lipopolysaccharide enhances FcɛRI‐mediated mast cell degranulation by increasing Ca2+ entry through store‐operated Ca2+ channels: implications for lipopolysaccharide exacerbating allergic asthma

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

2
37
0
1

Year Published

2013
2013
2019
2019

Publication Types

Select...
9

Relationship

2
7

Authors

Journals

citations
Cited by 44 publications
(40 citation statements)
references
References 41 publications
2
37
0
1
Order By: Relevance
“…Moreover, it was clear that whilst the Fc ε RI signal reflected a mix of mobilisation of intracellular calcium and calcium influx, as indicated by the observed transient spike in the absence of extracellular calcium (EGTA), the calcium response to LPS in all mast cell subtypes predominantly reflected calcium influx (Figures 4(c)–4(h)). Consistent with LPS inducing calcium influx, we also found as reported previously [43] that LPS enhanced Fc ε RI-mediated calcium mobilisation (data not shown). By contrast, although preexposure to ES-62 did not modulate the baseline calcium levels, the parasite product suppressed the subsequent calcium mobilisation in response to both Fc ε RI-crosslinking and LPS/TLR4 signalling in PDMC (Figures 5(a) and 5(b)).…”
Section: Resultssupporting
confidence: 92%
See 1 more Smart Citation
“…Moreover, it was clear that whilst the Fc ε RI signal reflected a mix of mobilisation of intracellular calcium and calcium influx, as indicated by the observed transient spike in the absence of extracellular calcium (EGTA), the calcium response to LPS in all mast cell subtypes predominantly reflected calcium influx (Figures 4(c)–4(h)). Consistent with LPS inducing calcium influx, we also found as reported previously [43] that LPS enhanced Fc ε RI-mediated calcium mobilisation (data not shown). By contrast, although preexposure to ES-62 did not modulate the baseline calcium levels, the parasite product suppressed the subsequent calcium mobilisation in response to both Fc ε RI-crosslinking and LPS/TLR4 signalling in PDMC (Figures 5(a) and 5(b)).…”
Section: Resultssupporting
confidence: 92%
“…Moreover, ES-62 exerts its effects via subversion of TLR4 signalling whilst the canonical TLR4 ligand LPS typically acts to enhance Fc ε RI functional responses [43, 44], the latter accounting at least in part for the widely established finding that LPS exacerbates airway hyperresponsiveness [43]. LPS has been reported to do this by increasing Fc ε RI-driven calcium mobilisation by upregulating the Orai1 and Stim1 subunits of the store-operated calcium (SOC) channel and hence stimulating calcium influx [43]. In addition, PKC signalling, including that of PKC α , has been shown to be important to LPS/TLR4 responses in a variety of innate cells [45].…”
Section: Resultsmentioning
confidence: 99%
“…Pyrogenic reactions to antivenom are thought to be caused by contamination of the antivenom preparation by endotoxin or lipopolysaccharide (LPS). Bacterial contamination of antivenom may also contribute to the development of anaphylaxis as LPS can directly activate mast cells [43]. Therefore, ensuring sterile manufacturing practises and filtering or heat-treating antivenom preparations may reduce both hypersensitivity and pyrogenic reactions [44].…”
Section: Discussionmentioning
confidence: 99%
“…LPS-induced mast cell activation was characterized by differential inflammation release without degranulation. Although LPS failed to have a direct effect on mast cell degranulation, it did appear to enhance degranulation in RBL-2H3 cells and mouse peritoneal mast cells upon FcεRI activation [28]. Reports demonstrate that Ang-1 inhibits NF-κB activation through interacting with NF-κB inhibitor ABIN-2 [29].…”
Section: Discussionmentioning
confidence: 98%