Search

It has been proposed that immune injury is the central mechanism of pathogenesis of the infectious disease, severe acute respiratory syndrome (SARS). To gain a better understanding of immune injury in the spleen, we investigated the number and distribution of various immune cell types in the spleens of SARS patients. We performed autopsies on six confirmed SARS cases, with six normal subjects as controls; spleen samples from these autopsies were examined with hematoxylin and eosin (H&E) sections, in situ hybridization for SARS virus genomic sequences, and immunohistochemistry with seven monoclonal antibodies to five cell types. The number and distribution of these cells were measured and analyzed using an image analysis system. SARS genomic sequences were detected in all SARS spleens. The SARS spleens all had severe damage to the white pulp and showed an alteration of the normal distribution of various cell types. Immunocytes in the red pulp were decreased by 68.0-90.7% except for CD68+ macrophages and human leukocyte antigen (HLA)-DR positive antigen-presenting cells (APC), which were decreased to a lesser degree. On average, CD68+ macrophages were increased in size by 2.21-fold. We hypothesize that the collapse of the splenic immune system plays a key role in the clinical outcome of these patients. [ABSTRACT FROM AUTHOR]

In this paper we tested the hypothesis that interrupting reperfusion (ischemic postconditioning) reduces the neuron death after transient global cerebral ischemia/reperfusion. Ten min transient cerebral ischemia was induced by four-vessel occlusion in male Sprague-Dawley rats. The animals underwent postconditioning consisting of 3 cycles of 15s/15s, 30s/30s or 60s/15s reperfusion/occlusion, respectively, which were applied after the start of reperfusion. Cytosolic expression of cytochrome c and caspase-3 was evaluated by immunohistochemistry. Ten min ischemia and 7 days reperfusion destroyed approximately 79% of CA1 neurons and 58% parietal cortex neurons, respectively. Three cycles of 30s/30s reperfusion/ischemia postconditioning decreased the neuron loss to 7% in CA1, and 10% in cortex. Another two postconditioning protocols failed to rescue the CA1 neuron death, but decreased the loss of cortex neurons. The expression of cytochrome c at 5h and 12h and caspase-3 at 12h increased significantly after reperfusion, which was prevented by three cycles of 30s/30s reperfusion/ischemia postconditioning. Our data provide the evidence that appropriate interrupting reperfusion is neuroprotective against global cerebral ischemia/reperfusion injury, and this protective effect is through preventing the activation of caspase and then neuronal apoptosis. [ABSTRACT FROM AUTHOR]