Biomedical subjects

S Batcher

Publications and source records attributed to S Batcher.

7 recordsLinked to original sources

PubMed1994

Nicotinic acetylcholine receptor subunits expressed in rat cochlea detected by the polymerase chain reaction.

Poly(A)+ RNA was extracted from rat cochleae using guanidinium thiocyanate and oligo(dT)-cellulose, and converted into cDNA by reverse transcriptase using an oligo(dT) primer. Oligonucleotides complementary to conserved 5' and 3' regions of alpha and beta subunits of the neuronal nicotinic acetylcholine receptor subunit (nAChR) family were then used as primers to screen the cochlear cDNA via the polymerase chain reaction (PCR) procedure. PCR products of approximately 900 bp length, purified by agarose gel electrophoresis, were nick translated to produce [32P]-dCTP labelled probes for Southern Blot screening of nAChR cDNAs. Of the four alpha and three beta subunits screened, only alpha 5 and beta 4 nAChR cDNAs hybridized. The alpha 5 PCR product was cloned and sequenced and proved to be identical to published sequence for alpha 5. The detection of alpha 5 and beta 4 nAChR subunit expression in cochlear tissue supports previous electrophysiological and immunocytochemical evidence for nAChR-mediated centrifugal control of hearing function.

Animals↗

PubMed1993

Cloning genes from an inner ear cDNA library.

A rat inner ear complementary DNA (cDNA) library containing 1.9 x 10(6) recombinants was constructed and evaluated. Inserts averaged 2.0 (+/- 2.1) kilobases in length. A subset of inserts was screened for site of expression. Two cDNA transcripts were isolated based on cochlear expression restricted to the spiral ganglion. One transcript showed a high degree of homology to several long interspersed DNA elements, neuron-specific nuclear transcripts thought to be involved in gene regulation. The second transcript showed no homology to known sequences and appears to encode a neuron-specific protein of about 248 amino acids. The library can be used to identify proteins important for inner ear function and disease.

Animals↗

PubMed1991

The response to human rIL-1, rIL-2, and rTNF in the middle ear of guinea pigs.

Human recombinant interleukin 1 (rIL-1), interleukin 2 (rIL-2), or tumor necrosis factor (rTNF) were injected transtympanically into the middle ear of normal guinea pigs. Effusion volume and cellular content were determined after sacrifice and rapid dissection of the ear. By 24 hours, rIL-2 (100 U) had produced a cellular effusion (77% to 92% polymorphonuclear neutrophil leukocytes), which cleared by 72 hours. rTNF (10 U) yielded a cellular effusion (12% to 67% lymphocytes) at 24 hours, which cleared by 48 hours. rIL-1 (100 U) did not produce significant effusion when compared to control. rIL-2 and rTNF cause an inflammatory effusion in the middle ear. To the extent they are generated in the middle ear during otitis media, these cytokines have the potential to contribute to the pathogenesis of otitis media with effusion.

Animals↗

PubMed1990

Pulmonary surfactant suppresses the immune lung injury response to inhaled antigen in guinea pigs.

Pulmonary surfactant (PS) has been shown to regulate the function of macrophages, T cells, B cells, and NK cells in vitro. We designed this study to explore the immunoregulatory role of PS in vivo. Guinea pigs were immunized to complete Freund's adjuvant (CFA) and 2 weeks later were subjected to an aerosol challenge with purified protein derivative (PPD) to induce immune lung injury (group I). Group II and group III were subjected to lung lavage by tracheostomy just before aerosol challenge. Group II was lavaged with 0.9% NaCl, which depleted PS by 32%. Group III was lavaged with 0.9% NaCl containing bovine surfactant, which did not alter total PS content. Control animals for each condition were not presensitized to CFA. All guinea pigs were killed 24 hours after the aerosol challenge; for each group n = 10 +/- 2. Bronchoalveolar lavage (BAL) protein and mononuclear leukocyte counts, as well as lung histopathologic grading, were performed. Group I animals showed evidence of mild immune lung injury by these parameters. Animals partially depleted of PS (group II) showed more severe lung injury with greater abnormalities in BAL leukocytes and histopathology compared with group I. Guinea pigs lavaged with fluid containing bovine surfactant (group III) were nearly identical to group I with respect to these two parameters. BAL protein levels were not related to PS depletion. This study suggests that surfactant may have an in vivo role in modulating the inflammatory response that accompanies immune lung injury in this model.

Aerosols↗

PubMed1988

Immunomodulation by pulmonary surfactant.

Canine pulmonary surfactant is recognized to modulate both T and B cell response in vitro. Because both responses involve cell proliferation, it has been suggested that surfactant interferes with the proliferation of lymphocytes. We herein report studies using human surfactant collected from amniotic fluid (HAFS). HAFS inhibited the proliferative response of human lymphocytes to antigen (PPD) and to allogeneic lymphocytes. Inhibition was linear within the dose range examined. Inhibition of the response to phytohemagglutinin was only evident when suboptimal doses of phytohemagglutinin were used. The effect of HAFS on the lysis of K562 human myeloid target cells by natural killer (NK) cells was also studied. Lysis in this system does not require proliferation. HAFS inhibited NK cell-induced lysis by 70% (250 micrograms HAFS per milliliter) to 95% (500 micrograms HAFS per milliliter). Inhibition was evident whether the cells were incubated with HAFS for 4 hours or for 18 hours. The NK suppressor activity was contained in the lipid fraction of HAFS, whereas the protein fraction revealed little activity. The washout experiments demonstrated that the action of HAFS was on NK cells and not on target cells. The immunomodulatory properties of surfactant affect NK cell activity and the proliferative response. Surfactant may protect the lungs from inappropriate immune reactions. Abnormalities of the lipid fraction of surfactant should be considered in studies of the mechanism of pulmonary diseases characterized by local pulmonary immune responses.

Amniotic Fluid↗

PubMed1987

Sequence of bronchoalveolar lavage and histopathologic findings in rat lungs early in inhalation asbestos exposure.

To assess the early cellular inflammatory response of the lungs, 7 rats per group were exposed nose-only to 13 mg/m3 of chrysotile asbestos, 7 h/day for 2, 4, or 6 wk. Lung histopathology and bronchoalveolar lavage (BAL) were analyzed. In exposed animals, dose-related bronchiolitis and fibrosis were found that were not seen in control rats (p less than 0.001). In exposed rats, total BAL cells were increased six-to sevenfold over matched controls, and more cells were retrieved with longer exposure (p less than 0.001). In the BAL, counts of macrophages, lymphocytes, and polymorphonuclear cells (PMNs) were each elevated in the exposed rats (each p less than 0.001). PMNs seen histologically and in the BAL may be related to the time period examined. PMNs and lymphocytes observed throughout this 6-wk study support the idea that these cells may have an important role in the early events of asbestos lung injury.

Administration, Inhalation↗

PubMed1983

A guinea pig model to study effects of persistent intrabronchial antigenic stimulation and inflammation.

Chronic antigenic stimulation and inflammation of the bronchial tree occurs in several diseases involving microbial airway colonization. We developed a guinea pig model to study the effects of persistent intrabronchial antigenic stimulation with keyhole limpet hemocyanin (KLH). Sepharose beads 200 to 300 micron in diameter conjugated with 300 micrograms KLH were injected via a tracheostomy catheter, causing them to lodge in the bronchial tree. When lung sections from these animals and animals given uncoupled sepharose beads were examined histologically, it became apparent that in this model the persistent antigenic stimulus is accompanied by local inflammation caused by an irritant effect of the beads. To determine how the intrabronchial antigen was distributed locally and systemically, 125I labeled KLH-coupled beads were administered. Radioactivity remained predominantly in the lung, where 13 +/- 5% of the administered dose was still detectable by Day 30. Autoradiographs of Day 30 lung sections demonstrated that the radioactivity was concentrated on the individual beads, indicating that it largely represented KLH persisting in the bronchial tree. Minute amounts of radioactivity were detected systemically and in the regional lymph nodes (LN). A radioimmune assay of serum collected on Day 1 demonstrated that some of the circulating radioactivity represented antigenic KLH. When anti-KLH antibody-forming cells (AFC) were measured in lung homogenate, regional LN, blood, and spleen cell preparations after KLH-coupled bead administration, they were initially detected only in the spleen. Significant concentrations appeared in the lung homogenate, regional LN, and spleen by Day 10 and thereafter through Day 20.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗