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1.
Emerg Infect Dis ; 27(8): 2081-2089, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34286681

RESUMEN

We evaluated the performance of self-collected anterior nasal swab (ANS) and saliva samples compared with healthcare worker-collected nasopharyngeal swab specimens used to test for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). We used the same PCR diagnostic panel to test all self-collected and healthcare worker-collected samples from participants at a public hospital in Atlanta, Georgia, USA. Among 1,076 participants, 51.9% were men, 57.1% were >50 years of age, 81.2% were Black (non-Hispanic), and 74.9% reported >1 chronic medical condition. In total, 8.0% tested positive for SARS-CoV-2. Compared with nasopharyngeal swab samples, ANS samples had a sensitivity of 59% and saliva samples a sensitivity of 68%. Among participants tested 3-7 days after symptom onset, ANS samples had a sensitivity of 80% and saliva samples a sensitivity of 85%. Sensitivity varied by specimen type and patient characteristics. These findings can help physicians interpret PCR results for SARS-CoV-2.


Asunto(s)
COVID-19 , SARS-CoV-2 , Anciano de 80 o más Años , Prueba de COVID-19 , Georgia , Humanos , Masculino , Nasofaringe , Saliva , Manejo de Especímenes
2.
Infect Immun ; 88(4)2020 03 23.
Artículo en Inglés | MEDLINE | ID: mdl-31964750

RESUMEN

Human genital Chlamydia infection is a major public health concern due to the serious reproductive system complications. Chlamydia binds several receptor tyrosine kinases (RTKs) on host cells, including the epidermal growth factor receptor (EGFR), and activates cellular signaling cascades for host invasion, cytoskeletal remodeling, optimal inclusion development, and induction of pathogenic epithelial-mesenchyme transition (EMT). Chlamydia also upregulates transforming growth factor beta (TGF-ß) expression, whose signaling pathway synergizes with the EGFR cascade, but its role in infectivity, inclusions, and EMT induction is unknown. We hypothesized that the EGFR and TGF-ß signaling pathways cooperate during chlamydial infection for optimal inclusion development and stable EMT induction. The results revealed that Chlamydia upregulated TGF-ß expression as early as 6 h postinfection of epithelial cells and stimulated both the EGFR and TGF-ß signaling pathways. Inhibition of either the EGFR or TGF-ßR1 signaling substantially reduced inclusion development; however, the combined inhibition of both EGFR and TGF-ßR1 signaling reduced inclusions by over 90% and prevented EMT induction. Importantly, EGFR inhibition suppressed TGF-ß expression, and an inhibitory thrombospondin-1 (Tsp1)-based peptide inhibited chlamydia-induced EMT, revealing a major source of active TGF-ß during infection. Finally, TGF-ßR signaling inhibition suppressed the expression of transforming acidic coiled-coil protein-3 (TACC3), which stabilizes EGFR signaling, suggesting reciprocal regulation between TGF-ß and EGFR signaling during chlamydial infection. Thus, RTK-mediated host invasion by chlamydia upregulated TGF-ß expression and signaling, which cooperated with other cellular signaling cascades and cytoskeletal remodeling to support optimal inclusion development and EMT induction. This finding may provide new targets for chlamydial disease biomarkers and prevention.


Asunto(s)
Infecciones por Chlamydia/fisiopatología , Chlamydia/crecimiento & desarrollo , Células Epiteliales/microbiología , Receptores ErbB/metabolismo , Interacciones Huésped-Patógeno , Transducción de Señal , Factor de Crecimiento Transformador beta/metabolismo , Animales , Línea Celular , Endocitosis , Transición Epitelial-Mesenquimal , Cuerpos de Inclusión/microbiología , Ratones , Modelos Biológicos
3.
Biochem Biophys Res Commun ; 508(2): 421-429, 2019 01 08.
Artículo en Inglés | MEDLINE | ID: mdl-30503337

RESUMEN

The unfolded protein response (UPR) contributes to chlamydial pathogenesis, as a source of lipids and ATP during replication, and for establishing the initial anti-apoptotic state of host cell that ensures successful inclusion development. The molecular mechanism(s) of UPR induction by Chlamydia is unknown. Chlamydia use type III secretion system (T3SS) effector proteins (e.g, the Translocated Actin-Recruiting Phosphoprotein (Tarp) to stimulate host cell's cytoskeletal reorganization that facilitates invasion and inclusion development. We investigated the hypothesis that T3SS effector-mediated assembly of myosin-II complex produces activated non-muscle myosin heavy chain II (NMMHC-II), which then binds the UPR master regulator (BiP) and/or transducers to induce UPR. Our results revealed the interaction of the chlamydial effector proteins (CT228 and Tarp) with components of the myosin II complex and UPR regulator and transducer during infection. These interactions caused the activation and binding of NMMHC-II to BiP and IRE1α leading to UPR induction. In addition, specific inhibitors of myosin light chain kinase, Tarp oligomerization and myosin ATPase significantly reduced UPR activation and Chlamydia replication. Thus, Chlamydia induce UPR through T3SS effector-mediated activation of NMMHC-II components of the myosin complex to facilitate infectivity. The finding provides greater insights into chlamydial pathogenesis with the potential to identify therapeutic targets and formulations.


Asunto(s)
Chlamydia muridarum/patogenicidad , Chlamydia trachomatis/patogenicidad , Interacciones Microbiota-Huesped/fisiología , Respuesta de Proteína Desplegada/fisiología , Animales , Infecciones por Chlamydia/etiología , Infecciones por Chlamydia/metabolismo , Infecciones por Chlamydia/microbiología , Chlamydia muridarum/metabolismo , Chlamydia trachomatis/metabolismo , Células HeLa , Humanos , Cuerpos de Inclusión/metabolismo , Ratones , Miosina Tipo II/metabolismo , Sistemas de Secreción Tipo III/metabolismo
4.
Infect Immun ; 86(1)2018 01.
Artículo en Inglés | MEDLINE | ID: mdl-29084894

RESUMEN

The reproductive system complications of genital chlamydial infection include fallopian tube fibrosis and tubal factor infertility. However, the molecular pathogenesis of these complications remains poorly understood. The induction of pathogenic epithelial-mesenchymal transition (EMT) through microRNA (miRNA) dysregulation was recently proposed as the pathogenic basis of chlamydial complications. Focusing on fibrogenesis, we investigated the hypothesis that chlamydia-induced fibrosis is caused by EMT-driven generation of myofibroblasts, the effector cells of fibrosis that produce excessive extracellular matrix (ECM) proteins. The results revealed that the targets of a major category of altered miRNAs during chlamydial infection are key components of the pathophysiological process of fibrogenesis; these target molecules include collagen types I, III, and IV, transforming growth factor ß (TGF-ß), TGF-ß receptor 1 (TGF-ßR1), connective tissue growth factor (CTGF), E-cadherin, SRY-box 7 (SOX7), and NFAT (nuclear factor of activated T cells) kinase dual-specificity tyrosine (Y) phosphorylation-regulated kinase 1a (Dyrk1a). Chlamydial induction of EMT resulted in the generation of α-smooth muscle actin (α-SMA)-positive myofibroblasts that produced ECM proteins, including collagen types I and III and fibronectin. Furthermore, the inhibition of EMT prevented the generation of myofibroblasts and production of ECM proteins during chlamydial infection. These findings may provide useful avenues for targeting EMT or specific components of the EMT pathways as a therapeutic intervention strategy to prevent chlamydia-related complications.


Asunto(s)
Infecciones por Chlamydia/complicaciones , Infecciones por Chlamydia/patología , Chlamydia/patogenicidad , Transición Epitelial-Mesenquimal/fisiología , Fibrosis/etiología , Fibrosis/patología , Actinas/metabolismo , Animales , Cadherinas/metabolismo , Línea Celular , Infecciones por Chlamydia/microbiología , Colágeno/metabolismo , Factor de Crecimiento del Tejido Conjuntivo/metabolismo , Proteínas de la Matriz Extracelular/metabolismo , Fibronectinas/metabolismo , Fibrosis/microbiología , Ratones , MicroARNs/metabolismo , Miofibroblastos/microbiología , Miofibroblastos/patología , Factores de Transcripción NFATC/metabolismo , Proteínas Serina-Treonina Quinasas/metabolismo , Proteínas Tirosina Quinasas/metabolismo , Receptor Tipo I de Factor de Crecimiento Transformador beta , Receptores de Factores de Crecimiento Transformadores beta/metabolismo , Factores de Transcripción SOXF/metabolismo , Factor de Crecimiento Transformador beta/metabolismo
5.
J Infect Dis ; 215(3): 456-465, 2017 02 01.
Artículo en Inglés | MEDLINE | ID: mdl-27932618

RESUMEN

Chlamydia is an obligate intracellular bacterium that relies on host cells for essential nutrients and adenosine triphosphate (ATP) for a productive infection. Although the unfolded protein response (UPR) plays a major role in certain microbial infectivity, its role in chlamydial pathogenesis is unknown. We hypothesized that Chlamydia induces UPR and exploits it to upregulate host cell uptake and metabolism of glucose, production of ATP, phospholipids, and other molecules required for its replicative development and host survival. Using a combination of biochemical and pathway inhibition assays, we showed that the 3 UPR pathway transducers-protein kinase RNA-activated (PKR)-like ER kinase (PERK), inositol-requiring enzyme-1α (IRE1α), and activating transcription factor-6α (ATF6α)-were activated during Chlamydia infection. The kinase activity of PERK and ribonuclease (RNase) of IRE1α mediated the upregulation of hexokinase II and production of ATP via substrate-level phosphorylation. In addition, the activation of PERK and IRE1α promoted autophagy formation and apoptosis resistance for host survival. Moreover, the activation of IRE1α resulted in the generation of spliced X-box binding protein 1 (sXBP1) and upregulation of lipid production. The vital role of UPR pathways in Chlamydia development and pathogenesis could lead to the identification of potential molecular targets for therapeutics against Chlamydia.


Asunto(s)
Infecciones por Chlamydia/microbiología , Chlamydia/patogenicidad , Respuesta de Proteína Desplegada , Factor de Transcripción Activador 6/metabolismo , Animales , Apoptosis , Supervivencia Celular , Infecciones por Chlamydia/metabolismo , Endorribonucleasas/metabolismo , Activación Enzimática , Femenino , Ratones , Ratones Endogámicos C57BL , Proteínas Serina-Treonina Quinasas/metabolismo , Transducción de Señal , eIF-2 Quinasa/metabolismo
6.
J Infect Dis ; 207(7): 1095-104, 2013 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-23303804

RESUMEN

Tubal factor infertility (TFI) represents 36% of female infertility and genital infection by Chlamydia trachomatis (C. trachomatis) is a major cause. Although TFI is associated with host inflammatory responses to bacterial components, the molecular pathogenesis of Chlamydia-induced infertility remains poorly understood. We investigated the hypothesis that activation of specific cysteine proteases, the caspases, during C. trachomatis genital infection causes the disruption of key fertility-promoting molecules required for embryo development and implantation. We analyzed the effect of caspase inhibition on infertility and the integrity of Dicer, a caspase-sensitive, fertility-promoting ribonuclease III enzyme, and key micro-RNAs in the reproductive system. Genital infection with the inflammation- and caspase-inducing, wild-type C. trachomatis serovar L2 led to infertility, but the noninflammation-inducing, plasmid-free strain did not. We confirmed that caspase-mediated apoptotic tissue destruction may contribute to chlamydial pathogenesis. Caspase-1 or -3 deficiency, or local administration of the pan caspase inhibitor, Z-VAD-FMK into normal mice protected against Chlamydia-induced infertility. Finally, the oviducts of infected infertile mice showed evidence of caspase-mediated cleavage inactivation of Dicer and alteration in critical miRNAs that regulate growth, differentiation, and development, including mir-21. These results provide new insight into the molecular pathogenesis of TFI with significant implications for new strategies for treatment and prevention of chlamydial complications.


Asunto(s)
Caspasa 1/metabolismo , Caspasa 3/metabolismo , Chlamydia trachomatis/patogenicidad , Infertilidad Femenina/microbiología , Infertilidad Femenina/prevención & control , Complicaciones Infecciosas del Embarazo/prevención & control , Animales , Apoptosis , Caspasa 1/genética , Caspasa 3/genética , Infecciones por Chlamydia/enzimología , Infecciones por Chlamydia/microbiología , Infecciones por Chlamydia/patología , Activación Enzimática , Femenino , Células HeLa , Humanos , Infertilidad Femenina/enzimología , Inflamación/microbiología , Inflamación/patología , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Embarazo , Complicaciones Infecciosas del Embarazo/enzimología , Complicaciones Infecciosas del Embarazo/microbiología , Complicaciones Infecciosas del Embarazo/patología
7.
J Clin Microbiol ; 51(4): 1298-300, 2013 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-23390274

RESUMEN

Trichomonas vaginalis infections are usually asymptomatic or can result in nonspecific clinical symptoms, which makes laboratory-based detection of this protozoan parasite essential for diagnosis and treatment. We report the development of a battery of highly sensitive and specific PCR assays for detection of T. vaginalis in urine, a noninvasive specimen, and development of a protocol for differentiating among Trichomonas species that commonly infect humans.


Asunto(s)
Técnicas de Laboratorio Clínico/métodos , Técnicas de Diagnóstico Molecular/métodos , Parasitología/métodos , Reacción en Cadena de la Polimerasa/métodos , Tricomoniasis/diagnóstico , Trichomonas vaginalis/aislamiento & purificación , Orina/parasitología , Adolescente , Niño , Preescolar , Femenino , Humanos , Lactante , Sensibilidad y Especificidad , Trichomonas vaginalis/clasificación , Trichomonas vaginalis/genética
8.
J Immunol ; 181(6): 4037-42, 2008 Sep 15.
Artículo en Inglés | MEDLINE | ID: mdl-18768859

RESUMEN

We investigated the hypothesis that the enhanced Ag-presenting function of IL-10-deficient dendritic cells (DCs) is related to specific immunoregulatory cytoskeletal molecules expressed when exposed to Ags. We analyzed the role of a prominent cytoskeletal protein, LEK1, in the immunoregulation of DC functions; specifically cytokine secretion, costimulatory molecule expression, and T cell activation against Chlamydia. Targeted knockdown of LEK1 expression using specific antisense oligonucleotides resulted in the rapid maturation of Chlamydia-exposed DCs as measured by FACS analysis of key activation markers (i.e., CD14, CD40, CD54, CD80, CD86, CD197, CD205, and MHC class II). The secretion of mostly Th1 cytokines and chemokines (IL-1a, IL-9, IL-12, MIP-1a, and GM-CSF but not IL-4 and IL-10) was also enhanced by blocking of LEK1. The function of LEK1 in DC regulation involves cytoskeletal changes, since the dynamics of expression of vimentin and actin, key proteins of the cellular cytoskeleton, were altered after exposure of LEK1 knockdown DCs to Chlamydia. Furthermore, targeted inhibition of LEK1 expression resulted in the enhancement of the immunostimulatory capacity of DCs for T cell activation against Chlamydia. Thus, LEK1 knockdown DCs activated immune T cells at least 10-fold over untreated DCs. These results suggest that the effect of IL-10 deficiency is mediated through LEK1-related events that lead to rapid maturation of DCs and acquisition of the capacity to activate an elevated T cell response. Targeted modulation of LEK1 expression provides a novel strategy for augmenting the immunostimulatory function of DCs for inducing an effective immunity against pathogens.


Asunto(s)
Chlamydia trachomatis/inmunología , Proteínas Cromosómicas no Histona/fisiología , Células Dendríticas/inmunología , Células Dendríticas/microbiología , Subgrupos de Linfocitos T/inmunología , Subgrupos de Linfocitos T/microbiología , Animales , Biomarcadores/análisis , Diferenciación Celular/inmunología , Células Cultivadas , Proteínas Cromosómicas no Histona/antagonistas & inhibidores , Proteínas Cromosómicas no Histona/biosíntesis , Proteínas Cromosómicas no Histona/deficiencia , Citocinas/biosíntesis , Citocinas/genética , Citocinas/metabolismo , Proteínas del Citoesqueleto/antagonistas & inhibidores , Proteínas del Citoesqueleto/biosíntesis , Proteínas del Citoesqueleto/deficiencia , Proteínas del Citoesqueleto/fisiología , Células Dendríticas/citología , Células Dendríticas/metabolismo , Femenino , Interleucina-10/antagonistas & inhibidores , Interleucina-10/biosíntesis , Interleucina-10/genética , Activación de Linfocitos/genética , Activación de Linfocitos/inmunología , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Proteínas de Microfilamentos , Oligonucleótidos Antisentido/farmacología , Subgrupos de Linfocitos T/metabolismo
9.
Ophthalmic Epidemiol ; 26(1): 1-6, 2019 02.
Artículo en Inglés | MEDLINE | ID: mdl-30543311

RESUMEN

PURPOSE: Trachoma, caused by repeated ocular infection with Chlamydia trachomatis, is the leading infectious cause of blindness worldwide and is targeted for elimination as a public health problem. We sought to determine whether a one-time azithromycin mass treatment would reduce trachomatous inflammation-follicular (TF) levels below the elimination threshold of 5% in communities with disease prevalence between 5 and 9.9%. METHODS: The study was conducted in 96 sub-village units (balozis) in the Kongwa district of Tanzania which were predicted from prior prevalence surveys to have TF between 5 and 9.9%. Balozis were randomly assigned to the intervention and control arms. The intervention arm received a single mass drug administration of azithromycin. At baseline and 12-month follow-up, ocular exams for trachoma, ocular swabs for detection of chlamydial DNA, and finger prick blood for analysis of anti-chlamydial antibody were taken. RESULTS: Comparison of baseline and 12-month follow-up showed no significant difference in the overall TF1-9 prevalence by balozi between control and treatment arms. In the treatment arm there was a significant reduction of ocular infection 12 months after treatment (p = 0.004) but no change in the control arm. No change in Pgp3-specific antibody responses were observed after treatment in the control or treatment arms. Anti-CT694 responses increased in both study arms (p = 0.009 for control arm and p = 0.04 for treatment arm). CONCLUSION: These data suggest that a single round of MDA may not be sufficient to decrease TF levels below 5% when TF1-9 is between 5 and 9.9% at baseline.


Asunto(s)
Azitromicina/administración & dosificación , Chlamydia trachomatis/genética , ADN Bacteriano/análisis , Infecciones Bacterianas del Ojo/tratamiento farmacológico , Tracoma/tratamiento farmacológico , Antibacterianos/administración & dosificación , Niño , Preescolar , Relación Dosis-Respuesta a Droga , Infecciones Bacterianas del Ojo/epidemiología , Infecciones Bacterianas del Ojo/microbiología , Femenino , Estudios de Seguimiento , Humanos , Lactante , Masculino , Prevalencia , Tanzanía/epidemiología , Factores de Tiempo , Tracoma/epidemiología , Tracoma/microbiología , Resultado del Tratamiento
10.
J Clin Microbiol ; 46(1): 355-6, 2008 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-18032619

RESUMEN

We genotyped Chlamydia trachomatis strains from 45 women or men living in either a rural indigenous community or in urban heterosexual communities. We found six different C. trachomatis serovars: E (n = 22; 48.9%), F (n = 10; 22.2%), J/Ja (n = 5; 11.1%), D/Da (n = 4; 8.9%), G (n = 3; 6.7%), and K (n = 1; 2.2%). The distribution of C. trachomatis serovars among members of the indigenous rural and the urban Australian communities appears similar to that in other Western countries.


Asunto(s)
Infecciones por Chlamydia/microbiología , Chlamydia trachomatis/clasificación , Chlamydia trachomatis/aislamiento & purificación , Adulto , Australia/epidemiología , Proteínas de la Membrana Bacteriana Externa/genética , Técnicas de Tipificación Bacteriana , Infecciones por Chlamydia/epidemiología , Femenino , Genotipo , Humanos , Masculino , Epidemiología Molecular , Reacción en Cadena de la Polimerasa/métodos , Población Rural , Análisis de Secuencia de ADN , Población Urbana , Orina/microbiología
11.
PLoS One ; 10(12): e0145198, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26681200

RESUMEN

Chlamydia trachomatis genital infection in women causes serious adverse reproductive complications, and is a strong co-factor for human papilloma virus (HPV)-associated cervical epithelial carcinoma. We tested the hypothesis that Chlamydia induces epithelial-mesenchyme transition (EMT) involving T cell-derived TNF-alpha signaling, caspase activation, cleavage inactivation of dicer and dysregulation of micro-RNA (miRNA) in the reproductive epithelium; the pathologic process of EMT causes fibrosis and fertility-related epithelial dysfunction, and also provides the co-factor function for HPV-related cervical epithelial carcinoma. Using a combination of microarrays, immunohistochemistry and proteomics, we showed that chlamydia altered the expression of crucial miRNAs that control EMT, fibrosis and tumorigenesis; specifically, miR-15a, miR-29b, miR-382 and MiR-429 that maintain epithelial integrity were down-regulated, while miR-9, mi-R-19a, miR-22 and miR-205 that promote EMT, fibrosis and tumorigenesis were up-regulated. Chlamydia induced EMT in vitro and in vivo, marked by the suppression of normal epithelial cell markers especially E-cadherin but up-regulation of mesenchymal markers of pathological EMT, including T-cadherin, MMP9, and fibronectin. Also, Chlamydia upregulated pro-EMT regulators, including the zinc finger E-box binding homeobox protein, ZEB1, Snail1/2, and thrombospondin1 (Thbs1), but down-regulated anti-EMT and fertility promoting proteins (i.e., the major gap junction protein connexin 43 (Cx43), Mets1, Add1Scarb1 and MARCKSL1). T cell-derived TNF-alpha signaling was required for chlamydial-induced infertility and caspase inhibitors prevented both infertility and EMT. Thus, chlamydial-induced T cell-derived TNF-alpha activated caspases that inactivated dicer, causing alteration in the expression of reproductive epithelial miRNAs and induction of EMT. EMT causes epithelial malfunction, fibrosis, infertility, and the enhancement of tumorigenesis of HPV oncogene-transformed epithelial cells. These findings provide a novel understanding of the molecular pathogenesis of chlamydia-associated diseases, which may guide a rational prevention strategy.


Asunto(s)
Infecciones por Chlamydia/metabolismo , Transición Epitelial-Mesenquimal , Animales , Cadherinas/genética , Cadherinas/metabolismo , Caspasas/metabolismo , Infecciones por Chlamydia/patología , Femenino , Fibronectinas/genética , Fibronectinas/metabolismo , Células HeLa , Proteínas de Homeodominio/genética , Proteínas de Homeodominio/metabolismo , Humanos , Factores de Transcripción de Tipo Kruppel/genética , Factores de Transcripción de Tipo Kruppel/metabolismo , Metaloproteinasa 9 de la Matriz/genética , Metaloproteinasa 9 de la Matriz/metabolismo , Ratones , Ratones Endogámicos C57BL , MicroARNs/genética , Factores de Transcripción de la Familia Snail , Trombospondina 1/genética , Trombospondina 1/metabolismo , Factores de Transcripción/genética , Factores de Transcripción/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Homeobox 1 de Unión a la E-Box con Dedos de Zinc
12.
J Med Microbiol ; 60(Pt 4): 472-476, 2011 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-21183598

RESUMEN

Despite a high prevalence of sexually transmitted Chlamydia trachomatis infections in Brazil and other countries in South America, very little is known about the distribution of C. trachomatis genovars. In this study, we genotyped C. trachomatis strains from urine or endocervical specimens collected from 163 C. trachomatis-positive female and male youths, and female adults, residing in two different regions of Brazil, the city of Goiânia located in the central part of Brazil, and the city of Vitória in the south-east region. C. trachomatis strains were genotyped by amplifying and sequencing the ompA gene encoding the chlamydial major outer-membrane protein, which is genovar specific. We found nine different C. trachomatis genovars: E (39.3%), F (16.6%), D (15.9%), I (8.6%), J (7.4%), G (4.9%), K (3.1%), H (2.4%) and B (1.8%). The distribution of the C. trachomatis genovars in the two regions of Brazil was similar, and there was no statistically significant association of serovars with age, gender, number of sexual partners or clinical symptoms. The overall distribution of C. trachomatis genovars in Brazil appears similar to that found in other regions of the world, where E, D and F are the most common. This supports the notion that, during the last few decades, the overall distribution of C. trachomatis genovars throughout the world has been relatively stable.


Asunto(s)
Infecciones por Chlamydia/epidemiología , Infecciones por Chlamydia/microbiología , Chlamydia trachomatis/clasificación , Chlamydia trachomatis/aislamiento & purificación , Adolescente , Adulto , Proteínas de la Membrana Bacteriana Externa/genética , Técnicas de Tipificación Bacteriana , Brasil/epidemiología , Cuello del Útero/microbiología , Chlamydia trachomatis/genética , Femenino , Genotipo , Humanos , Masculino , Tipificación Molecular , Prevalencia , Orina/microbiología , Adulto Joven
13.
J Infect Dis ; 200(6): 926-34, 2009 Sep 15.
Artículo en Inglés | MEDLINE | ID: mdl-19656067

RESUMEN

Vaccines are needed to prevent the oculogenital diseases of Chlamydia trachomatis. Infected hosts develop immunity, although temporary, and experimental vaccines have yielded significant protective immunity in animal models, fueling the impetus for a vaccine. Because infections cause sequelae, the functional relationship between infection- and vaccine-induced immunity is unclear. We hypothesized that infection- and vaccine-induced immunity are functionally distinct, particularly in the ability to prevent sequelae. Chlamydia-immune mice, with immunity generated by either a previous infection or vaccination, exhibited a significant degree of protective immunity, marked by a lower-intensity, abbreviated course of infection. However, vaccinated mice were protected from infertility, whereas preinfected mice were not. Thus, infection-induced immunity does not prevent the pathologic process leading to infertility. Furthermore, T cell subsets, especially CD8 T cells, play a major role in Chlamydia-induced infertility. The results have important implications for the immunopathogenesis of chlamydial disease and new vaccine strategies.


Asunto(s)
Infecciones por Chlamydia/inmunología , Chlamydia trachomatis , Subgrupos de Linfocitos T/fisiología , Animales , Antígenos CD4/genética , Antígenos CD8/genética , Línea Celular , Femenino , Fertilidad , Humanos , Interleucina-10/genética , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados
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