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)

The sensitivity of primary splenic B cells to Fas-mediated apoptosis is modulated in a receptor-specific fashion. Here we used a differential display strategy to detect cDNAs present in B cells rendered Fas resistant but absent in those rendered Fas sensitive. This led to the cloning and characterization of a novel 1.2-kb gene that encodes a Fas apoptosis inhibitory molecule (FAIM). faim-transfected BAL-17 B lymphoma cells were less sensitive by half or more to Fas-mediated apoptosis than were vector-transfected controls, using Fas ligand-bearing T cells or a cytotoxic anti-Fas antibody to trigger Fas, and this was associated with inhibition of Fas- induced poly-ADP ribose polymerase (PARP) cleavage. In primary B cells, the time course of faim mRNA and FAIM protein expression correlated with the induction of Fas resistance by surface (s)Ig engagement. Thus, FAIM is an inducible effector molecule that mediates Fas resistance produced by sIg engagement in B cells. However, faim is broadly expressed in various tissues and the faim sequence is highly conserved evolutionarily, suggesting that its role extends beyond lymphocyte homeostasis. As FAIM has no significant regions of homology to other gene products that modulate Fas killing, it appears to represent a distinct, new class of antiapoptotic protein.
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PMID:A novel gene coding for a Fas apoptosis inhibitory molecule (FAIM) isolated from inducibly Fas-resistant B lymphocytes. 1007 78

We compared apoptosis in eosinophils from bronchoalveolar lavage (BAL-Eos) with that in eosinophils from peripheral blood (PB-Eos) of 4 patients with chronic eosinophilic pneumonia (CEP). The survival rate of the BAL-Eos on the 3rd day of the culture was significantly higher than that of the PB-Eos (39.1 vs. 1.3%). The percentage of apoptotic cells in the PB-Eos after a 24-hour incubation was higher than that in the BAL-Eos (21.7 vs. 10.6%) according to an analysis with annexin V. We further found that ECF-PI9, an eosinophil chemotactic factor (ECF) derived from an established T cell line (STO-2), significantly suppressed the apoptosis of both PB-Eos and BAL-Eos and prolonged their survival. The expression of Fas on PB-Eos was significantly suppressed by ECF-PI9 (18.5 to 7.37%, p < 0. 05), whereas ECF-PI9 failed to suppress the Fas expression on BAL-Eos (3.3 to 3.6%). In addition, an ECF with similar physicochemical properties and biological functions was isolated from the BAL fluid of patients with CEP. These data demonstrate differences between PB-Eos and BAL-Eos, and indicate that ECF-PI9 is involved in the pathogenesis of CEP.
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PMID:Difference in apoptotic function between eosinophils from peripheral blood and bronchoalveolar lavage in chronic eosinophilic pneumonia. 1052 13

To clarify the pathogenesis of chronic eosinophilic pneumonia (CEP), the apoptosis of eosinophils from bronchoalveolar lavage (BAL-Eos) was compared with that of eosinophils from peripheral blood (PB-Eos) in six cases of CEP. The survival rate of eosinophils and the percentage of apoptotic cells of both types of eosinophils were examined, and the effects of interleukin 5 (IL-5) were evaluated. The role of Fas expression in apoptosis of these eosinophils was also studied. The survival rate of BAL-Eos on the third day of culture was significantly higher than that of PB-Eos (p < 0.01). This was associated with a lower proportion of apoptotic cells in BAL-Eos than in PB-Eos; the percentages of apoptotic cells in PB-Eos and BAL-Eos after 24 h of incubation were 21.7 +/- 3.4% and 10.6 +/- 1.7% respectively. IL-5 suppressed apoptosis and increased the survival rate of both PB-Eos and BAL-Eos. It was found that the apoptotic character of BAL-Eos differed from that of PB-Eos in at least three ways. Firstly, the positive rate of Fas expression on PB-Eos was increased after 24 h of incubation, whereas that on BAL-Eos did not change. Secondly, the expression of Fas on PB-Eos was suppressed by IL-5 (18.5 +/- 4.2% - 8.3 +/- 3.2%, p < 0.05), whereas IL-5 failed to suppress Fas expression on BAL-Eos (3.3 +/- 1.6% - 3.6 +/- 1.0%). Lastly, binding of antibody to Fas antigen induced apoptosis of PB-Eos, but not of BAL-Eos. These data suggested that Fas seemed to be involved in the apoptosis of PB-Eos, whereas BAL-Eos were Fas-resistant in chronic eosinophilic pneumonia. In conclusion, apoptosis of eosinophils might be suppressed by proinflammatory cytokines such as IL-5 leading to their accumulation in the lung. Chronic stimulation of eosinophils in the alveolar space with IL-5 may play a crucial role chronic eosinophilic disorders.
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PMID:Apoptotic response of eosinophils in chronic eosinophilic pneumonia. 1133 18

Alveolar type 2 (AT-2) cell apoptosis is an important mechanism during lung inflammation, lung injury, and regeneration. Blunt chest trauma has been shown to activate inflammatory cells such as alveolar macrophages (AMs) or neutrophils (polymorphonuclear granulocytes [PMNs]), resulting in an inflammatory response. The present study was performed to determine the capacity of different components/cells of the alveolar compartment (AMs, PMNs, or bronchoalveolar lavage [BAL] fluids) to induce apoptosis in AT-2 cells following blunt chest trauma. To study this, male Sprague-Dawley rats were subjected to either sham procedure or blunt chest trauma induced by a single blast wave. Various time points after injury (6 h to 7 d), the lungs were analyzed by immunohistochemistry, for AT-2 cells, or with antibodies directed against caspase 3, caspase 8, Fas, Fas ligand (FasL), BAX, and BCL-2. Bronchoalveolar lavage concentrations of TNF-alpha, IL-1beta, and soluble FasL were determined by enzyme-linked immunosorbent assay. Furthermore, cultures of AT-2 cells isolated from healthy rats were incubated with supernatants of AMs, PMNs, or BAL fluids obtained from either trauma or sham-operated animals in the presence or absence of oxidative stress. Annexin V staining or TUNEL (terminal deoxynucleotidyl transferase) assay was used to detect apoptotic AT-2 cells. Histological evaluation revealed that the total number of AT-2 cells was significantly reduced at 48 h following trauma. Fas, FasL, active caspase 8, and active caspase 3 were markedly up-regulated in AT-2 cells after chest trauma. BAX and BCL-2 did not show any significant changes between sham and trauma. IL-1beta, but not TNF-alpha, levels were markedly increased at 24 h after the injury, and soluble FasL concentrations were significantly enhanced at 6, 12, 24, and 48 h after the insult. Apoptosis of AT-2 cells incubated with supernatants from cultured AMs, isolated at 48 h following chest trauma was markedly increased when compared with shams. In contrast, no apoptosis was induced in AT-2 cells incubated with supernatants of activated PMNs or BAL fluids of traumatized animals. In summary, blunt chest trauma induced apoptosis in AT-2 cells, possibly involving the extrinsic death receptor pathway. Furthermore, mediators released by AMs appeared to be involved in the induction of AT-2 cell apoptosis.
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PMID:Pulmonary contusion induces alveolar type 2 epithelial cell apoptosis: role of alveolar macrophages and neutrophils. 1831 5

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease with unfavourable outcome. Tobacco consumption in IPF exacerbates the clinical manifestations and limits the time of patient survival. The cyto-immunological alterations caused by smoking in IPF patients need particular explanation. BAL was carried out in 21 non-treated patients with IPF, subdivided according to the smoking status (n=7 for smokers). BAL routine cytology was completed by; immunotyping, including T cell major subsets (CD4 and CD8) stained for Fas, Fas ligand (FasL) and TNFR-1, late apoptosis/cell cycle analyses (BAL cells were permeabilized and stained with PI) and TUNEL assay. BAL cytology in IPF, as compared with control group, was characterized by significantly higher total cell and macrophage number, increased lymphocyte, neutrophile and eosinophile percentage and relatively low CD4/CD8 ratio. Cigarette smoking in IPF resulted in enhanced BAL lymphocyte CD8 cell percentage and number, as compared with nonsmoking subgroup and further decline in CD4/CD8 ratio (0.41+/-0.15 vs 1.23+/-0.29 in nonsmokers, median +/- SEM, p<0.05). The percentage of CD8, but not CD4 cells carrying Fas Ligand was significantly increased in IPF smokers (12.0+/-3.1% vs 3.7+/-0.9% in nonsmokers, median +/- SEM, p<0.05). Apoptosis rate of BAL macrophages and lymphocytes was enhanced in IPF, as compared with controls (confirmed by both techniques), but without remarkable changes, if compared one IPF subgroup to another. The number and percentage of CD8+FasL+ was negatively correlated with vital capacity (VC) values in IPF patients, but not with BAL inflammatory cell apoptosis rate. Cigarette smoking enhanced a percentage as well as a total number of both BAL CD8 and BAL CD8+FasL+ cells in IPF patients. BAL cytotoxic cells (CD8+FasL+ lymphocytes) seem to have impact on impaired lung function in smoking IPF patients.
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PMID:[Cigarette smoking results in the number of CD8+Fas Ligand+ T cytotoxic lymphocytes in bronchoalveolar lavage (BAL) fluid of patients with idiopathic pulmonary fibrosis (IPF)]. 1840 87