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Biomedical subjects

I N Montgomery

Publications and source records attributed to I N Montgomery.

At least 19 recordsLinked to original sources
PubMed1989

Paternal alcohol consumption: effects on ocular response and serum antibody response to Pseudomonas aeruginosa infection in offspring.

Male Swiss-Webster mice that consumed liquid alcohol diets containing 25, 20, 15, 10, 5, or 0% ethanol-derived calories (EDC) for 7 weeks were bred to untreated females that were not exposed to alcohol diets. Males receiving the 20-0% EDC diets were pair-fed to those consuming the 25% EDC diet. At approximately 60 days of age, male offspring were challenged with 10(8) colony forming units of Pseudomonas aeruginosa onto the scarified cornea of one eye. The ocular response was then evaluated macroscopically for 4 weeks. Male offspring sired by alcohol-consuming fathers exhibited more severe ocular infection at 24 hr postinfection compared with mice sired by control fathers and, after 8 days postinfection, more corneas of the 25% EDC-sired progeny perforated than did the other groups. At 30 days after infection, serum immunoglobulin titers (IgM, IgG, IgA) specific to P. aeruginosa were determined by ELISA. Although the majority of the mice were unable to restore corneal clarity within 30 days postinfection, a strong serum IgG response was detected in pooled sera from those animals tested. Offspring were reinfected in the contralateral control eye at 30 days postprimary infection. Most control animals were able to restore corneal clarity in the contralateral control eye within 30 days postinfection, but less than a third of the alcohol-sired offspring did so. Again, the pooled sera that was tested indicated a strong humoral response, despite differences in corneal clarity. These studies indicate an increased susceptibility to infection and an impairment in restoration of corneal clarity in offspring sired by alcohol-consuming males, which does not appear to be mediated by serum antibody mechanisms.

Alcoholism↗
PubMed1988

Serum antibody and ocular responses to murine corneal infection caused by Pseudomonas aeruginosa.

The serum antibody response and differential corneal response to primary and secondary infections by Pseudomonas aeruginosa were investigated in DBA/2J (resistant) and C57BL/6J (susceptible) mice, since they respond differently to intracorneal challenge. Using an enzyme-linked immunosorbent assay, we found that naturally resistant DBA/2J mice mounted a significant immunoglobulin M (IgM) and IgG response to P. aeruginosa within 7 days postinfection of one eye; this was subsequently followed by a drop in the IgM response. Of 31 mice, 30 were able to restore corneal clarity within 3 to 4 weeks. However, when C57BL/6J mice were infected intracorneally, their levels of serum antibody developed more slowly than did those of the DBA/2J mice, and they were unable to restore corneal clarity within 8 to 12 weeks. None of the mice from either test strain mounted a detectable serum IgA response to P. aeruginosa over a 90-day holding period. However, infection of the contralateral, normal cornea of mice of both test strains resulted in a heightened IgG response to P. aeruginosa within 30 days after the secondary infection. Many (50%) of the susceptible C57BL/6J mice recovered or exhibited less severe corneal damage within the 30-day holding period. If the C57BL/6J mice were reinfected 60 days after the primary infection instead of after 30 days, most (89%) of the mice had restored corneal clarity within 3 to 6 days. Passive transfer of immune serum from either recovered DBA/2J or C57BL/6J mice to naive C57BL/6J mice resulted in the restoration of corneal clarity in many of the recipients following infection.

Animals↗
PubMed1987

Effects of cardiotoxin D from Naja naja siamensis snake venom upon murine splenic lymphocytes.

Cardiotoxin D from Naja naja siamensis is cytotoxic to T-lymphocytes above 150 femtomoles/10(6) cells. Equivalent lysis of macrophages or B-lymphocytes requires at least 1000 times more toxin. Reduction and carboxamidomethylation of cardiotoxin D does not effect T cell lysis. At higher toxin concentrations, 50% T-cell lysis occurs within 10 min. Splenocytes cultured with mitogens are up to five times more susceptible to toxin than unstimulated cells. Cardiotoxin D may directly disrupt the plasma membrane, since lysis is unaltered at 4 degrees C.

Animals↗
PubMed1987

Experimental allergic encephalomyelitis in mice: presence of myelin basic protein in cerebrospinal fluid.

The concentration of myelin basic protein (MBP) in cerebrospinal fluid (CSF) correlates with the development of experimental allergic encephalomyelitis following intradermal injection with encephalitogen in adjuvant; MBP is absent in controls inoculated with adjuvants only. The presence of MBP is a sensitive indicator of disease inasmuch as CNS-inoculated mice with neurologic signs had an average of 0.29 ng/microliter of MBP in their CSF and controls, including normal or adjuvants only, had an average of 0.03 ng/microliter. The amount present per microliter of CSF, as well as the absolute amount, obtained from an individual mouse do not always reflect the severity of disease as indicated by clinical signs and the pathology observed in a sampling of the neuraxis. The presence of MBP does correlate with demyelination, although the extent of pathology observed by light microscopy in the mouse model is minimal, associated only with the inflammatory response, and does not extend beyond the zone of the perivascular cuff.

Animals↗
PubMed1987

Production and characterization of high titer antibodies to galactocerebroside.

High titer antibodies primarily of the IgG class were produced against galactocerebroside (GalC) by including keyhole limpet hemocyanin (KLH) and supplemental M. tuberculosis in the adjuvant mixture used for immunization of rabbits. Antibody titers were determined by an ELISA in which microtiter wells were coated with liposomes containing lecithin, cholesterol and GalC. The antibodies showed reactivity with GalC and psychosine, but not glucocerebroside, sulfatide, mixed gangliosides or asialo GM1. Specificity was further demonstrated by absorption of antibodies with GalC. Binding was inhibited by galactose, but only at high concentrations. Further, the antibodies did not bind to any brain proteins on immunoblots, indicating lack of reactivity with glycoproteins which might contain a terminal galactose. Antibodies to GalC are directed against different determinants than those reacting with peanut agglutinin since the lectin will not react with GalC, and the antibodies will not react with asialo GM1. The antibodies raised to GalC by this method show specific staining for oligodendroglia in culture. Peanut agglutinin binds intensely to process-bearing GalC+ oligodendroglia, but very poorly to the membrane sheets elaborated by oligodendroglia after longer times in culture. Other process-bearing GalC-, GFAP- cells were also stained with peanut agglutinin; these cells may represent glial precursors.

Animals↗
PubMed1987

Chronic Theiler's virus infection in mice: appearance of myelin basic protein in the cerebrospinal fluid and serum antibody directed against MBP.

Myelin basic protein (MBP) appears frequently in the cerebrospinal fluid (CSF) of mice with chronic demyelination following intracerebral infection with Theiler's murine encephalomyelitis virus (TMEV); antibody to MBP can frequently be found in the sera. The peaks of the immune responses to both MBP and TMEV coincide with the time course of the clinical signs of disease. Adsorption of mouse sera with TMEV or MBP indicate the non-identity of the antigens and the specificity of the antisera as measured by ELISA. Immunoblot analysis of sera confirmed the ELISA findings. The mechanism of induction of antibody directed against MBP and its role in TMEV-associated demyelination remain to be determined.

Animals↗
PubMed1986

The role of the immune response in TMEV infection and the development of late onset demyelination.

The nature of the role of the immune response to TMEV in the development of LODD after TMEV infection was examined by different means. Immunosuppression by both cyclophosphamide (postinfection) or adult thymectomy and ATS treatment (preinfection) did not inhibit clinical LODD. Adoptive transfer of spleen cells from infected donors with LODD facilitates LODD in the recipients compared with i.v. transfer of the freeze-thaw supernatants from such suspensions (although virus is present in splenocyte suspensions). The immune response to TMEV, both lymphoproliferative and antibody, reaches a peak coincidental with the development of LODD. The role of the immune response is equivocal depending on the stage of the viral infection, the timing of immunosuppressive treatment, and assessment.

Animals↗
PubMed1986

Clinical correlates of enzyme-immunoassay versus radioimmunoassay measurements of antibody against acetylcholine receptor in patients with myasthenia gravis.

Antibody against human nicotinic acetylcholine receptor [Ab(AcChR)] was measured in the sera obtained from 55 patients with myasthenia gravis (MG) using both radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA). By at least one assay, 91% of the patients had elevated Ab(AcChR). We found no correlation between the amount of Ab(AcChR) measured by RIA and that measured by ELISA. Patient subpopulations defined by ELISA- or RIA-measured Ab(AcChR) were associated with different disease durations. All of those who had high Ab(AcChR) levels by both assays had experienced symptoms for less than 2 years. 87% of those with high Ab(AcChR) levels by ELISA had had MG for less than 4 years. Those patients with high Ab(AcChR) only by RIA had a mean disease duration of over 8 years. With regard to correlations of Ab(AcChR) with patient age and sex, females under 50 years of age had high levels of Ab(AcChR) by RIA, but had lower levels by ELISA, whereas men over 50 had high Ab(AcChR) levels by ELISA. Using either assay, no relationship was established between concentrations of Ab(AcChR) and the patient's functional status, previous thymectomy, or current therapy. In this study, 16% of the MG patients with elevated Ab(AcChR) would have been considered within the non-disease range of Ab(AcChR) had only the RIA been performed, thus recommending the routine use of both assays for diagnostic purposes.

Adult↗
PubMed1985

Natural killer cell activity in multiple sclerosis and myasthenia gravis.

Because of the potential role of Natural Killer (NK) cells in viral immunity and immunoregulation, we have undertaken a study of NK activity of peripheral blood lymphocytes from both Multiple Sclerosis (MS) and Myasthenia Gravis (MG) patients, two chronic diseases in which a viral etiology and an induced autoregulatory abnormality are strongly implicated. No significant difference between the mean NK activity in MS patients and controls was observed. A difference was observed between the NK activity of female MG patients and female controls, but no difference was seen between male MG patients and controls.

Adult↗
PubMed1984

Experimental allergic encephalomyelitis in mice: adoptive transfer of disease is modulated by the presence of natural suppressor cells.

Normal, untreated syngeneic recipients of lymphocytes from mice with experimental allergic encephalomyelitis (EAE) do not generally express adoptively transferred disease. Cell transfer of EAE is more successful when syngeneic recipients are treated with cyclophosphamide (CY) prior to the injection of donor cells. Normal, untreated recipients that do not develop EAE after receiving EAE donor lymphocytes are also unresponsive to subsequent encephalitogenic challenge. Those CY-treated recipients that fail to develop EAE after cell transfer do develop EAE after subsequent challenge. After reconstitution with normal splenic lymphocytes, CY-treated recipients do not develop EAE after subsequent challenge. These findings suggest the presence of an intrinsic natural suppressor cell subpopulation in naive mice which modulate the expression of adoptively transferred T lymphocytes.

Animals↗
PubMed1982

Experimental allergic encephalomyelitis (EAE) in mice: primary control of EAE susceptibility is outside the H-2 complex.

We report here the results of EAE induction in 1758 mice from 9 inbred strains, 5 H-2 congenic strains, and 6 F1 hybrids. EAE responsiveness is under the primary control of genes outside the H-2 complex. The F1 data do not show a unifactorial inheritance of EAE responsiveness. The F1 data do imply a maternal factor, sex hormone, or sex-linked gene(s) that modifies EAE responsiveness. The data suggest that the H-2 complex modifies the degree of EAE responsiveness. This modulatory effect by H-2 could account for the contradictory reports in the literature on the association of H-2 type and EAE responsiveness.

Animals↗
PubMed1981

Expression of mosaicism in females heterozygous for Jimpy.

The Jimpy mouse is a sex-linked neurological mutant characterized by a paucity of myelin in the central nervous system (CNS). The distribution of myelin in the optic nerves of female carriers of the Jimpy gene exhibits a mosaic pattern such that patches of tissue along the nerve are identical in appearance to the hemizygote male, while other areas appear normal.

Age Factors↗
PubMed1981

Inhibition of experimental allergic encephalomyelitis by carrier administered prior to challenge with encephalitogenic peptide-carrier conjugate.

Guinea pigs can be rendered unresponsive to experimental allergic encephalomyelitis (EAE) challenge by prior injections of myelin basic protein (BP) or peptides derived from BP. The synthesized tryptophan-containing peptide (TrpP, corresponding to residues 114-122) which is the primary encephalitogenic sequence in BP (for guinea pigs) had been conjugated to the non-central nervous system protein bovine serum albumin (BSA) and used for EAE challenge. It has been shown in this study that prechallenge treatment with the BSA carrier alone can significantly inhibit the induction of EAE by TrpP-BSA conjugate. That carrier treatment is immunologically specific was determined when prior treatment with cytochrome c did not protect animals from EAE challenge with TrpP conjugated to BSA. In addition, in disease induced with BP or TrpP, and while TrpP did protect guinea pigs challenged with TrpP, it did not protect those challenged with BP. This last finding raises the possibility of a second encephalitogenic sequence in BP or an important role for the carrier in the TrpP conjugate.

Animals↗
PubMed1981

Experimental allergic encephalomyelitis in mice: encephalitogenicity of mouse central myelin basic proteins.

Two co-extractable myelin basic proteins (MBP) were isolated and purified from mouse brain and designated: large (L), estimated to be composed of 160-164 amino acid residues, and small (S), estimated to contain 114-115 residues. The two proteins migrate separately in polyacrylamide gel electrophoresis (PAGE) in a pattern similar to rat MBP-S and MBP-L; mouse MBP-L resembles rat MBP-L, human, bovine and guinea pig MBP by PAGE and by amino acid analysis. This report demonstrates for the first time that mouse MPB-L alone, and not mouse MBP-S, is encephalitogenic for guinea pigs and mice.

Amino Acids↗
PubMed1980

Bovine-derived spinal cord protein (SCP) protects guinea pigs from experimental allergic encephalomyelitis (EAE) - a confirmatory report.

An axonally localized, non-encephalitogenic protein derived from bovine spinal cord can protect guinea pigs from EAE following challenge with bovine myelin basic protein. Protection from neurologic signs is significant although CNS pathology is present. The protective regimen apparently varies depending upon the species and strain of animal; this specific requirement may account for a previous negative report.

Animals↗
PubMedDate not supplied

Histopathologic evaluation following chronic implantation of chromium and steel based metal alloys in the rabbit central nervous system.

Histopathologic evaluation of three metal alloys for chronic implantation in the central nervous system (CNS) was undertaken in rabbits. Throughout the 8 month evaluation period the inflammatory response to the alloys was bland. Two of the alloys tested (chromium based MP35N, Trademark of the Standard Pressed Steel Company, and a stainless steel alloy, BG42 VacArc, Trademark of Latrobe Steel) appeared suitable as CNS implants. The third alloy (stainless steel 440C, Carpenter Steel Company) showed more corrosion than the other alloys, and may be less suitable for implantation. While E. cuniculi infection was found in four rabbits, the infection did not directly interfere with the assessment of the histologic changes directly due to the implants. Autoantibodies to a brain constituent were not observed.

Animals↗