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K Keller

Publications and source records attributed to K Keller.

At least 19 recordsLinked to original sources
PubMed1995

From triple cysteine mutants to the cysteine-less glucose transporter GLUT1: a functional analysis.

Two triple cysteine mutants containing Cys-less N- or C-terminal halves and the Cys-less GLUT1 were generated by site-directed mutagenesis. Following expression in Xenopus oocytes, the intrinsic transport activities of the multiple cysteine mutants were slightly decreased when either the cysteine residues of the C-terminal half or all six residues were changed; substitution of serine for cysteine residues located at the N-terminal half was without consequence for the catalytic activity. The exofacial ligand ethylidene glucose inhibited 2-deoxy-D-glucose uptake of wild-type and Cys-less GLUT1-expressing Xenopus oocytes with comparable half-saturation constants (11.5 and 13.2 mM). However, each of the multiple cysteine mutants exhibited an increase in affinity for the endofacial inhibitor cytochalasin B, with the greatest effect being observed for the Cys-less construct (decrease in Ki by the factor 5-6).

Animals↗
PubMed1995

Proinflammatory cytokines regulate cyclooxygenase-2 mRNA expression in human macrophages.

Prostaglandins play a major role in the inflammatory and immune response. Macrophages constitutively produce prostaglandins by the enzyme cyclooxygenase-1 (cox) whereas inflammatory mediators and cytokines stimulate the inducible enzyme cox-2 for high output prostaglandin production. In this study, we investigated the effect of LPS, IFN-gamma and TNF-alpha in the regulation of cox-1 and cox-2 mRNA expression in PMA-differentiated U937 human macrophages. LPS, but not IFN-gamma or TNF-alpha, caused the induction of cox-2 mRNA in a dose- and time-dependent fashion. In IFN-gamma-primed macrophages, LPS stimulated a marked increase in the accumulation of cox-2 mRNA, whereas TNF-alpha and IFN-gamma induced a moderate level. However, IFN-gamma in combination with either LPS or TNF-alpha induced a synergistic increase in the accumulation of cox-2 mRNA after 24 hours. Regardless of the conditions, cox-1 mRNA remained unchanged. These results indicate that IFN-gamma priming is required for full expression of cox-2 mRNA in response to LPS or TNF-alpha stimulation and suggest that cox-2 mRNA is highly regulated by cytokines during macrophage activation.

Cells, Cultured↗
PubMed1995

Functional consequences of proline mutations in the putative transmembrane segments 6 and 10 of the glucose transporter GLUT1.

Proline residues are thought to play a characteristic structural and/or dynamic role in various membrane proteins [Williams, K.A. & Deber, C.M. (1991) Biochemistry 30, 8919-8923]. By use of site-directed mutagenesis and functional expression of mutant glucose transporters in Xenopus oocytes, we investigated the effects of single proline substitutions in the putative helices 6 and 10 on GLUT1-mediated glucose transport. Proline residues of helix 6, that are conserved in all human glucose-transporter isoforms except for the human GLUT2, were mutated either to alanine or to the corresponding residues of GLUT2, i.e. to histidine (P187H), arginine (P196R) or phenylalanine (P205F). In addition, the three proline amino acids within the domain G382-P-G-P-I-P of helix 10 were individually replaced with either alanine or glutamine residues. In all cases, transport function was retained when each individual proline residue was replaced with alanine. Substitution of proline 196 by arginine (P196R), however, resulted in reduction of 2-deoxy-D-glucose uptake rates by approximately 70%. Since the amount of this mutant transporter protein in plasma membrane and total membrane preparations was found to be decreased, as detected by immunoblotting, no single proline residue seemed to play a critical role in maintaining the catalytic activity of GLUT1. However, structural changes introduced by incorporation of the neutral polar amino acid glutamine at each single proline position of helix 10 almost completely abolished 2-deoxy-D-glucose uptake. Thus, the specific chemical structure of the side chain of the substituted amino acid rather than the unique property of proline residues for cis-trans isomerization seemed to determine the consequences on glucose transport.

Animals↗
PubMed1995

Estimation of water content and water mobility in the nucleus and cytoplasm of Xenopus laevis oocytes by NMR microscopy.

NMR microscopy is a noninvasive approach for studying cell structure and properties. Spatially resolved measurements of the relaxation times T1 and T2 provided information on the water proton spin density and water mobility in different parts of Xenopus laevis oocytes. The spin-lattice relaxation time T1 was determined using a saturation-recovery sequence and the common spin-echo sequence with increasing repetition times, while the transverse relaxation time T2 was measured by means of the spin-echo sequence with varying echo times. From the relaxation times, the mole fractions of possible reorientational correlation times tau c for different types of intracellular water were calculated according to a simple two-phase model. The values for T1, T2, and proton spin density (i.e., water content) are: nucleus >> animal cytoplasm > vegetal cytoplasm. Based on the estimation of tau c, nearly 90% of the nuclear water and 74.4% of the water of the animal pole was considered as free mobile water, whereas 55.5% of the water of the vegetal pole appeared as bound water.

Animals↗
PubMed1995

The relationships between skin hardness, pressure perception and two-point discrimination in the fingertip.

With the recent introduction of computer-assisted sensibility testing devices, it is possible to investigate the hypothesis that the neurological mechanisms responsible for perception of pressure and two-point discrimination are influenced by skin hardness. This study examined the relationships between the skin hardness of the human index and little finger pulp and the perception of pressure in 25 adults. Skin hardness was measured using the Derma-Durometer. Pressure perception was measured with the Pressure-Specified Sensory Device for both static and moving touch stimuli and for two-point discrimination. The mean hardness of the fingertip pulp was 12.5 +/- 0.6 gm/mm2. There was no statistically significant difference in hardness between the dominant and non-dominant, right and left, index and little, or male and female fingertips. Skin hardness was independent of age for this population. The highest correlation, which was r = 0.46, was found between the cutaneous pressure threshold for one-point static touch and skin hardness. While this degree of correlation is significant at the P < 0.02 level, the r2 = 21%, demonstrating that this degree of correlation leaves 79% of the variability unexplained. These results suggest a physical interaction between mechanoreceptors and dermis that is only partially explained by the hardness of the skin.

Adolescent↗
PubMed1995

Transforming growth factor-beta 1 primes macrophages for enhanced expression of the nitric oxide synthase gene for nitric oxide-dependent cytotoxicity against Entamoeba histolytica.

Nitric oxide (NO) produced by activated macrophages is the major cytotoxic molecule for in vitro cytotoxicity against Entamoeba histolytica trophozoites. Transforming growth factor-beta 1 (TGF-beta 1) is a potent negative regulator of several macrophage functions, including NO production. In this study, we investigated the effect of TGF-beta 1 on macrophage nitric oxide synthase (mac-NOS) mRNA expression and NO production for macrophage cytotoxicity against E. histolytica trophozoites. TGF-beta 1 by itself was incapable of inducing mouse bone marrow-derived macrophage (BMM) amoebicidal activity and NO production (as measured by nitrite). In contrast, TGF-beta 1 pretreatment (4 hr) primed BMM for an enhanced amoebicidal activity of 15% and 23% in response to (interferon-gamma) IFN-gamma+tumour necrosis factor-alpha (TNF-alpha) or IFN-gamma+lipopolysaccharide LPS, concomitant with increased NO production of 85% and 27%, respectively. TGF-beta 1 pretreatment increased NO production in response to IFN-gamma+TNF-alpha/LPS stimulation in a time- and dose-dependent manner. By Northern blot analysis, the increased NO production of TGF-beta 1-pretreated BMM was preceded by markedly enhanced expression of mac-NOS mRNA. The priming effect of TGF-beta 1 on NO production was critically dependent on both a TNF-alpha (> or = 100 U) and a LPS (> or = 100 ng) triggering dose in the presence of IFN-gamma. TGF-beta 1 pretreatment enhanced TNF-alpha mRNA expression, but had no effect on TNF-alpha production in culture supernatants after 4 hr of stimulation with IFN-gamma+TNF-alpha/LPS; however, at a later time-point (16-48 hr), even though the levels of TNF-alpha mRNA expression were unaffected, TNF-alpha production was reduced. These data demonstrate that TGF-beta 1 priming for increased mac-NOS mRNA expression for NO-dependent cytotoxicity against E. histolytica in response to IFN-gamma+TNF-alpha/LPS stimulation may be involved in the modulation of a TNF-alpha triggering signal by TGF-beta 1.

Animals↗
PubMed1995

Entamoeba histolytica stimulates the unstable transcription of c-fos and tumour necrosis factor-alpha mRNA by protein kinase C signal transduction in macrophages.

Macrophages play an important role in the control of and resistance to Entamoeba histolytica (E. histolytica). However, E. histolytica infections are characterized by suppression of cell-mediated immunity. To elucidate the molecular mechanisms whereby amoebae modulate host defences, we investigated whether the parasite elicits the 'immediate early' gene c-fos and cytokine tumour necrosis factor-alpha (TNF)-alpha mRNA and determined the signal transduction pathways involved in naive bone marrow-derived macrophages (BMM). E. histolytica stimulated a rapid and transient expression of c-fos and low levels of TNF-alpha mRNA, whereas the non-pathogenic Entamoeba moshkovshii (E. moshkovskii) did not. Inhibition of the protein kinase C (PKC) pathway with the pharmacological inhibitor H7 and by PKC depletion with phorbol myristate acetate showed that E. histolytica modulates TNF-alpha and c-fos gene expression through a PKC-dependent stimulus-response coupling event. E. histolytica activated and translocated PKC to the membrane fraction in BMM demonstrating a rapid and direct effect on PKC enzyme activity. Unlike lipopolysaccharide (LPS), BMM stimulated with E. histolytica had reduced stability of both c-fos and TNF-alpha mRNA transcripts (> 50%) and failed to secrete TNF-alpha protein. BMM treated with amoebic proteins and stimulated with LPS, or interferon-gamma (IFN-gamma)+LPS, resulted in a 33% and 50% reduction in TNF-alpha mRNA levels, respectively. These data argue that although E. histolytica stimulates c-fos and TNF-alpha gene expression through PKC signal transduction, the rapid degradation of the mRNAs, the lack of secreted TNF-alpha protein and the observed decreased responsiveness to a stimulatory signal may be a novel mechanism whereby the parasite modulates host defence mechanisms.

Animals↗
PubMed1994

Tumor necrosis factor alpha augments nitric oxide-dependent macrophage cytotoxicity against Entamoeba histolytica by enhanced expression of the nitric oxide synthase gene.

Nitric oxide (NO measured as nitrite, NO2-) is the major effector molecule produced by activated macrophages for in vitro cytotoxicity against Entamoeba histolytica trophozoites. In this study, we determine whether tumor necrosis factor alpha (TNF-alpha) produced by activated bone marrow-derived macrophages (BMM) is involved in the induction of the inducible NO synthase gene (mac-NOS) for NO-dependent amebicidal activity. TNF-alpha alone did not directly induce macrophage NO2- production to kill amebae; however, in combination with increasing concentrations of TNF-alpha and gamma interferon (IFN-gamma), BMM amebicidal activity and NO2- production progressively increased and showed a significant linear correlation. Antiserum to TNF-alpha and the NO synthase inhibitor NG-monomethyl L-arginine (L-NMMA) inhibited the synergistic effects of TNF-alpha and IFN-gamma. BMM activated with increasing concentrations of lipopolysaccharide (LPS) and IFN-gamma showed a significant linear correlation between TNF-alpha release and NO2- production. Antiserum to TNF-alpha suppressed TNF-alpha release, NO2- production, and amebicidal activity by 93, 53, and 86%, respectively. L-NMMA diminished NO2- production by 74% and macrophage amebicidal activity by 83% but had no effect on TNF-alpha release. Quantification by Northern (RNA) blot analyses demonstrated that IFN-gamma in combination with TNF-alpha or LPS increased markedly the accumulation of mac-NOS and TNF-alpha mRNAs in a time-dependent manner with a concomitant increase in NO and TNF-alpha production. Peak induction of mac-NOS occurred after 24 h, whereas TNF-alpha mRNA was rapidly expressed after 4 h and remained stable for 48 h. Taken together, these data argue that TNF-alpha augments NO-dependent macrophage cytotoxicity against E. histolytica via elevated levels of mac-NOS mRNA expression which may be associated with the accumulation of TNF-alpha mRNA.

Amino Acid Oxidoreductases↗
PubMed1994

Entamoeba histolytica modulates the nitric oxide synthase gene and nitric oxide production by macrophages for cytotoxicity against amoebae and tumour cells.

Nitric oxide (NO) is the major cytotoxic molecule produced by activated macrophages for cytotoxicity against Entamoeba histolytica trophozoites. In the present study, we determined whether E. histolytica infection and soluble amoebic proteins affected macrophage cytotoxicity against amoebae and tumour cells by modulating the inducible NO synthase gene (iNOS) and NO (measured as nitrite, NO2-) and tumour necrosis factor-alpha (TNF-alpha) production. Amoebic liver abscess-derived macrophages [days 10, 20, 30 post-infection (p.i.)] stimulated with interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) showed increased cytotoxicity against L929 cells (TNF-alpha-sensitive), but were refractory for killing amoebae and P815 cells (both NO-sensitive), concomitant with low NO2- production (< 4 microM/10(6) cells). In contrast, peritoneal and spleen macrophages at 10 and 20 days p.i. activated with IFN-gamma and LPS demonstrated increased killing of amoebae, and L929 and P815 cells concomitant with high NO2- production (> 12 microM/10(6) cells). Pretreatment of mouse bone marrow-derived macrophages with amoebic proteins suppressed IFN-gamma and LPS-induced amoebicidal (33%) and tumoricidal (44-49%) activities, with a corresponding decrease in TNF-alpha (56%) and NO (41%) production as well as TNF-alpha (41%) and iNOS (27%) mRNA by Northern blot analyses as compared to untreated activated controls. Inhibition of prostaglandin E2 (PGE2) biosynthesis in abscess and naive macrophages pretreated with amoebic proteins augmented IFN-gamma- and LPS-induced killing of L929 cells and TNF-alpha production, but failed to increase killing of P815 cells and amoebae as well as iNOS mRNA levels or NO production. These results suggest that E. histolytica selectively induces dysfunction of macrophage cytotoxicity by modulating iNOS mRNA expression and NO production independent from TNF-alpha and PGE2 allowing the parasites to survive within the host by impairing host immune responses.

Amino Acid Oxidoreductases↗
PubMed1992

The differential role of Cys-421 and Cys-429 of the Glut1 glucose transporter in transport inhibition by p-chloromercuribenzenesulfonic acid (pCMBS) or cytochalasin B (CB).

Cys-421 and Cys-429 of Glut1 were replaced by site-directed mutagenesis in order to investigate their involvement in basal glucose transport and transport inhibition. Neither of the two cysteine residues was essential for basal 2-deoxy-D-glucose uptake in Xenopus oocytes expressing the respective mutant M421 and M429. If applied from the external side, the poorly permeable sulfhydryl-reactive agent pCMBS inhibited 2-deoxy-D-glucose uptake of Glut1- and M421-expressing Xenopus oocytes but failed to affect uptake of the Cys-429 mutant. This is in agreement with the proposed two-dimensional model of Glut1 confirming that Cys-429 is the only residue exposed to the surface of the plasma membrane. The replacement of Cys-421 at the exofacial end of helix eleven caused a partial protection of 3-O-methylglucose transport inhibition by CB; this residue may thus be involved in stabilizing an adjacent local tertiary structure necessary for the full activity of this inhibitor.

4-Chloromercuribenzenesulfonate↗
PubMed1992

Subcellular distribution and activity of glucose transporter isoforms GLUT1 and GLUT4 transiently expressed in COS-7 cells.

In adipose and muscle cells, the glucose transporter isoform GLUT4 is mainly located in an intracellular, vesicular compartment from which it is translocated to the plasma membrane in response to insulin. In order to test the hypothesis that this preferential targeting of a glucose transporter to an intracellular storage site is conferred only by its primary sequence, we compared the subcellular distribution of the fat/muscle glucose transporter GLUT4 with that of the erythrocyte/brain-type glucose transporter GLUT1 after transient expression in COS-7 cells. Full-length cDNA was ligated into the expression vector pCMV that is driven by the cytomegalovirus promoter, and introduced into COS cells by the DEAE-dextran method. Cells were homogenized and fractionated by differential centrifugation to yield plasma membranes and a Golgi-enriched fraction of intracellular membranes (low-density microsomes). In these membrane fractions, the abundance of glucose transporters was assessed by immunoblotting with specific antibodies against GLUT1 and GLUT4, and their transport activity was assayed after solubilization and reconstitution into lecithin liposomes. Uptake rates of 2-deoxyglucose assayed in parallel samples were higher in cells expressing GLUT1 or GLUT4 as compared with control cells (transfection of pCMV without transporter cDNA). Reconstituted glucose transport activity in plasma membranes was about 5-fold higher after expression of GLUT1 and GLUT4 as compared with control cells. The relative amount of GLUT4 in the low-density microsomes as detected by reconstitution and immunoblotting exceeded that of the GLUT1, but was much lower than that observed in typical insulin-sensitive cells, e.g., rat fat cells or 3T3-L1 adipocytes. These data indicate that COS-7 cells transfected with glucose transporter cDNA express the active transport proteins and can be used for functional studies.

Amino Acid Sequence↗
PubMed1992

Amino acid substitutions at tryptophan 388 and tryptophan 412 of the HepG2 (Glut1) glucose transporter inhibit transport activity and targeting to the plasma membrane in Xenopus oocytes.

All 6 tryptophan residues in the human HepG2-type glucose transporter (Glut1) were individually altered by site-directed mutagenesis to investigate the role of these residues in transport function. Tryptophan residues in positions 48, 65, 186, 363, 388, and 412 of Glut1 were changed to either a glycine or leucine residue. Mutant mRNAs were synthesized and injected into Xenopus laevis oocytes. Transporter function as assessed by uptake of 2-deoxy-D-[3H]glucose or transport of 3-O-[3H]methylglucose was decreased in the 388 and 412 mutants but was unaltered in all other mutants. The amount of the mutant transporters expressed in total membrane and plasma membrane fractions was measured using Glut1-specific antibodies. Calculation of the intrinsic transport activity of each of the mutants using these data demonstrated that the reduced transport activity of the 412 mutants was caused entirely by a dramatic decrease in the intrinsic activity of the mutant proteins whereas the reduced activity of the 388 mutants was a result of a decreased level of the protein in oocytes, decreased targeting to the plasma membrane, and a modest decrease in the intrinsic activity. Protease/glycosidase mapping of in vitro translation products indicated that the effects of the 388 and 412 point mutations could not be attributed to a disruption in the ability of the mutant proteins to insert properly into the membrane. The ID50 for cytochalasin B inhibition of 2-deoxyglucose uptake was increased from 5 x 10(-7) M for the wild-type Glut1 to 4 x 10(-6) M in the 388 mutants but was unaltered in the 412 mutants. These observations suggest that 1) Trp-412 may comprise part of a hexose binding site or is involved in maintaining a local tertiary structure critical for transport function; 2) Trp-388 is involved in stabilizing the equilibrium binding of cytochalasin B to the transporter. Trp-388 may therefore lie near a substrate binding site and also appears to participate in stabilization of local tertiary structure important for full catalytic activity and efficient targeting to the Xenopus plasma membrane.

Animals↗
PubMed1992

Modulation of tumor necrosis factor production by macrophages in Entamoeba histolytica infection.

The macrophage-derived mediator tumor necrosis factor alpha (TNF) is a cytokine with pleiotropic effects. TNF exhibits potent immunologic and inflammatory properties in parasitic diseases. The present study examined the production of TNF by macrophages isolated from gerbils infected with Entamoeba histolytica and by naive macrophages in response to amoebae in vitro. Amoebic liver abscess-derived macrophages produced low constitutive basal levels of TNF; in response to lipopolysaccharide (LPS) stimulation, TNF production was enhanced by 14-, 11-, and 6-fold at 10, 20, and 30 days postinfection, respectively. Amoebic liver abscess-derived macrophages pretreated with either recombinant gamma interferon (IFN-gamma) or the cyclooxygenase inhibitor indomethacin augmented TNF production in response to soluble amoebic proteins and LPS. Kupffer cells and peritoneal and spleen macrophages from infected animals did not release TNF constitutively in vitro. However, TNF production in response to LPS stimulation was significantly higher at 10 and 20 days postinfection. Macrophages from infected and naive animals pretreated with recombinant IFN-gamma or indomethacin produced increased amounts of TNF in response to LPS but not in response to soluble amoebic protein stimulation. Pretreatment of naive macrophages with amoebic proteins inhibited LPS-induced TNF production by 69 to 79%; the effect of the amoebic proteins was partially reversed by indomethacin pretreatment. In contrast, IFN-gamma- and LPS-activated naive macrophages produced enhanced levels of TNF in response to live amoebae and soluble amoebic proteins. Our results demonstrate that TNF production by macrophages is altered during E. histolytica infection and in response to amoebae and suggest a role for IFN-gamma and prostaglandin E2 in regulating TNF production during the infection.

Animals↗
PubMed1992

The fast release of mucin secretion from human colonic cells induced by Entamoeba histolytica is dependent on contact and protein kinase C activation.

The mucus producing colonic cell line, LS174T, was used as a model to study E. histolytica-induced mucin secretion. E. histolytica trophozoites in contact with the mucus layer overlying the LS174T cells and in response to PMA, a protein kinase C activator, and Ca2+ ionophore A23187 which elevates intracellular Ca2+ ([Ca]i), caused a time-dependent (0.25-2.00 h) release of mucin. PKC inhibitors, H7 and staurosporine inhibited E. histolytica (37 and 75%) and PMA (46 and 100%)-induced mucin secretion, whereas in response to Ca2+ ionophore mucin secretion was augmented (56 and 17%). Both PMA and E. histolytica-induced the translocation of the PKC enzyme from the cytoplasm to the membrane fraction with increased enzyme activity. These results suggest that even though mucin secretion can be induced by PKC and Ca(2+)-dependent pathways, E. histolytica evokes the fast release of mucins by a PKC-dependent mechanism.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1992

[The legal status of homeopathic medicines. Quality requirements, registration and permit procedures].

Homeopathic medicaments which are ready for application have to be approved or registered before they can be made available. This procedure is regulated by the "Arzneimittelgesetz (AMG)", a law regulating licensing and registration of medicaments. The commission in charge of the registration and licensing of homeopathic medicaments is the "Aufbereitungskommission D" of the German "Bundesgesundheitsamt (BGA)", the Board of Public Health. Application forms are dealt with on the basis of controlled and non-controlled clinical studies, application observations, and case studies, as well as specialized literature. The commission is trying to do justice to the particular features of the special field of homeopathy.

Animals↗
PubMed1991

Down-regulation of murine lymphocyte responsiveness to mitogens after treatment with antigens of Entamoeba histolytica.

Injection of mice with pathogenic Entamoeba histolytica (strain HM1-IMSS) antigens resulted in a decreased capacity of splenocytes to respond to mitogen-induced blastogenesis following a challenge with concanavalin A (Con A), phytohemagglutinin (PHA), and lipopolysaccharide (LPS), whereas no inhibition was observed in mice that had previously been injected with equivalent amounts of non-pathogenic E. histolytica-like Laredo antigens. Depletion of adherent cells in the splenocyte preparation indicated that these cells were not a major contributor to the observed immunosuppression. Quantification of splenic T-lymphocyte subsets demonstrated a significant decrease in Thy-1+ and Lyt-1+ cells, but Lyt-2+ cells were not affected. Splenocytes treated with pathogenic amoebic antigens in vitro affected the capacity of these cells to respond optimally to Con A- and LPS-induced blastogenesis but not to that induced by PHA. These findings demonstrate that amoebic antigens affect lymphocyte function and may be important co-factors in the immunoregulation and pathogenesis of amoebiasis.

Animals↗
PubMed1991

Mucin and nonmucin secretagogue activity of Entamoeba histolytica and cholera toxin in rat colon.

Depletion of colonic mucus occurs before invasion of the colonic mucosa by Entamoeba histolytica trophozoites. It is hypothesized that E. histolytica releases a mucus secretagogue; this was studied in a rat colonic loop model. In colonic loops exposed to live amebae, mucus secretion was quantitated by release of acid-precipitable [3H]glucosamine-labeled luminal glycoprotein and by specific immunoassay. Mucus secretion increased in dose-dependent fashion in response to greater than or equal to 1 X 10(5) trophozoites; cholera toxin (20 micrograms per loop), a known mucus secretagogue, elicited a similar response. Thin-section histological analysis of amebae and cholera toxin-exposed loops showed increased mucus release and streaming from mucosal goblet cells with cellular cavitation compared with control loops. Sepharose-4B chromatography of amebae and cholera toxin-stimulated glycoproteins demonstrated secretion of mucins and an 80%-90% increase in low-molecular-weight proteins. E. histolytica trophozoites and cholera toxin enhanced the secretion of preformed and newly synthesized mucin glycoproteins and stimulated colonic glycoprotein synthesis. The level of mucus secretion elicited by axenic E. histolytica strains correlated with their virulence in vivo and in vitro. The amebic secretagogue was released into the culture medium and was heat stable. Mucus secretagogue activity of E. histolytica may contribute to depletion or alteration of the protective mucus blanket, facilitating pathogenesis of invasive amebiasis.

Animals↗