Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pgp-1 expression was studied as a marker of memory/activation on systemic and mucosal T cells of BALB/c and C57BL/6 mice after infection with respiratory syncytial virus (RSV), using two-color dual fluorescence flow cytometry employing anti-L3T4 (CD4), anti-Ly2 (CD8), and anti-Pgp-1 (CD44) monoclonal antibodies. Pgp-1 was expressed in relatively low densities on T cells of C57BL/6 mice, allowing differentiation of a dual population of Pgp-1(10) and Pgp-1hi T cells after antigenic stimulation in vivo. On the contrary, T cells of BALB/c mice were uniformly Pgp-1hi, making this mouse strain less suitable for studies with this marker. In blood and spleen consistently more CD8+ than CD4+ T cells were Pgp-1hi, while in BAL more CD4+ than CD8+ T cells were Pgp-1hi. After primary but not after secondary infection, CD4+ Pgp-1hi T cells increased significantly in the blood and spleen. After secondary infection both CD4+ Pgp-1hi and CD8+ Pgp-1hi T cells increased in the BAL. It is hypothesized that after primary infection systemic RSV-specific T cells acquire an activation/memory phenotype as characterized by an enhanced expression of Pgp-1, resulting in a faster and stronger influx of these cells in the lungs after secondary infection.
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PMID:Mucosal T cells recovered from mice after infection with respiratory syncytial virus display a memory/activation phenotype. 758 21

World conditions place large populations at risk from ionizing radiation (IR) from detonation of dirty bombs or nuclear devices. In a subgroup of patients, ionizing radiation exposure would be followed by a secondary infection. The effects of radiation combined injury are potentially more lethal than either insult in isolation. The purpose of this study was to determine mechanisms of mortality and possible therapeutic targets in radiation combined injury. Mice were exposed to IR with 2.5 Gray (Gy) followed four days later by intratracheal methicillin-resistant Staphylococcus aureus (MRSA). While either IR or MRSA alone yielded 100% survival, animals with radiation combined injury had 53% survival (p = 0.01). Compared to IR or MRSA alone, mice with radiation combined injury had increased gut apoptosis, local and systemic bacterial burden, decreased splenic CD4 T cells, CD8 T cells, B cells, NK cells, and dendritic cells, and increased BAL and systemic IL-6 and G-CSF. In contrast, radiation combined injury did not alter lymphocyte apoptosis, pulmonary injury, or intestinal proliferation compared to IR or MRSA alone. In light of the synergistic increase in gut apoptosis following radiation combined injury, transgenic mice that overexpress Bcl-2 in their intestine and wild type mice were subjected to IR followed by MRSA. Bcl-2 mice had decreased gut apoptosis and improved survival compared to WT mice (92% vs. 42%; p<0.01). These data demonstrate that radiation combined injury results in significantly higher mortality than could be predicted based upon either IR or MRSA infection alone, and that preventing gut apoptosis may be a potential therapeutic target.
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PMID:Inhibition of intestinal epithelial apoptosis improves survival in a murine model of radiation combined injury. 2420 69