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Journal ArticleDOI

Human and tuberculosis co-evolution: An integrative view

01 Jun 2015-Tuberculosis (Churchill Livingstone)-Vol. 95
TL;DR: Tuberculosis is considered as a multifactorial disorder in which environmental factors interact tightly with human and pathogen genetic, and accessing ancient human pathogens allows a better understanding of infectious agents over a longer time scale and confrontation with the dynamic of modern TB strains.
About: This article is published in Tuberculosis.The article was published on 2015-06-01. It has received 22 citations till now. The article focuses on the topics: Mycobacterium tuberculosis complex & Tuberculosis.
Citations
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Journal ArticleDOI
TL;DR: It is suggested that this unusual situation of causality by chlamydiae in rheumatic disease requires establishment of a consensus regarding microorganism-specific terminology as well as the development of new diagnostic and classification criteria.
Abstract: Current molecular genetic understanding of the metabolically active persistent infection state of Chlamydia trachomatis and Chlamydia pneumoniae in the synovium in patients with arthritis and spondyloarthritis favors a causal relationship. Here, we examine how adequately the accepted criteria for that etiologic relationship are fulfilled, emphasizing the situation in which these microorganisms cannot be cultivated by standard or other means. We suggest that this unusual situation of causality by chlamydiae in rheumatic disease requires establishment of a consensus regarding microorganism-specific terminology as well as the development of new diagnostic and classification criteria. Recent studies demonstrate the value of molecular testing for diagnosis of reactive arthritis, undifferentiated spondyloarthritis, and undifferentiated arthritis caused by C. trachomatis and C. pneumoniae in clinical practice. Data regarding combination antibiotic therapy is consistent with the causative role of chlamydiae for these diseases. Observations of multiple intra-articular coinfections require more research to understand the implications and to respond to them.

28 citations

Journal ArticleDOI
TL;DR: PhoPR directly activates whiB3 expression in response to low pH and mutating the residues important for the phosphorylation pathway of PhoPR in M. marinum abolished the activation of whi B3 expression by Pho PR under acidic conditions.
Abstract: During infection, Mycobacterium tuberculosis colonizes macrophages or necrotic granulomas, in which low pH is one of the major challenges. The PhoPR two-component regulatory system and the cytosolic redox sensor WhiB3 both play important roles in the response to low pH by M. tuberculosis However, whether close association exists between PhoPR and WhiB3 remains unclear. In this study, the positive regulation of whiB3 by PhoPR in mycobacteria was characterized. We observed that the expression patterns of the whiB3 gene under acidic conditions are different among mycobacterial species, suggesting that the regulation of whiB3 differs among mycobacteria. A sequence analysis of the whiB3 promoters (whiB3p) from M. tuberculosis and two closely related species, namely, M. marinum and M. smegmatis, showed that the whiB3p regions from M. tuberculosis and M. marinum contain a new type of PhoP box that is absent in the M. smegmatiswhiB3p Direct binding of PhoP to whiB3p from M. tuberculosis and M. marinum but not that from M. smegmatis was validated by in vitro protein-DNA binding assays. The direct activation of whiB3 by PhoPR under acidic conditions was further verified by reverse transcription-quantitative PCR (qRT-PCR) analysis in M. marinum Moreover, mutating the residues important for the phosphorylation pathway of PhoPR in M. marinum abolished the activation of whiB3 expression by PhoPR under acidic conditions, suggesting that low pH triggers the phosphorylation of PhoPR, which in turn activates the transcription of whiB3 Since the PhoP box was only identified in whiB3p of pathogenic mycobacteria, we suggest that the PhoPR-whiB3 regulatory pathway may have evolved to facilitate mycobacterial infection.IMPORTANCE The low pH in macrophages is an important barrier for infection by microbes. The PhoPR two-component regulatory system is required for the response to low pH and plays a role in redox homeostasis in Mycobacterium tuberculosis WhiB3, a cytosolic redox-sensing transcriptional regulator, is also involved in these processes. However, there is no direct evidence to demonstrate the regulation of WhiB3 by PhoPR. In this study, we found that PhoPR directly activates whiB3 expression in response to low pH. An atypical PhoP box in the whiB3 promoters has been identified and is only found in pathogenic mycobacteria, which suggests that the PhoPR-whiB3 regulatory pathway may facilitate mycobacterial infection. This study provides novel information for further characterization of the PhoPR regulon.

18 citations

Journal ArticleDOI
TL;DR: Past human populations were associated with different lineages of the Mycobacterium tuberculosis complex, thereby elucidating early human migrations and the importance of human population density in such circumstances.

9 citations

Journal ArticleDOI
TL;DR: Using case-control analysis, it is identified that two genetic polymorphism sites in the ASAP1 relate to host susceptibility of TB in a Chinese Xinjiang Muslim population.
Abstract: Seven single-nucleotide polymorphism (SNP) sites located in ASAP1 gene have been found associated with tuberculosis (TB) susceptibility by genome-wide association studies in Russia The case-control study was carried out to test whether these seven SNPs were associated with susceptibility to TB in a Chinese Xinjiang Muslim population The seven SNPs were genotyped in a case-control design that included 780 Xinjiang Muslim subjects (400 TB patients and 380 controls) Multiplex PCR and direct sequencing were used to detect ASAP1 gene polymorphisms Hardy-Weinberg equilibrium test was performed to test whether the sample was from genetic equilibrium population The associations of SNPs with TB risk were determined by the distributions of allelic frequencies and different genetic models Significant differences of the allelic distribution of rs4733781 and rs1017281 in ASAP1 gene were observed between control group and TB group A allele of rs4733781 was associated with TB risk (TB vs control, OR=1242; 95% CI: 1004-1537, P=0046); While in rs1017281 site, G allele was associated with increased risk for TB (TB vs control, OR: 0792, 95% CI: 0643-0976, P=0028) The recessive model of rs4733781 (CC vs AC+AA) in Xinjiang Muslim populations was associated with a lower TB risk [P=0003, OR=051 (0324-0802)], while the recessive model of rs1017281 (GG vs AG+AA) was associated with a higher TB risk [P=0011, OR=1792 (1135-2828)] Using case-control analysis, we identified that two genetic polymorphism sites in the ASAP1 relate to host susceptibility of TB in a Chinese Xinjiang Muslim population

7 citations


Cites background from "Human and tuberculosis co-evolution..."

  • ...Other co-variables may not be excluded, such as socio-economic factors, nutritional status, and interactions between genes (29)....

    [...]

Journal ArticleDOI
TL;DR: The genetic, phenotypic, and clinical similarities and differences between strains of M. tuberculosis and M. africanum are discussed and how it possibly articulates with distinct disease progression and with the geographical restriction attributed to this pathogen is discussed.
Abstract: Tuberculosis (TB), one of the deadliest threats to human health, is mainly caused by 2 highly related and human-adapted bacteria broadly known as Mycobacterium tuberculosis and Mycobacterium africanum. Whereas M. tuberculosis is widely spread, M. africanum is restricted to West Africa, where it remains a significant cause of tuberculosis. Although several differences have been identified between these 2 pathogens, M. africanum remains a lot less studied than M. tuberculosis. Here, we discuss the genetic, phenotypic, and clinical similarities and differences between strains of M. tuberculosis and M. africanum. We also discuss our current knowledge on the immune response to M. africanum and how it possibly articulates with distinct disease progression and with the geographical restriction attributed to this pathogen. Understanding the functional impact of the diversity existing in TB-causing bacteria, as well as incorporating this diversity in TB research, will contribute to the development of better, more specific approaches to tackle TB.

6 citations

References
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Journal ArticleDOI
TL;DR: Findings indicating that developmental aspects of the adaptive immune system are influenced by bacterial colonization of the gut are discussed, and the possibility that the mammalian immune system, which seems to be designed to control microorganisms, is in fact controlled by microorganisms is raised.
Abstract: Immunological dysregulation is the cause of many non-infectious human diseases such as autoimmunity, allergy and cancer. The gastrointestinal tract is the primary site of interaction between the host immune system and microorganisms, both symbiotic and pathogenic. In this Review we discuss findings indicating that developmental aspects of the adaptive immune system are influenced by bacterial colonization of the gut. We also highlight the molecular pathways that mediate host–symbiont interactions that regulate proper immune function. Finally, we present recent evidence to support that disturbances in the bacterial microbiota result in dysregulation of adaptive immune cells, and this may underlie disorders such as inflammatory bowel disease. This raises the possibility that the mammalian immune system, which seems to be designed to control microorganisms, is in fact controlled by microorganisms.

4,079 citations


"Human and tuberculosis co-evolution..." refers background in this paper

  • ...know that disturbances in the bacterial microbiome is a major regulator of inflammatory disorders [30], it can acts as modulator in non-infectious diseases like obesity and autoimmune diseases....

    [...]

Journal ArticleDOI
TL;DR: The distribution of 20 variable regions resulting from insertion-deletion events in the genomes of the tubercle bacilli has been evaluated and contradict the often-presented hypothesis that M. tuberculosis, the etiological agent of human tuberculosis evolved from M. bovis, the agent of bovine disease.
Abstract: The distribution of 20 variable regions resulting from insertion-deletion events in the genomes of the tubercle bacilli has been evaluated in a total of 100 strains of Mycobacterium tuberculosis, Mycobacterium africanum, Mycobacterium canettii, Mycobacterium microti, and Mycobacterium bovis. This approach showed that the majority of these polymorphisms did not occur independently in the different strains of the M. tuberculosis complex but, rather, resulted from ancient, irreversible genetic events in common progenitor strains. Based on the presence or absence of an M. tuberculosis specific deletion (TbD1), M. tuberculosis strains can be divided into ancestral and “modern” strains, the latter comprising representatives of major epidemics like the Beijing, Haarlem, and African M. tuberculosis clusters. Furthermore, successive loss of DNA, reflected by region of difference 9 and other subsequent deletions, was identified for an evolutionary lineage represented by M. africanum, M. microti, and M. bovis that diverged from the progenitor of the present M. tuberculosis strains before TbD1 occurred. These findings contradict the often-presented hypothesis that M. tuberculosis, the etiological agent of human tuberculosis evolved from M. bovis, the agent of bovine disease. M. canettii and ancestral M. tuberculosis strains lack none of these deleted regions, and, therefore, seem to be direct descendants of tubercle bacilli that existed before the M. africanum→M. bovis lineage separated from the M. tuberculosis lineage. This observation suggests that the common ancestor of the tubercle bacilli resembled M. tuberculosis or M. canettii and could well have been a human pathogen already.

1,497 citations

Journal ArticleDOI
TL;DR: It is demonstrated that the global population structure of M. tuberculosis is defined by six phylogeographical lineages, each associated with specific, sympatric human populations, and in an urban cosmopolitan environment, mycobacterial lineages were much more likely to spread in sympatrics than in allopatric patient populations.
Abstract: Mycobacterium tuberculosis remains a major cause of morbidity and mortality worldwide Studies have reported human pathogens to have geographically structured population genetics, some of which have been linked to ancient human migrations However, no study has addressed the potential evolutionary consequences of such longstanding human-pathogen associations Here, we demonstrate that the global population structure of M tuberculosis is defined by six phylogeographical lineages, each associated with specific, sympatric human populations In an urban cosmopolitan environment, mycobacterial lineages were much more likely to spread in sympatric than in allopatric patient populations Tuberculosis cases that did occur in allopatric hosts disproportionately involved high-risk individuals with impaired host resistance These observations suggest that mycobacterial lineages are adapted to particular human populations If confirmed, our findings have important implications for tuberculosis control and vaccine development

972 citations

Journal ArticleDOI
07 Mar 2003-Science
TL;DR: Helicobacter pylori, a chronic gastric pathogen of human beings, can be divided into seven populations and subpopulations with distinct geographical distributions.
Abstract: Helicobacter pylori, a chronic gastric pathogen of human beings, can be divided into seven populations and subpopulations with distinct geographical distributions. These modern populations derive their gene pools from ancestral populations that arose in Africa, Central Asia, and East Asia. Subsequent spread can be attributed to human migratory fluxes such as the prehistoric colonization of Polynesia and the Americas, the neolithic introduction of farming to Europe, the Bantu expansion within Africa, and the slave trade.

939 citations

Journal ArticleDOI
TL;DR: A genome-wide phylogeny based on genomes of 21 strains representative of the global diversity and six major lineages of the M. tuberculosis complex showed, as expected, that essential genes in MTBC were more evolutionarily conserved than nonessential genes.
Abstract: Mycobacterium tuberculosis is an obligate human pathogen capable of persisting in individual hosts for decades. We sequenced the genomes of 21 strains representative of the global diversity and six major lineages of the M. tuberculosis complex (MTBC) at 40- to 90-fold coverage using Illumina next-generation DNA sequencing. We constructed a genome-wide phylogeny based on these genome sequences. Comparative analyses of the sequences showed, as expected, that essential genes in MTBC were more evolutionarily conserved than nonessential genes. Notably, however, most of the 491 experimentally confirmed human T cell epitopes showed little sequence variation and had a lower ratio of nonsynonymous to synonymous changes than seen in essential and nonessential genes. We confirmed these findings in an additional data set consisting of 16 antigens in 99 MTBC strains. These findings are consistent with strong purifying selection acting on these epitopes, implying that MTBC might benefit from recognition by human T cells.

621 citations

Trending Questions (1)
How does the evolution of tuberculosis in humans and animals affect human health?

The evolution of tuberculosis in humans and animals has shaped the immune system and susceptibility factors, but the direct interaction between human and TB variation is not confirmed.