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We propose that Gpa33 −/− mice provide a valuable model to study the mechanisms linking intestinal permeability and multiple inflammatory pathologies.
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Elevated MPO (myeloperoxidase) levels are associated with multiple human inflammatory pathologies.
These oxidants generated by both MPO [ 5], and other peroxidases (including salivary, gastric and eosinophil peroxidases; [ 1]) are important in the innate immune response against invading pathogens [ 2, 3], but have been implicated as damaging agents in multiple human inflammatory pathologies (reviewed in [ 1– 3]).
Our findings are consistent with elevated SCN− contributing to an enhanced risk of developing pathologies associated with multiple inflammatory diseases.
On the other hand, patients having traumatic, neoplastic, or inflammatory pathologies were excluded.
Altogether, these findings outline promising candidate molecules and design approaches for targeting RIPK1- and RIPK3-driven inflammatory pathologies.
Consequently, ASK1 inhibitors may have the potential to treat clinically important inflammatory pathologies including renal, pulmonary and liver diseases.
CX3CL1 is involved in the development of numerous inflammatory pathologies including rheumatoid arthritis and graft rejection.
This same gene is involved in other inflammatory pathologies, including bronchial asthma [ 15].
Delayed neutrophil apoptosis is often detected in inflammatory pathologies, including sepsis [ 1].
Disruption of the cytokine-HPA axis feedback loop can aggravate inflammatory pathologies [ 11].
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