Bam32/DAPP1-Dependent Neutrophil Reactive Oxygen Species in WKYMVm-Induced Microvascular Hyperpermeability.
Abstract
B cell adaptor molecule of 32 kDa (Bam32), known as dual adapter for phosphotyrosine and 3-phosphoinositides 1 (DAPP1), has been implicated in regulating lymphocyte proliferation and recruitment during inflammation. However, its role in neutrophils during inflammation remains unknown. Using intravital microscopy, we examined the role of Bam32 in formyl peptide receptor agonist WKYMVm-induced permeability changes in post-capillary venules and assessed simultaneously neutrophil adhesion and emigration in cremaster muscles of Bam32-deficient (Bam32-/-) and wild-type (WT) control mice. We observed significantly reduced WKYMVm-induced microvascular hyperpermeability accompanied by markedly decreased neutrophil emigration in Bam32-/- mice. The Bam32-specific decrease in WKYMVm-induced hyperpermeability was neutrophil-dependent as this was verified in bone marrow transplanted chimeric mice. We discovered that Bam32 was critically required for WKYMVm-induced intracellular and extracellular production of reactive oxygen species (ROS) in neutrophils. Pharmacological scavenging of ROS eliminated the differences in WKYMVm-induced hyperpermeability between Bam32-/- and WT mice. Deficiency of Bam32 decreased WKYMVm-induced ERK1/2 but not p38...Continue Reading
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Small-molecule screen identifies reactive oxygen species as key regulators of neutrophil chemotaxis.
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