RESUMEN
The immune system plays an indispensable role in the process of tissue regeneration following damage as well as during homeostasis. Inflammation and immune cell recruitment are signs of early onset injury. At the wound site, immune cells not only help to clear debris but also secrete numerous signalling molecules that induce appropriate cell proliferation and differentiation programmes essential for successful regeneration. However, the immune system does not always perform a complementary role in regeneration and several reports have suggested that increased inflammation can inhibit the regeneration process. Successful regeneration requires a balanced immune cell response, with the recruitment of accurately polarised immune cells in an appropriate quantity. The regulatory interactions of the immune system with regeneration are not unidirectional. Stem cells, as key players in regeneration, can also modulate the immune system in several ways to facilitate regeneration. In this review, we will focus on recent research demonstrating the key role of immune system in the regeneration process as well as the immunomodulatory effects of stem cells. Finally, we propose that research investigating the interplay between the immune system and stem cells within highly regenerating animals can benefit the identification of the key interactions and molecules required for successful regeneration.
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Células Madre Adultas/inmunología , Sistema Inmunológico/inmunología , Regeneración/fisiología , Animales , Humanos , Regeneración/inmunologíaRESUMEN
Bartonella quintana is a facultative intracellular bacterium responsible for relapsing fever, an example of non-sterilizing immunity. The cellular sanctuary of B. quintana in-between febrile relapses remains unknown but repeated detection of B. quintana in dental pulp specimens suggested long-term half-life dental pulp stem cells (DPSCs) as candidates. As the capacity of DPSCs to internalize microscopic particles was unknown, we confirmed that DPSCs internalized B. quintana bacteria: Gimenez staining and fluorescence microscopy localized B. quintana bacteria inside DPSCs and this internalization did not affect the cellular multiplication of DPSCs during a one-month follow-up despite the increase in the bacterial load. B. quintana-infected DPSCs did not produce Tumor Necrosis Factor-α whereas an important production of Monocytes Chemoattractant Protein-1 was observed. These unprecedented observations suggest the possibility that DPSCs are shelters for the long-term persistence of B. quintana in the host, warranting further experimental and clinical investigations.
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Bartonella quintana , Fiebre de las Trincheras , Pulpa Dental , Humanos , Recurrencia , Células MadreRESUMEN
Coxiella burnetii is the agent of Q fever, or "query fever," a zoonosis first described in Australia in 1937. Since this first description, knowledge about this pathogen and its associated infections has increased dramatically. We review here all the progress made over the last 20 years on this topic. C. burnetii is classically a strict intracellular, Gram-negative bacterium. However, a major step in the characterization of this pathogen was achieved by the establishment of its axenic culture. C. burnetii infects a wide range of animals, from arthropods to humans. The genetic determinants of virulence are now better known, thanks to the achievement of determining the genome sequences of several strains of this species and comparative genomic analyses. Q fever can be found worldwide, but the epidemiological features of this disease vary according to the geographic area considered, including situations where it is endemic or hyperendemic, and the occurrence of large epidemic outbreaks. In recent years, a major breakthrough in the understanding of the natural history of human infection with C. burnetii was the breaking of the old dichotomy between "acute" and "chronic" Q fever. The clinical presentation of C. burnetii infection depends on both the virulence of the infecting C. burnetii strain and specific risks factors in the infected patient. Moreover, no persistent infection can exist without a focus of infection. This paradigm change should allow better diagnosis and management of primary infection and long-term complications in patients with C. burnetii infection.
Asunto(s)
Coxiella burnetii/patogenicidad , Fiebre Q/diagnóstico , Fiebre Q/epidemiología , Animales , Genoma Bacteriano , Humanos , Fiebre Q/veterinaria , Virulencia , Zoonosis/epidemiologíaRESUMEN
Mycobacterium ulcerans, a decaying Mycobacterium marinum derivative is responsible for Buruli ulcer, a notifiable non-contagious disabling infection highly prevalent in some West African countries. Aquatic environments are suspected to host M. ulcerans, however, the exact reservoirs remain unknown. While M. marinum was found to resist amoebal microbicidal activities, this remains unknown for M. ulcerans. In this study M. ulcerans was co-cultured with the moderately halophile Acanthamoeba griffini at 30 °C to probe this tropical amoeba as a potential reservoir for M. ulcerans. In triplicate experiments, we observed engulfment of M. ulcerans by A. griffini trophozoites, followed by an unexpected significant difference of 98.4% (day 1), 99.5% (day 2), 99.5% (day 3) and 99.9% (day 7) between the number of intra-amoebal mycobacteria detected by PCR and the number of viable intra-amoebal mycobacteria measured by 10-week culture. Further encystment revealed only one Mycobacterium organism for 150 A. griffini cysts observed by electron microscopy and the culture of excysted amoebae remained sterile. In conclusion, these data install M. ulcerans as susceptible to A. griffini microbicidal activities rendering this amoeba species an unlikely host of M. ulcerans in natural environments.
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Acanthamoeba/microbiología , Acanthamoeba/fisiología , Técnicas de Cocultivo/métodos , Mycobacterium ulcerans/fisiología , Amoeba/microbiología , Úlcera de Buruli/microbiología , ADN Bacteriano , Reservorios de Enfermedades/microbiología , Microbiología Ambiental , Viabilidad Microbiana , Mycobacterium ulcerans/crecimiento & desarrolloRESUMEN
A small gram-negative bacterium, Coxiella burnetii (C. burnetii), is responsible for a zoonosis called Q fever. C. burnetii is an intracellular bacterium that can survive inside microbicidal cells like monocytes and macrophages by hijacking several functions of the immune system. Among several virulence factors, the lipopolysaccharide (LPS) of C. burnetii is one of the major factors involved in this immune hijacking because of its atypical composition and structure. Thus, the aim of this mini-review is to summarize the repressive effects of C. burnetii LPS on the antibacterial immunity of cells.
Asunto(s)
Coxiella burnetii/inmunología , Coxiella burnetii/metabolismo , Lipopolisacáridos/inmunología , Fiebre Q/inmunología , Fiebre Q/microbiología , Animales , Antígenos Bacterianos/química , Antígenos Bacterianos/inmunología , Antígenos Bacterianos/metabolismo , Interacciones Huésped-Patógeno/inmunología , Humanos , Lipopolisacáridos/química , Lipopolisacáridos/metabolismo , Fagocitos/inmunología , Fagocitos/microbiología , Fagocitosis/inmunología , Fagosomas/inmunología , Fagosomas/metabolismoRESUMEN
BACKGROUND: Necrotizing enterocolitis (NEC) is the most common and serious gastrointestinal disorder among preterm neonates. We aimed to assess a specific gut microbiota profile associated with NEC. METHODS: Stool samples and clinical data were collected from 4 geographically independent neonatal intensive care units, over a 48-month period. Thirty stool samples from preterm neonates with NEC (n = 15) and controls (n = 15) were analyzed by 16S ribosomal RNA pyrosequencing and culture-based methods. The results led us to develop a specific quantitative polymerase chain reaction (qPCR) assay for Clostridium butyricum, and we tested stool samples from preterm neonates with NEC (n = 93) and controls (n = 270). We sequenced the whole genome of 16 C. butyricum strains, analyzed their phylogenetic relatedness, tested their culture supernatants for cytotoxic activity, and searched for secreted toxins. RESULTS: Clostridium butyricum was specifically associated with NEC using molecular and culture-based methods (15/15 vs 2/15; P < .0001) or qPCR (odds ratio, 45.4 [95% confidence interval, 26.2-78.6]; P < .0001). Culture supernatants of C. butyricum strains from preterm neonates with NEC (n = 14) exhibited significant cytotoxic activity (P = .008), and we identified in all a homologue of the ß-hemolysin toxin gene shared by Brachyspira hyodysenteriae, the etiologic agent of swine dysentery. The corresponding protein was secreted by a NEC-associated C. butyricum strain. CONCLUSIONS: NEC was associated with C. butyricum strains and dysbiosis with an oxidized, acid, and poorly diversified gut microbiota. Our findings highlight the plausible toxigenic mechanism involved in the pathogenesis of NEC.
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Clostridium butyricum/genética , Disbiosis/complicaciones , Disbiosis/microbiología , Enterocolitis Necrotizante/complicaciones , Enterocolitis Necrotizante/microbiología , Supervivencia Celular , Estudios de Cohortes , Disbiosis/epidemiología , Enterocolitis Necrotizante/epidemiología , Heces/microbiología , Francia/epidemiología , Humanos , Recién Nacido , Recien Nacido Prematuro , Células JurkatRESUMEN
Pregnancy is dependent on maternal-fetal tolerance that may be compromised because of infections or inflammation of the placenta. In this study, we examined whether the context of placental immune tolerance affected the functions of resident macrophages and if their functions were altered during chorioamnionitis, an infectious pathology of the placenta. Macrophages from at-term placentas expressed CD14, exhibited macrophage microbicidal functions, but were less inflammatory than monocyte-derived macrophages. Moreover, placental macrophages spontaneously matured into multinucleated giant cells (MGCs), a property not exhibited by monocyte-derived macrophages, and we detected MGCs of myeloid origin in placental tissue. Compared with placental macrophages, MGCs exhibited a specific phenotype and gene expression signature, consisting of increased cytoskeleton-associated gene expression along with depressed expression of inflammatory response genes. Furthermore, placental macrophages from patients with chorioamnionitis were unable to form MGCs, but this defect was partially corrected by incubating these placental macrophages with control trophoblast supernatants. MGCs formation likely serves to regulate their inflammatory and cytocidal activities in a context that imposes semiallograft acceptance and defense against pathogens.
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Corioamnionitis/inmunología , Macrófagos/inmunología , Placenta/inmunología , Complicaciones Infecciosas del Embarazo/inmunología , Infecciones Estreptocócicas/inmunología , Streptococcus/inmunología , Adulto , Animales , Diferenciación Celular/efectos de los fármacos , Células Cultivadas , Corioamnionitis/etiología , Medios de Cultivo Condicionados/farmacología , Citoesqueleto/genética , Femenino , Regulación de la Expresión Génica/inmunología , Células Gigantes/inmunología , Humanos , Receptores de Lipopolisacáridos/metabolismo , Macrófagos/efectos de los fármacos , Placenta/patología , Embarazo , Infecciones Estreptocócicas/complicaciones , Tolerancia al Trasplante , Adulto JovenRESUMEN
Expressing mspA porin gene from Mycobacterium smegmatis in Mycobacterium tuberculosis attenuated this pathogen. Intracellular growth of the transformants into free-living amoeba and murine and human macrophages decreased. Furthermore, transformants decreased the microbicidal program of human monocyte-derived macrophages. BALB/c mice inoculated with transformants exhibited higher weights, lower histological lesions and lower M. tuberculosis inoculum in the liver, spleen and lungs than control mice challenged with wild-type M. tuberculosis. Preliminary evaluation indicated that mice inoculated with this transformant showed higher weights and lower numbers of lung nodules and tissular mycobacteria than control mice when challenged with wild-type M. tuberculosis. Similar to the paradoxical "unbirthday" gift coined by Lewis Carroll in Alice's Adventures in Wonderland, adding mspA gene reduced the virulence of M. tuberculosis and yielded a protective effect. Lost of non-virulence genes is a mechanism for virulence in mycobacteria. Engineering non-virulence genes in M. tuberculosis may yield strains with decreased virulence and increased immunogenicity.
Asunto(s)
Mycobacterium smegmatis/genética , Mycobacterium tuberculosis/crecimiento & desarrollo , Mycobacterium tuberculosis/genética , Porinas/genética , Transformación Bacteriana , Amoeba/microbiología , Animales , Carga Bacteriana , Peso Corporal , Modelos Animales de Enfermedad , Histocitoquímica , Humanos , Pulmón/microbiología , Pulmón/patología , Macrófagos/microbiología , Ratones Endogámicos BALB C , Tuberculosis/microbiología , Tuberculosis/patología , VirulenciaRESUMEN
BACKGROUND: Q fever is caused by Coxiella burnetii, a bacterium that persists in M2-polarized macrophages. We wondered whether the concept of M1/M2 polarization is applicable to Q fever patients. METHODS: Monocytes from healthy controls were cultured with IFN-γ and IL-4, agonists of M1 and M2 macrophages, respectively, and their gene expression was assessed using whole-genome microarrays. Selected biomarkers were assessed in blood from Q fever patients by real-time reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Monocytes exhibited early (6-hour) patterns of activation specific to IFN-γ or IL-4 and a late (18-hour) pattern of common activation. Because these responses were not reducible to M1/M2 polarization, we selected biomarkers and tested their relevance in Q fever patients. The early genes NLRC5, RTP4, and RHOH, which were modulated in response to IFN-γ, were up-regulated in patients with acute Q fever, and the expression levels of the late genes ALOX15, CLECSF1, CCL13, and CCL23 were specifically increased in patients with Q fever endocarditis. The RHOH and ALOX15 genes were associated with the activity of acute Q fever and Q fever endocarditis, respectively. CONCLUSIONS: Our results show that the kinetic model of monocyte activation enables a dynamic approach for the evaluation of Q fever patients.
Asunto(s)
Activación de Macrófagos , Monocitos/inmunología , Fiebre Q/inmunología , Enfermedad Aguda , Adulto , Anciano , Biomarcadores/sangre , Estudios de Casos y Controles , Coxiella burnetii , Endocarditis Bacteriana/inmunología , Regulación de la Expresión Génica , Humanos , Interferón gamma/inmunología , Interleucina-4/inmunología , Macrófagos/inmunología , Análisis por Micromatrices , Persona de Mediana Edad , Transcripción Genética , Regulación hacia ArribaRESUMEN
E3 ubiquitin ligases give specificity to the ubiquitylation process by selectively binding substrates. Recently, their function has emerged as a crucial modulator of T-cell tolerance and immunity. However, substrates, partners and mechanism of action for most E3 ligases remain largely unknown. In this study, we identified the human T-cell co-receptor CD8 α-chain as binding partner of the ligand of Numb proteins X1 (LNX1p80 isoform) and X2 (LNX2). Both LNX mRNAs were found expressed in T cells purified from human blood, and both proteins interacted with CD8α in human HPB-ALL T cells. By using an in vitro assay and a heterologous expression system we showed that the interaction is mediated by the PDZ (PSD95-DlgA-ZO-1) domains of LNX proteins and the cytosolic C-terminal valine motif of CD8α. Moreover, CD8α redistributed LNX1 or LNX2 from the cytosol to the plasma membrane, whereas, remarkably, LNX1 or LNX2 promoted CD8α ubiquitylation, downregulation from the plasma membrane, transport to the lysosomes, and degradation. Our findings highlight the function of LNX proteins as E3 ligases and suggest a mechanism of regulation for CD8α localization at the plasma membrane by ubiquitylation and endocytosis.
Asunto(s)
Antígenos CD8/metabolismo , Proteínas Portadoras/metabolismo , Endocitosis , Ubiquitina-Proteína Ligasas/metabolismo , Antígenos CD8/química , Antígenos CD8/genética , Proteínas Portadoras/química , Proteínas Portadoras/genética , Línea Celular , Membrana Celular/química , Membrana Celular/genética , Membrana Celular/metabolismo , Humanos , Dominios PDZ , Unión Proteica , Ubiquitina-Proteína Ligasas/química , Ubiquitina-Proteína Ligasas/genética , UbiquitinaciónRESUMEN
Scrub typhus is a life-threatening disease caused by Orientia tsutsugamushi, a bacterium that primarily infects endothelial cells both in vitro and in vivo. Evidence suggests that the interaction of O. tsutsugamushi with myeloid cells may play a pivotal role in O. tsutsugamushi infection. We demonstrated that O. tsutsugamushi replicated within human monocyte-derived macrophages. Bacteria stimulated the expression of a large number of genes, including type I interferon genes, interferon-stimulated genes, inflammation-associated genes and apoptosis-related genes, and the release of inflammatory cytokines such as Tumor Necrosis Factor and interleukin-1ß. In addition, O. tsutsugamushi induced an M1-type genetic program in macrophages. O. tsutsugamushi viability was required for the type I interferon response and, to a lesser degree, for the inflammatory response. As interferon-γ is known to elicit M1 polarization, we assessed the effect of interferon-γ on the fate of O. tsutsugamushi in macrophages. Exogenous interferon-γ partially inhibited O. tsutsugamushi replication within macrophages. Our results suggest that the inflammatory response induced by O. tsutsugamushi may account for the local and systemic inflammation observed in scrub typhus.
Asunto(s)
Macrófagos/inmunología , Orientia tsutsugamushi/inmunología , Tifus por Ácaros/inmunología , Células Cultivadas , Humanos , Interferón Tipo I/genética , Interferón Tipo I/inmunología , Interferón gamma/genética , Interferón gamma/inmunología , Interleucina-1beta/genética , Interleucina-1beta/inmunología , Macrófagos/microbiología , Orientia tsutsugamushi/fisiología , Tifus por Ácaros/genética , Tifus por Ácaros/microbiología , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/inmunologíaRESUMEN
BACKGROUND: The outcome of Q fever, an infectious disease caused by Coxiella burnetii, is associated with granuloma formation. Granulomas are present in patients with resolutive Q fever but are lacking in patients with chronic Q fever. METHODS: Study of granuloma formation requires invasive approaches. Here, we took advantage of a recently described method that enables in vitro generation of human granulomas specific for C. burnetii. RESULTS: Circulating mononuclear cells progressively accumulated around beads coated with C. burnetii extracts, and complete granulomas were generated in 8 days. Granuloma cells consisted of macrophages, lymphocytes, and, to a lesser extent, epithelioid cells and multinucleated giant cells. Early events that govern granuloma formation were studied using live-imaging microscopy. Monocytes migrated toward C. burnetii-coated beads independently of the presence of T lymphocytes and then recruited T lymphocytes. About 90% of patients with chronic Q fever failed to form granulomas. This deficiency was associated with defective migration of monocytes toward coated beads. CONCLUSIONS: Monocytes were involved in the early stages of granuloma formation and recruited T lymphocytes to complete granuloma formation. This article describes a direct relationship between defective granuloma formation and defective migration of monocytes.
Asunto(s)
Coxiella burnetii/inmunología , Coxiella burnetii/patogenicidad , Granuloma/inmunología , Monocitos/inmunología , Fiebre Q/inmunología , Anciano , Anciano de 80 o más Años , Células Cultivadas , Femenino , Humanos , Masculino , Persona de Mediana Edad , Linfocitos T/inmunologíaRESUMEN
Macrophages are the first line of defense against pathogens. Upon infection macrophages usually produce high levels of proinflammatory mediators. However, macrophages can undergo an alternate polarization leading to a permissive state. In assessing global macrophage responses to the bacterial agent of Whipple's disease, Tropheryma whipplei, we found that T. whipplei induced M2 macrophage polarization which was compatible with bacterial replication. Surprisingly, this M2 polarization of infected macrophages was associated with apoptosis induction and a functional type I interferon (IFN) response, through IRF3 activation and STAT1 phosphorylation. Using macrophages from mice deficient for the type I IFN receptor, we found that this type I IFN response was required for T. whipplei-induced macrophage apoptosis in a JNK-dependent manner and was associated with the intracellular replication of T. whipplei independently of JNK. This study underscores the role of macrophage polarization in host responses and highlights the detrimental role of type I IFN during T. whipplei infection.
Asunto(s)
Apoptosis/inmunología , Perfilación de la Expresión Génica , Interferón Tipo I/inmunología , Macrófagos/microbiología , Transducción de Señal/inmunología , Enfermedad de Whipple/inmunología , Animales , Western Blotting , Ensayo de Inmunoadsorción Enzimática , Técnica del Anticuerpo Fluorescente , Expresión Génica , Etiquetado Corte-Fin in Situ , Factor 3 Regulador del Interferón/inmunología , Factor 3 Regulador del Interferón/metabolismo , Interferón Tipo I/metabolismo , Activación de Macrófagos/inmunología , Macrófagos/inmunología , Macrófagos/metabolismo , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Análisis de Secuencia por Matrices de Oligonucleótidos , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Factor de Transcripción STAT1/inmunología , Factor de Transcripción STAT1/metabolismo , Transfección , Tropheryma/inmunología , Tropheryma/metabolismo , Enfermedad de Whipple/genética , Enfermedad de Whipple/metabolismoRESUMEN
Coxiella burnetii is a bacterial intracellular parasite of eucaryotic cells that replicates within a membrane-bound compartment, or "parasitophorous vacuole" (PV). With the exception of human macrophages/monocytes, the consensus model of PV trafficking in host cells invokes endolysosomal maturation culminating in lysosome fusion. C. burnetii resists the degradative functions of the vacuole while at the same time exploiting the acidic pH for metabolic activation. While at first glance the mature PV resembles a large phagolysosome, an increasing body of evidence indicates the vacuole is in fact a specialized compartment that is actively modified by the pathogen. Adding to the complexity of PV biogenesis is new data showing vacuole engagement with autophagic and early secretory pathways. In this chapter, we review current knowledge of PV nature and development, and discuss disparate data related to the ultimate maturation state of PV harboring virulent or avirulent C. burnetii lipopolysaccharide phase variants in human mononuclear phagocytes.
Asunto(s)
Coxiella burnetii/metabolismo , Sistema Mononuclear Fagocítico/metabolismo , Vacuolas/metabolismo , Animales , Humanos , Lisosomas/metabolismo , Lisosomas/microbiología , Sistema Mononuclear Fagocítico/microbiología , Fagosomas/metabolismo , Fagosomas/microbiología , Vacuolas/microbiologíaRESUMEN
Rickettsia species are endosymbionts hosted by arthropods and are known to cause mild to fatal diseases in humans. Here, we analyse the evolution and diversity of 34 Rickettsia species using a pangenomic meta-analysis (80 genomes/41 plasmids). Phylogenomic trees showed that Rickettsia spp. diverged into two Spotted Fever groups, a Typhus group, a Canadensis group and a Bellii group, and may have inherited their plasmids from an ancestral plasmid that persisted in some strains or may have been lost by others. The results suggested that the ancestors of Rickettsia spp. might have infected Acari and/or Insecta and probably diverged by persisting inside and/or switching hosts. Pangenomic analysis revealed that the Rickettsia genus evolved through a strong interplay between genome degradation/reduction and/or expansion leading to possible distinct adaptive trajectories. The genus mainly shared evolutionary relationships with α-proteobacteria, and also with γ/ß/δ-proteobacteria, cytophagia, actinobacteria, cyanobacteria, chlamydiia and viruses, suggesting lateral exchanges of several critical genes. These evolutionary processes have probably been orchestrated by an abundance of mobile genetic elements, especially in the Spotted Fever and Bellii groups. In this study, we provided a global evolutionary genomic view of the intracellular Rickettsia that may help our understanding of their diversity, adaptation and fitness.
Asunto(s)
Artrópodos , Gammaproteobacteria , Rickettsia , Rickettsiosis Exantemáticas , Animales , Artrópodos/genética , Evolución Molecular , Genómica , Filogenia , Rickettsia/genéticaRESUMEN
Marseille-P9602T is a Chryseobacterium-like strain that we isolated from planarian Schmidtea mediterranea and characterized by taxono-genomic approach. We found that Marseille-P9602T strain exhibits a 16S rRNA gene sequence similarity of 98.76% with Chryseobacterium scophthalmum LMG 13028T strain, the closest phylogenetic neighbor. Marseille-P9602T strain was observed to be a yellowish-pigmented, Gram-negative, rod-shaped bacterium, growing in aerobic conditions and belonging to the Flavobacteriaceae family. The major fatty acids detected are 13-methyl-tetradecanoic acid (57%), 15-methylhexadecenoic acid (18%) and 12-methyl-tetradecanoic acid (8%). Marseille-P9602 strain size was found from genome assembly to be of 4,271,905 bp, with a 35.5% G + C content. The highest values obtained for Ortho-ANI and dDDH were 91.67% and 44.60%, respectively. Thus, hereby we unravel that Marseille-P9602 strain is sufficiently different from other closed related species and can be classified as a novel bacterial species, for which we propose the name of Chryseobacterium schmidteae sp. nov. Type strain is Marseille-P9602T (= CSUR P9602T = CECT 30295T).
Asunto(s)
Chryseobacterium , Mediterranea , Filogenia , ARN Ribosómico 16SRESUMEN
Adult stem cells (ASCs) are the undifferentiated cells that possess self-renewal and differentiation abilities. They are present in all major organ systems of the body and are uniquely reserved there during development for tissue maintenance during homeostasis, injury, and infection. They do so by promptly modulating the dynamics of proliferation, differentiation, survival, and migration. Any imbalance in these processes may result in regeneration failure or developing cancer. Hence, the dynamics of these various behaviors of ASCs need to always be precisely controlled. Several genetic and epigenetic factors have been demonstrated to be involved in tightly regulating the proliferation, differentiation, and self-renewal of ASCs. Understanding these mechanisms is of great importance, given the role of stem cells in regenerative medicine. Investigations on various animal models have played a significant part in enriching our knowledge and giving In Vivo in-sight into such ASCs regulatory mechanisms. In this review, we have discussed the recent In Vivo studies demonstrating the role of various genetic factors in regulating dynamics of different ASCs viz. intestinal stem cells (ISCs), neural stem cells (NSCs), hematopoietic stem cells (HSCs), and epidermal stem cells (Ep-SCs).
Asunto(s)
Células Madre Adultas/fisiología , Diferenciación Celular , Proliferación Celular , Regulación de la Expresión Génica , Transducción de Señal , Animales , Movimiento Celular , Células Madre Hematopoyéticas , Humanos , Modelos Animales , Células-Madre NeuralesRESUMEN
The planarian species Schmidtea mediterranea is a flatworm living in freshwater that is used in the research laboratory as a model to study developmental and regeneration mechanisms, as well as antibacterial mechanisms. However, the cultivable microbial repertoire of the microbes comprising its microbiota remains unknown. Here, we characterized the bacterial constituents of a 10-year-old laboratory culture of planarian species S. mediterranea via culturomics analysis. We isolated 40 cultivable bacterial species, including 1 unidentifiable species. The predominant phylum is Proteobacteria, and the most common genus is Pseudomonas. We discovered that parts of the bacterial flora of the planarian S. mediterranea can be classified as fish pathogens and opportunistic human pathogens.
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Bacterias/clasificación , Bacterias/crecimiento & desarrollo , Laboratorios/estadística & datos numéricos , Microbiota , Planarias/microbiología , Animales , Bacterias/genética , Bacterias/aislamiento & purificación , Técnicas de Cultivo , ARN Ribosómico 16S/genética , Regeneración , Manejo de EspecímenesRESUMEN
Here, we report the draft genome sequence of Comamonas jiangduensis strain YW1T (= DSM 100319T = CSUR Q1714T = CCTCC AB 2012033Tâ = âKACC 16697T). Comamonas jiangduensis is a new Comamonas species that was isolated from agricultural soil. The genome sequence from strain YW1T has been assembled into 322 contigs for a total size of 2,758,586 bp with a G+C content of 59.1%.
RESUMEN
Comamonas aquatilis was defined as a new Comamonas species based on its 16S rRNA sequence, but the genome from the type strain SB30-Cr27-3T (= CIP 111491T = CCM 8815T) is not available. We have cultivated from the planarian Schmidtea mediterranea a Comamonas aquatilis strain, LK (= CSUR P6418 = CECT 9772), that exhibits 100% 16S rRNA sequence similarity to strain SB30-Cr27-3T We have sequenced the genome of strain LK and obtained a chromosome of 4,899,818 bp, with a G+C content of 61.75%, assembled into two contigs.