Is increased bacterial translocation in gluten-sensitive mice independent of small intestinal paracellular permeability defect?
Pharmacological restoration of paracellular permeability was not sufficient to prevent bacterial translocation in gluten-sensitive mice. We hypothesize that transcellular mechanisms involving CD103(+)DC and CD11c(+)DC may explain in gluten-sensitive HCD4/HLA-DQ8 transgenic mice the sustained increased bacterial translocation observed in the absence of a significant inflammatory response.
While 90 mg 2-CP or 25 mg B may be reliable alternatives to epinephrine test doses in unpremedicated subjects, they are unreliable indicators of intravascular injection in the premedicated patient.