[Is dental plaque a normal Helicobacter pylori reservoir?]. / Es la placa dentaria reservorio habitual de Helicobacter pylori?

The mechanisms of transmission and reservoir of Helicobacter pylori is still unclear; even it has been suggested that dental plaque could be the bacterial reservoir and one important factor in the reinfection. The aim of the study was to evaluate the prevalence of Helicobacter pylori in dental plaque in 20 patients with non ulcer dyspepsia (12 females, 7 males; mean age 40.5 years) and antral infection; and to establish the presence of bacteria in dental plaque and gastric mucosa after eradication. Gastric colonization in all of them was confirmed by five samples (three of antrum and two of body) with Giemsa conventional technique, clotest and culture. When clotest was positive in gastric mucosa, we performed the scrape of dental plaque and sending the material for culture. All patients were treated with a scheme of seven days with one protom pump inhibitor and two antibiotics. After four weeks all the patients were controlled with endoscopy and culture of dental plaque to confirm eradication. Dental plaque culture was positive in 1/20 patients (5%), and this results was similar to developed countries, using as detection method culture or polymerase chain reaction (PCR).

Es la placa dentaria reservorio habitual de Helicobacter pylory? / Is dental plaque reservoir of Helicobacter pylori?

Si bien la forma de transmisión y el reservorio del Helicobacter pylori no son claros, se ha sugerido que la placa dentaria puede ser reservorio del germen y poseer inplicancias en la reinfección, una vez erradicada la bacteria. El objetivo de este trabajo fue evaluar la prevalencia del Helicobacter pylori en placa dentaria en 20 pacientes portadores de dispepsia no ulcerosa (12 mujeres y 7 varones con media etaria de 40.5 años)e infección antral por Helicobacter pylori y establecer la presencia en placa dentaria y mucosa gástrica luego de la erradicación. En todas ellas se confirmó la colonización gástrica mediante 5 biopsias (3 de antro y 2 de cuerpo) realizándose histología convencional com Giemsa clotest y cultivo en medio de anaerobiosis com generador de microaerofilia, usando como medio de transporte Stuard-carbón activado. Confirmada la positividad del clotest en mucosa gástrica, se procedió al raspado de placa dentaria en el servicio de odontología, enviándose el material en las mismas condiciones descriptas para el cultivo de la bacteria. Todos los pacientes fueron tratados com un esquema de erradicación a 7 días que incluía un IBP en dos tomas diarias; amoxicilina 1 gr. X 2 y claritromicina 500 mg. X 2. Cuatro semanas después de finalizado el esquema se realizó nueva endoscopía y cultivo de placa dentaria para confirmar erradicación. El cultivo de placa dentaria fue positivo en 1 de 20 es decir el 5 por ciento, confirmándose su erradicación com la terapeútica en el control a las 4 semanas. Nuestros resultados en cuanto a prevalencia de Hp en placa dentaria son similares a los obtenidos en países desarrollados, utilizando como método de detección de la bacteria el cultivo de PCR.

Es la placa dentaria reservorio habitual de Helicobacter pylory? / Is dental plaque reservoir of Helicobacter pylori?

Si bien la forma de transmisión y el reservorio del Helicobacter pylori no son claros, se ha sugerido que la placa dentaria puede ser reservorio del germen y poseer inplicancias en la reinfección, una vez erradicada la bacteria. El objetivo de este trabajo fue evaluar la prevalencia del Helicobacter pylori en placa dentaria en 20 pacientes portadores de dispepsia no ulcerosa (12 mujeres y 7 varones con media etaria de 40.5 años)e infección antral por Helicobacter pylori y establecer la presencia en placa dentaria y mucosa gástrica luego de la erradicación. En todas ellas se confirmó la colonización gástrica mediante 5 biopsias (3 de antro y 2 de cuerpo) realizándose histología convencional com Giemsa clotest y cultivo en medio de anaerobiosis com generador de microaerofilia, usando como medio de transporte Stuard-carbón activado. Confirmada la positividad del clotest en mucosa gástrica, se procedió al raspado de placa dentaria en el servicio de odontología, enviándose el material en las mismas condiciones descriptas para el cultivo de la bacteria. Todos los pacientes fueron tratados com un esquema de erradicación a 7 días que incluía un IBP en dos tomas diarias; amoxicilina 1 gr. X 2 y claritromicina 500 mg. X 2. Cuatro semanas después de finalizado el esquema se realizó nueva endoscopía y cultivo de placa dentaria para confirmar erradicación. El cultivo de placa dentaria fue positivo en 1 de 20 es decir el 5 por ciento, confirmándose su erradicación com la terapeútica en el control a las 4 semanas. Nuestros resultados en cuanto a prevalencia de Hp en placa dentaria son similares a los obtenidos en países desarrollados, utilizando como método de detección de la bacteria el cultivo de PCR. (AU)

CD4, CXCR-4, and CCR-5 dependencies for infections by primary patient and laboratory-adapted isolates of human immunodeficiency virus type 1.

We have used a focal infectivity method to quantitatively analyze the CD4, CXCR-4, and CCR-5 dependencies for infections by diverse primary patient (PR) and laboratory-adapted (LA) isolates of human immunodeficiency virus type 1 (HIV-1). Infectivities of T-cell-tropic viruses were analyzed in a panel of HeLa-CD4 cell clones that have distinct quantities of CD4 and in human astroglioma U87MG-CD4 cells that express a large quantity of CD4 and become highly susceptible to infection after transfection with a CXCR-4 expression vector. The latter analysis indicated that PR as well as LA T-cell-tropic viruses efficiently employ CXCR-4 as a coreceptor in an optimal human cell line that contains abundant CD4. Previous uncertainties regarding coreceptor usage by PR T-cell-tropic HIV-1 isolates may therefore have derived from the assay conditions. As reported previously, unrelated LA and PR T-cell-tropic HIV-1 isolates differ in infectivities for the HeLa-CD4 clonal panel, with LA viruses infecting all clones equally and PR viruses infecting the clones in proportion to cellular CD4 quantities (D. Kabat, S. L. Kozak, K. Wherly, and B. Chesebro, J. Virol. 68:2570-2577, 1994). To analyze the basis for this difference, we used the HeLa-CD4 panel to compare a molecularly cloned T-cell-tropic PR virus (ELI1) with six of its variants that grow to different extents in CD4-positive leukemic cell lines and that differ only at specific positions in their gp120 and gp41 envelope glycoproteins. All mutations in gp120 or gp41 that contributed to laboratory adaptation preferentially enhanced infectivity for cells that had little CD4 and thereby decreased the CD4 dependencies of the infections. There was a close correlation between abilities of T-cell-tropic ELI viruses to grow in an expanded repertoire of leukemic cell lines, the reduced CD4 dependencies of their infections of the HeLa-CD4 panel, and their sensitivities to inactivation by soluble CD4 (sCD4). Since all of the ELI viruses can efficiently use CXCR-4 as a coreceptor, we conclude that an increase in viral affinity for CD4 rather than a switch in coreceptor specificity is principally responsible for laboratory adaption of T-cell-tropic HIV-1. Syncytium-inducing activities of the ELI viruses, especially when analyzed on cells with low amounts of CD4, were also highly correlated with their laboratory-adapted properties. Results with macrophage-tropic HIV-1 were strikingly different in both coreceptor and CD4 dependencies. When assayed in HeLa-CD4 cells transfected with an expression vector for CCR-5, macrophage-tropic HIV-1 isolates that had been molecularly cloned shortly after removal from patients were equally infectious for cells that had low or high CD4 quantities. Moreover, despite their substantial infectivities for cells that had only a trace of CD4, macrophage-tropic isolates were relatively resistant to inactivation by sCD4. We conclude that T-cell-tropic PR viruses bind weakly to CD4 and preferentially infect cells that coexpress CXCR-4 and large amounts of CD4. Their laboratory adaptation involves corresponding increases in affinities for CD4 and in abilities to infect cells that have relatively little CD4. In contrast, macrophage-tropic HIV-1 appears to interact weakly with CD4 although it can infect cells that coexpress CCR-5 and small quantities of CD4. We propose that cooperative binding of macrophage-tropic HIV-1 onto CCR-5 and CD4 may enhance virus adsorption and infectivity for cells that have only a trace of CD4.

Deletions in one domain of the Friend virus-encoded membrane glycoprotein overcome host range restrictions for erythroleukemia.

Although the Friend virus-encoded membrane glycoprotein (gp55) activates erythropoietin receptors (EpoR) to cause erythroblastosis only in certain inbred strains of mice but not in other species, mutant viruses can overcome aspects of mouse resistance. Thus, mice homozygous for the resistance allele of the Fv-2 gene are unaffected by gp55 but are susceptible to mutant glycoproteins that have partial deletions in their ecotropic domains. These and other results have suggested that proteins coded for by polymorphic Fv-2 alleles might directly or indirectly interact with EpoR and that changes in gp55 can overcome this defense. A new viral mutant with an exceptionally large deletion in its ecotropic domain is now also shown to overcome Fv-2rr resistance. In all cases, the glycoproteins that activate EpoR are processed to cell surfaces as disulfide-bonded dimers. To initiate analysis of nonmurine resistances, we expressed human EpoR and mouse EpoR in the interleukin 3-dependent mouse cell line BaF3 and compared the abilities of Friend virus-encoded glycoproteins to convert these cells to growth factor independence. Human EpoR was activated in these cells by erythropoietin but was resistant to gp55. However, human EpoR was efficiently activated in these cells by the same viral mutants that overcome Fv-2rr resistance in mice. By construction and analysis of human-mouse EpoR chimeras, we obtained evidence that the cytosolic domain of human EpoR contributes to its resistance to gp55 and that this resistance is mediated by accessory cellular factors. Aspects of host resistance in both murine and nonmurine species are targeted specifically against the ecotropic domain of gp55.

A Friend virus mutant encodes a small glycoprotein that causes erythroleukemia.

The Pvu delta mutant of Friend spleen focus-forming virus encodes the smallest env glycoprotein (apparent M(r), 41,000) known to activate erythropoietin receptors. In vivo, Pvu delta causes erythroblastosis and the development of erythroleukemia. We isolated two leukemic cell lines that contain Pvu delta; both synthesize hemoglobin in response to dimethyl sulfoxide. The Pvu delta env gene contains a 204-base deletion in the ecotropic-specific region, suggesting that this domain of the glycoprotein is not essential for viral pathogenesis.

A Friend virus mutant that overcomes Fv-2rr host resistance encodes a small glycoprotein that dimerizes, is processed to cell surfaces, and specifically activates erythropoietin receptors.

The env gene of Friend spleen focus-forming virus (SFFV) encodes a membrane glycoprotein (gp55) that is inefficiently (3 to 5%) processed from the rough endoplasmic reticulum to form a larger dimeric plasma membrane derivative (gp55p). Moreover, the SFFV env glycoprotein associates with erythropoietin receptors (EpoR) to cause proliferation of infected erythroblasts [J.-P. Li, A. D. D'Andrea, H. F. Lodish, and D. Baltimore, Nature (London) 343:762-764, 1990]. Interestingly, the mitogenic effect of SFFV is blocked in mice homozygous for the Fv-2r resistance gene, but mutant SFFVs can overcome this resistance. Recent evidence suggested that these mutants contain partial env deletions that truncate the membrane-proximal extracellular domain of the encoded glycoproteins (M. H. Majumdar, C.-L. Cho, M. T. Fox, K. L. Eckner, S. Kozak, D. Kabat, and R. W. Geib, J. Virol. 66:3652-3660, 1992). Mutant BB6, which encodes a gp42 glycoprotein that has a large deletion in this domain, causes erythroblastosis in DBA/2 (Fv-2s) as well as in congenic D2.R (Fv-2r) mice. Analogous to gp55, gp42 is processed inefficiently as a disulfide-bonded dimer to form cell surface gp42p. Retroviral vectors with SFFV and BB6 env genes have no effect on interleukin 3-dependent BaF3 hematopoietic cells, but they cause growth factor independency of BaF3/EpoR cells, a derivative that contains recombinant EpoR. After binding 125I-Epo to surface EpoR on these factor-independent cells and adding the covalent cross-linking reagent disuccinimidyl suberate, complexes that had immunological properties and sizes demonstrating that they consisted of 125I-Epo-gp55p and 125I-Epo-gp42p were isolated from cell lysates. Contrary to a previous report, SFFV or BB6 env glycoproteins did not promiscuously activate other members of the EpoR superfamily. Although the related env glycoproteins encoded by dualtropic murine leukemia viruses formed detectable complexes with EpoR, strong mitogenic signalling did not ensue. Our results indicate that the SFFV and BB6 env glycoproteins specifically activate EpoR; they help to define the glycoprotein properties important for its functions; and they strongly suggest that the Fv-2 leukemia control gene encodes an EpoR-associated regulatory factor.

Cell surface site for mitogenic interaction of erythropoietin receptors with the membrane glycoprotein encoded by Friend erythroleukemia virus.

The membrane glycoprotein (gp55) encoded by the env gene of Friend spleen focus-forming virus (SFFV) causes mitogenesis of infected erythroblasts and is inefficiently (3-5%) processed from the rough endoplasmic reticulum (RER) to plasma membranes. Recent evidence suggested that gp55 binds to erythropoietin receptors (EpoR) in the RER, and it was proposed that this intracellular interaction causes mitogenesis (Li, J.-P., D'Andrea, A. D., Lodish, H. F., and Baltimore, D. (1990) Nature 343, 762-764). Other evidence has indicated that the plasma membrane component (gp55P) can also complex with EpoR. To identify the site of functional complexes and to study the factors that control their formation, we analyzed eight SFFV env mutants that contain in-frame deletions or linker insertions. The three nonpathogenic mutants encode gp55s that fail to leave the RER, whereas the five pathogenic mutants encode glycoproteins that occur on cell surfaces. Although BaF3 hematopoietic cells are interleukin 3 (IL-3)-dependent, a cellular derivative BaF3/EpoR that contains EpoR survives and grows in either IL-3 or erythropoietin (Epo). The five pathogenic SFFV env mutants converted BaF3/EpoR but not BaF3 cells to growth factor independence, whereas the nonpathogenic mutants did not eliminate growth factor requirements of any cells. Studies using 125I-Epo and the covalent cross-linking reagent disuccinimidyl suberate provided unambiguous evidence for ternary complexes of 125I-Epo.EpoR.gp55P on surfaces of all factor-independent cells. Size of the cell surface complex was correspondingly reduced in the case of a newly isolated SFFV mutant that encodes a severely truncated (M(r) approximately 41,000) but mitogenically active env glycoprotein. Our results support the hypothesis that activation of EpoR by the SFFV env glycoprotein occurs exclusively on cell surfaces.

Acalasia y cancer de esofago / Achalasia and esophageal cancer

En el período comprendido entre enero de 1970 y diciembre de 1990, fueron estudiados 242 pacientes portadores de acalasia esofágica. De ellos 8 (3.3%) desarrollaron durante la evolución de la enfermedad una neoplasia esofágica. Los 8 casos correspondieron al tipo histológico de carcinoma epidermoide: 3 diferenciados, 3 semidiferenciados y 2 anaplásicos. La terapéutica recibida con anterioridad para la enfermedad de base fue: 1 paciente operado efectuándose miotomía extramucosa de Heller, 4 pacientes recibieron dilatación con bujías prógradas en numerosas oportunidades y los 2 restantes no recibieron tratamiento alguno para su acalasia. Dos pacientes presentaron fístulas traqueobronquiales como complicación de la neoplasia. El tratamiento recibido fue: 3 pacientes, radioterapia (4000 rad); 1 paciente, quimioterapia (bleomicina más cisplatino): 1 paciente quimio más radioterapia; 1 paciente cirugía de resección; 2 pacientes gastrostomía de alimentación. Los 8 pacientes fallecieron dentro del ano de demostrado su cáncer esofágico

Acalasia y cancer de esofago / Achalasia and esophageal cancer

En el período comprendido entre enero de 1970 y diciembre de 1990, fueron estudiados 242 pacientes portadores de acalasia esofágica. De ellos 8 (3.3%) desarrollaron durante la evolución de la enfermedad una neoplasia esofágica. Los 8 casos correspondieron al tipo histológico de carcinoma epidermoide: 3 diferenciados, 3 semidiferenciados y 2 anaplásicos. La terapéutica recibida con anterioridad para la enfermedad de base fue: 1 paciente operado efectuándose miotomía extramucosa de Heller, 4 pacientes recibieron dilatación con bujías prógradas en numerosas oportunidades y los 2 restantes no recibieron tratamiento alguno para su acalasia. Dos pacientes presentaron fístulas traqueobronquiales como complicación de la neoplasia. El tratamiento recibido fue: 3 pacientes, radioterapia (4000 rad); 1 paciente, quimioterapia (bleomicina más cisplatino): 1 paciente quimio más radioterapia; 1 paciente cirugía de resección; 2 pacientes gastrostomía de alimentación. Los 8 pacientes fallecieron dentro del ano de demostrado su cáncer esofágico (AU)

[Achalasia and esophageal cancer]. / Acalasia y cáncer de esófago.

During the period included between January 1970 and December 1990, we studied 242 patients with manometric and radiological diagnosis of esophageal achalasia. Eight of these patients (3.3%) developed during the evolution of their disease an esophageal carcinoma. Eight cases showed histologic type of epidermoid carcinoma: 3 differentiated, 3 semi-differentiated and 2 anaplastic. Therapy for achalasia was: one patient, Heller myotomy, 4 patients, dilatations with bougies in numerous opportunities, and the other two patients receive no treatment for achalasia. Two patients reported tracheobronchial fistulas as complication of carcinoma. Treatment received for carcinoma included: three patients, radiotherapy (4000 rads); one patient, chemotherapy; one patient, chemotherapy and radiotherapy, one resection surgery and two patients feeding gastrostomy. All of the eight patients died within the year of diagnosis of epidermoid carcinoma.

Acalasia y cáncer de esófago. / [Achalasia and esophageal cancer]

During the period included between January 1970 and December 1990, we studied 242 patients with manometric and radiological diagnosis of esophageal achalasia. Eight of these patients (3.3

) developed during the evolution of their disease an esophageal carcinoma. Eight cases showed histologic type of epidermoid carcinoma: 3 differentiated, 3 semi-differentiated and 2 anaplastic. Therapy for achalasia was: one patient, Heller myotomy, 4 patients, dilatations with bougies in numerous opportunities, and the other two patients receive no treatment for achalasia. Two patients reported tracheobronchial fistulas as complication of carcinoma. Treatment received for carcinoma included: three patients, radiotherapy (4000 rads); one patient, chemotherapy; one patient, chemotherapy and radiotherapy, one resection surgery and two patients feeding gastrostomy. All of the eight patients died within the year of diagnosis of epidermoid carcinoma.

Acalasia y cáncer de esófago. / [Achalasia and esophageal cancer]

During the period included between January 1970 and December 1990, we studied 242 patients with manometric and radiological diagnosis of esophageal achalasia. Eight of these patients (3.3

) developed during the evolution of their disease an esophageal carcinoma. Eight cases showed histologic type of epidermoid carcinoma: 3 differentiated, 3 semi-differentiated and 2 anaplastic. Therapy for achalasia was: one patient, Heller myotomy, 4 patients, dilatations with bougies in numerous opportunities, and the other two patients receive no treatment for achalasia. Two patients reported tracheobronchial fistulas as complication of carcinoma. Treatment received for carcinoma included: three patients, radiotherapy (4000 rads); one patient, chemotherapy; one patient, chemotherapy and radiotherapy, one resection surgery and two patients feeding gastrostomy. All of the eight patients died within the year of diagnosis of epidermoid carcinoma.