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Results for “Pathogen diversity”

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PubMed2006

High recombination frequency creates genotypic diversity in colonies of the leaf-cutting ant Acromyrmex echinatior.

Honeybees are known to have genetically diverse colonies because queens mate with many males and the recombination rate is extremely high. Genetic diversity among social insect workers has been hypothesized to improve general performance of large and complex colonies, but this idea has not been tested in other social insects. Here, we present a linkage map and an estimate of the recombination rate for Acromyrmex echinatior, a leaf-cutting ant that resembles the honeybee in having multiple mating of queens and colonies of approximately the same size. A map of 145 AFLP markers in 22 linkage groups yielded a total recombinational size of 2076 cM and an inferred recombination rate of 161 kb cM(-1) (or 6.2 cM Mb(-1)). This estimate is lower than in the honeybee but, as far as the mapping criteria can be compared, higher than in any other insect mapped so far. Earlier studies on A. echinatior have demonstrated that variation in division of labour and pathogen resistance has a genetic component and that genotypic diversity among workers may thus give colonies of this leaf-cutting ant a functional advantage. The present result is therefore consistent with the hypothesis that complex social life can select for an increased recombination rate through effects on genotypic diversity and colony performance.

Animals↗

PubMed1990

Pathogenic idiotypes of autoantibodies in autoimmunity: lessons from new experimental models of SLE.

Systemic lupus erythematosus (SLE) is considered a classical autoimmune disease that involves many biological systems. Similar to other autoimmune conditions, its etiology is multifactorial entailing genetic, environmental, hormonal, and immunologic factors. In this review we demonstrate that by using a pathogenic idiotype of anti-DNA autoantibodies, it is possible to explain some of the pathogenesis and diversity of clinical and serological manifestations reported by SLE patients. The 16/6 idiotype (Id) is a representative pathogenic idiotype of anti-DNA autoantibodies. The serum titers of 16/6 Id in SLE patients correlate with clinical activity of the disease, and are deposited in afflicted tissues in SLE patients. SLE was experimentally induced in naive mice after immunization with 1 microgram of the Id. The disease is characterized clinically (proteinuria), serologically (e.g., anti-dsDNA, anti-Sm antibodies), and by pathological findings (e.g., deposition of 16/6 Id in the kidneys). The condition can be induced by other human and mouse antibodies carrying the 16/6 Id, as well as by mouse antimonoclonal-16/6 Id and by T cell lines and clones specifically reactive with 16/6 Id. There are strain-dependent differences in susceptibility to the induction of systemic lupus erythematosus (SLE). Induction of SLE is directly correlated with the ability to respond to the 16/6 idiotype (or 16/6 Id)2 by anti-Id antibody production. It is easier to induce the disease in females, and it can be modulated by manipulation of sex hormones. Being able to identify the pathogenic idiotype allowed us to generate T suppressor (Ts) cells specific for the 16/6 Id. Treatment of mice with these T cells abrogated the disease. Our studies point to the importance of pathogenic idiotypes of autoantibodies in autoimmunity, which suggests that SLE may represent a dysregulation of a functional network of idiotypes-anti-idiotypes interactions among autoreactive B cells, T helper cells, and T suppressor cells.

Animals↗

PubMed1995

DNA fingerprinting of pathogenic bacteria by fluorophore-enhanced repetitive sequence-based polymerase chain reaction.

Fluorophore-labeled oligonucleotide primers complementary to defined interspersed repetitive sequences conserved in diverse bacteria were used in the polymerase chain reaction to generate DNA fingerprint patterns from selected pathogenic bacteria. Fluorophore-enhanced, repetitive sequence-based polymerase chain reaction allowed discrimination between unrelated isolates of penicillin-resistant Streptococcus pneumoniae recovered from pediatric patients and Mycobacterium avium cultured from patients with acquired immunodeficiency syndrome. Combinations of oligonucleotide primers labeled with distinct fluorescent dyes enabled simultaneous DNA fingerprinting and Shiga-like toxin gene detection in enterohemorrhagic Escherichia coli isolates. Fluorophore-enhanced, repetitive sequence-based polymerase chain reaction was performed with either purified DNA or intact cells that were lysed during the polymerase chain reaction. Fluorophore-enhanced, repetitive sequence-based polymerase chain reaction successfully combines polymerase chain reaction amplification and fluorescent label detection for DNA fingerprinting of cultured bacterial pathogens.

Base Sequence↗

PubMed2002

Memorizing innate instructions requires a sufficiently specific adaptive immune system.

During its primary encounter with a pathogen, the immune system has to decide which type of immune response is most appropriate. Based on signals from the innate immune system and the immunological context in which the pathogen is presented, responding lymphocytes will adopt a particular phenotype, e.g. secrete a particular profile of cytokines. Once stimulated, lymphocytes store the appropriate type of response by differentiating from a naive to a memory phenotype. This allows the appropriate type of immune reaction to be regenerated upon re-stimulation of those memory clones. We developed a computer simulation model in which cross-reacting effector/memory clones contribute to the immunological context of pathogens. If a pathogen is recognized by both naive clones and pre-existing effector/memory clones, the naive lymphocytes adopt the effector mechanism of the memory clone. The adaptive immune system thereby stores immunological decisions and somatically learns to induce the right type of immune response to pathogens sharing epitopes. The influence of effector/memory lymphocytes may be detrimental when they cross-react to new pathogens that require a different kind of immune response. Here, we show that the immune system needs to be sufficiently specific to avoid such mistakes and to profit from the information that is stored in effector/memory lymphocytes. Repertoire diversity is required to reconcile this specificity with reactivity against many pathogens.

Aged↗

PubMed2001

Genetic engineering of live rabies vaccines.

Rabies virus is not a single entity but consists of a wide array of variants that are each associated with different host species. These viruses differ greatly in the antigenic makeup of their G proteins, the primary determinant of pathogenicity and major inducer of protective immunity. Due to this diversity, existing rabies vaccines have largely been targeted to individual animal species. In this report, a novel approach to the development of rabies vaccines using genetically modified, reverse-engineered live attenuated rabies viruses is described. This approach entails the engineering of vaccine rabies virus containing G proteins from virulent strains and modification of the G protein to further reduce pathogenicity. Strategies employed included exchange of the arginine at position 333 for glutamine and modification of the cytoplasmic domain. The recombinant viruses obtained were non-neuroinvasive when administered via a peripheral route. The ability to confer protective immunity depended largely upon conservation of the G protein antigenic structure between the vaccine and challenge virus, as well as on the route of immunization.

Animals↗

PubMed1978

Sequential expression of immunoglobulin on developing mouse B lymphocytes: a systematic survey that suggests a model for the generation of immunoglobulin isotype diversity.

Paired immunofluorescent staining with antibodies specific for the major isotypes of mouse immunoglobulin was used to study the ontogenetic expression of diversity of cell surface immunoglobulin. The first B lymphocytes to emerge, derived from cytoplasmic IgM+ precursors, express sIgM exclusively. Between birth and 3 days of age separate populations of sIgM+ B lymphocyte acquire a second isotype: sIgD, one of the subclasses of sIgG, or sIgA. At 3 days, all splenic B lymphocytes that bear sIg or sIgA also express sIgM, but virtually none stain for sIgD. By 7 days, a substantial porportion of sIgG+ or sIgA+ lymphocytes in spleen and most of those in lymph node express both sIgM ans sIgD. Anti-mu antibody treatment from birth prevented development of B lymphocytes expressing any isotype. These observations suggest that the immature sIgM+ B lymphocyte is the pivotal cell in the generation of the different sublines of B cells and that sIgD ig or IgA. The frequency of lymphocytes bearing only sIgG or sIgA is higher in old than in young mice, suggesting that sIgD and sIgM may be lost after stimulation by antigens. The occurrence of a nearly identical distribution of sIg isotypes on B lymphocytes from athymic, pathogen-free mice suggests that primary expression of isotype diversity does not require T cells.

Aging↗

PubMed1999

Search for an antibody profile of Rhodococcus equi infection in AIDS patients despite the diversity of isolates and patient immune dysfunction.

Diversity of virulence-associated antigens of Rhodococcus equi was detected among thirteen strains isolated from AIDS patients on two continents. One out of four Brazilian isolates presented the virulence-associated antigen of 15- to 17-kDa, and the other three isolates had the 20-kDa virulence-associated antigen. In contrast, only three out of nine Italian isolates were positive for virulence-associated antigens - two for the 15- to 17-kDa antigen and one for the 20-kDa antigen. In four other Italian strains, one or more other low-molecular-weight antigens were identified. Because of R. equi variability and host immune dysfunction, no characteristic antibody profile was detected among patients, although the presence of specific antibodies in serum samples suggested prognostic value: good patient outcome and recovery from pneumonia were correlated with R. equi antibody detection, whereas the lack or disappearance of specific antibodies, mainly those to low-molecular-weight antigens, was correlated with disease progression and patient death. These results confirmed the nonobligatory presence of the well-known virulence-associated antigens for the pathogenicity of R. equi in humans, and also the diversity of R. equi strains isolated from AIDS patients, which may be related to the geographic origin of the isolates or may be a consequence of the route of R. equi transmission in different countries. Some mechanisms underlying the results obtained are discussed, suggesting immune complex formation during the progress of the disease.

AIDS-Related Opportunistic Infections↗

PubMed2026

Identification and in-depth characterization of clinical isolates of Peribacillus frigoritolerans.

UNLABELLED: Peribacillus frigoritolerans is a bacterial species commonly found in the environment and used as a plant-growth promoter and biocontrol agent in agriculture. Recent evidence has proven that Peribacillus spp. are also able to cause severe infections in humans, thus emerging as new human pathogens. In this study, for the first time, 10 P. frigoritolerans strains were isolated from human samples (both superficial and sterile deep body sites) and characterized in terms of morphology, lifestyle, genetics, and virulence. The molecular identification by MALDI-TOF mass spectrometry and 16S rRNA gene sequencing was inconclusive, while whole-genome sequencing was effective in properly identifying isolates within the species P. frigoritolerans. The pangenome analysis provided an overview of the virulence potential of P. frigoritolerans, revealing the presence of genes involved in antibiotic resistance and toxin/exoenzyme production. Phenotypically, the strains displayed different features and behaviors, indicating strain-specific properties and high intra-species variability. A part of the strains exhibited virulence factors, being able to swim and swarm, form biofilms, and produce enzymes and toxins. Antibiotic susceptibility testing revealed resistance to ampicillin for all strains and resistance to erythromycin and clindamycin for some of them. Antimicrobial activity against Gram-positive bacteria and fungi was demonstrated, further corroborating the presence of putative bacteriocin/antimicrobial peptide-encoding genes. An association between the overall virulence potential and infection site/severity was hypothesized. Altogether, these findings highlight the extreme diversity within the species, reveal the strain-dependent pathogenic potential of P. frigoritolerans, and support its role as a candidate human pathogen. IMPORTANCE: This study provides insights into the infectious role of Peribacillus frigoritolerans, an almost unknown bacterial species with agrobiotechnological potential but no history of human infections. This is the first report of P. frigoritolerans isolation from human clinical samples. Ten P. frigorit-olerans strains were herein characterized for their morphology, lifestyle, genetics, and virulence, highlighting an extreme intra-species variability and the potential to act as pathogens in humans. Importantly, this study points out the need for unconventional methods for proper identification of this species, since traditional techniques result inconclusive. Resistance to commonly prescribed antibiotics was also evidenced, confirming the importance of antimicrobial testing on clinical iso-lates. This study lays the foundation for a more in-depth characterization of Peribacillus spp. in the clinical context.

Humans↗

PubMed1999

Selecting and maintaining a diverse T-cell repertoire.

To provide a T-cell population that will respond promptly to foreign antigen, the immune system looks inward, using the variety of self-antigens to select and maintain a diverse repertoire of receptors. A protective immune system must include a T-lymphocyte population that is poised to respond to foreign antigenic peptides presented by self-major histocompatibility complex molecules. As the organism cannot predict the precise pathogen-derived antigens that will be encountered, the system uses the diverse array of self-peptides bound to self-major histocompatibility complex molecules, not only to select a receptor repertoire in the thymus, but also to keep naïve T cells alive and 'ready for action' in the periphery.

Animals↗

PubMed2000

T cell tolerance and autoimmunity.

A functional immune system requires a T cell repertoire that is extremely diverse so as to allow for the elimination of all possible pathogens. However, the production of an immense T cell repertoire also increases the likelihood of generating autoreactive T cells. The immune system must therefore also incorporate a means of silencing or eliminating autoreactive T cells, while minimally sacrificing T cell diversity. The induction and maintenance of T cell unresponsiveness to self antigens is thus defined as T cell tolerance. This review provides an overview of the T cell tolerance mechanisms invoked in the thymus and in the periphery to prevent the induction of autoimmunity. Factors that can influence the induction of tolerance and autoimmunity are also discussed.

Animals↗

PubMed2006

The obligate intracellular pathogen Chlamydia trachomatis targets host lipid droplets.

Lipid droplets (LDs) are ubiquitous but poorly understood neutral-lipid-rich eukaryotic organelles that may participate in functions as diverse as lipid homeostasis, membrane traffic, and signaling . We report that infection with the obligate intracellular pathogen Chlamydia trachomatis, the causative agent of trachoma and many sexually transmitted diseases , leads to the accumulation of neutral-lipid-rich structures with features of LDs at the cytoplasmic surface of the bacteria-containing vacuole. To identify bacterial factors that target these organelles, we screened a collection of yeast strains expressing GFP-tagged chlamydial ORFs and identified several proteins with tropism for eukaryotic LDs. We determined that three of these LD-associated (Lda) proteins are translocated into the mammalian host and associate with neutral-lipid-rich structures. Furthermore, the stability of one Lda protein is dependent on binding to LDs, and pharmacological inhibition of LD formation negatively impacted chlamydial replication. These results suggest that C. trachomatis targets LDs to enhance its survival and replication in infected cells. The co-option of mammalian LD function by a pathogenic bacterium represents a novel mechanism of eukaryotic organelle subversion and provides unique research opportunities to explore the function of these understudied organelles.

Bacterial Proteins↗

PubMed1997

Dominance of a single peptide bound to the class I(B) molecule, Qa-1b.

One of the hallmarks of class I(A) molecules is their ability to bind and present a wide array of peptides to CD8 T cells. This diversity is consistent with their ability to restrict a variety of pathogenic peptide epitopes as well as elicit strong transplantation responses. In contrast, class I(B) molecules appear to be involved in presentation of pathogenic epitopes to a relatively lesser extent as well as play a minor role in transplantation responses. Here we have examined the peptides bound and presented by the class I(B) molecule Qa-1b in order to determine if their diversity was similar to that reported for class I(A) Ags. First, we show that bulk-cultured anti-Qa-1b CTL predominantly recognize a single peptide (Qdm) derived from the leader segment of class I(A) alloantigens. These CTL are peptide specific and reflect the activity of previously described CTL clones. Second, we find approximately 4.6 x 10(4) copies of the Qdm peptide/cell. Most of the peptide is Qa-1b associated since the recovery of this peptide from anti-Qa-1b immunoprecipitates is approximately 75% of that seen in whole cell extracts and no detectable activity is observed in Kb or Db extracts from H-2b lymphoblasts. Third, the expression of Qa-1b on lymphoblasts is approximately 1 to 1.25 x 10(4) molecules/cell indicating that the Qdm peptide must be derived from both cell membrane and intracellular compartments. Finally, examination of the diversity of peptides associated with Qa-1b as determined by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry indicates few detectable peptide species associated with this molecule. Taken together, Qa-1b appears to predominantly bind a single peptide species that is recognized by alloreactive CD8 T cells. This feature may account, in part, for the class I(B) properties of this molecule.

Animals↗

PubMed2002

Genetic diversity of three lgt loci for biosynthesis of lipooligosaccharide (LOS) in Neisseria species.

Lipooligosaccharide (LOS) is a major virulence factor of the pathogenic Neisseria. Nine lgt genes at three chromosomal loci (lgt-1, 2, 3) encoding the glycosyltransferases responsible for the biosynthesis of LOS oligosaccharide chains were examined in 26 Neisseria meningitidis, 51 Neisseria gonorrhoeae and 18 commensal Neisseria strains. DNA hybridization, PCR and nucleotide sequence data were compared to previously reported lgt genes. Analysis of the genetic organization of the lgt loci revealed that in N. meningitidis, the lgt-1 and lgt-3 loci were hypervariable genomic regions, whereas the lgt-2 locus was conserved. In N. gonorrhoeae, no variability in the composition or organization of the three lgt loci was observed. lgt genes were detected only in some commensal Neisseria species. The genetic organization of the lgt-1 locus was classified into eight types and the lgt-3 locus was classified into four types. Two types of arrangement at lgt-1 (II and IV) and one type of arrangement at lgt-3 (IV) were novel genetic organizations reported in this study. Based on the three lgt loci, 10 LOS genotypes of N. meningitidis were distinguished. Phylogenetic analysis revealed a gene cluster, lgtH, which separated from the homologous genes lgtB and lgtE. The lgtH and lgtE genes were mutually exclusive and were located at the same position in lgt-1. The data demonstrated that pathogenic and commensal Neisseria share a common lgt gene pool and horizontal gene transfer appears to contribute to the genetic diversity of the lgt loci in Neisseria.

Genes, Bacterial↗

PubMed1992

Esophageal disease in the acquired immunodeficiency syndrome: etiology, diagnosis, and management.

Esophageal disease is a common complication and cause of morbidity in patients with human immunodeficiency virus (HIV) infection. Opportunistic esophageal diseases may occur in patients with long-standing infection or may be the initial manifestation of HIV disease. Although a variety of both opportunistic and nonopportunistic disorders result in esophageal disease in this population, candidal esophagitis is the most common cause of symptomatic disease. Ulcerative esophagitis resulting from cytomegalovirus and idiopathic esophageal ulceration constitute the next most important etiologies. In contrast to other immunocompromised hosts, herpes simplex virus esophagitis appears to be relatively uncommon. Multiple simultaneously discovered esophageal disorders have been documented in up to 50% of patients. Opportunistic neoplasms are an infrequent cause of symptomatic disease. Candidal esophagitis may present with either dysphagia or odynophagia, and oropharyngeal candidiasis is usually present at the time of diagnosis. In contrast, ulcerative esophagitis is usually first manifested by moderate to severe odynophagia. Barium esophagography and upper endoscopy are the most commonly employed diagnostic modalities for the evaluation of the symptomatic patient. Although barium esophagography may identify specific abnormalities, this procedure appears to be relatively insensitive for the detection of mild candidal disease as well as nondiagnostic for ulcerative lesions when compared with endoscopy. In the HIV-infected patient with new-onset esophageal symptoms, an empiric trial of a systemically acting oral antifungal agent should probably be the initial management strategy. If the patient does not respond to standard therapy within 1 to 2 weeks, an endoscopic evaluation appears to be the most cost-effective diagnostic test given the diversity of potential disorders, the possibility of one or more co-pathogens or diseases, the potential for an immediate diagnosis, and the availability of mucosal biopsy to make a definite diagnosis of ulcerative or mass lesions. Given the presently available therapy for these diverse processes, establishing a definitive diagnosis in the symptomatic patient not responsive to empiric antifungal therapy is warranted.

Acquired Immunodeficiency Syndrome↗

PubMed2004

Epidemiological processes involved in the emergence of vector-borne diseases: West Nile fever, Rift Valley fever, Japanese encephalitis and Crimean-Congo haemorrhagic fever.

Over the past few decades, the geographical distribution of arthropod-borne zoonoses has dramatically expanded. The influence of human-induced or ecological changes on the risk of disease outbreaks is undeniable. However, few hypotheses have been proposed which address the re-emergence of these diseases, the spread of these viruses to previously uninfected areas and their establishment therein. Host and vector movements play an important role in the dissemination of pathogens, and the ability of these diseases to colonise previously uninfected areas may be explained by the diversity of hosts and vectors, the presence of favourable ecological conditions, and the successful adaptations of vectors or pathogens to new ecosystems. The objective of this paper is to describe the epidemiological processes of the vector-borne diseases Rift Valley fever, West Nile fever, Japanese encephalitis and Crimean-Congo haemorrhagic fever.

Animals↗

PubMed2001

[Plants and pathogenic agents, a refined and dangerous relationship: the example of fungi].

Plant-fungus interactions are highly diverse, either being beneficial to the host plant such as those leading to mycorhizal symbiosis, or very detrimental when leading to severe diseases. Since the beginning of agriculture, improvement of plant resistance to pathogens has remained a major challenge. Breeding for resistance, first conducted empirically in the past centuries, was then performed on a more theoretical basis after the statement of heredity laws by Mendel at the end of the XIXth century. As a result, most cultivated species contain various cultivars whose resistance or susceptibility to a given pathogen species depend on their interaction with various races of that pathogen. Such highly specific race-cultivar systems are particularly suited for understanding the molecular dialogue which underlies compatible (host susceptible/pathogen virulent) or incompatible (host resistant/pathogen avirulent) interactions. During the twentieth century, one of the major events that paved the way for future research was the statement by Flor [1946, 1947] of the gene-for-gene concept. Studying inheritance of the disease phenotype in the interaction between flax and Melampsora lini he showed that resistance in the host and avirulence in the pathogen are dictated by single dominant genes which correspond one to one, i.e. one resistance gene for one avirulence gene. The fact that incompatibility may depend on the presence of only one resistance (R) gene in the host and one avirulence (Avr) gene in the pathogen was fully confirmed about 40 years later. Molecular genetics and complementation experiments have allowed to isolate numerous R and Avr genes from various plant-pathogen systems, and to verify the gene-for-gene concept. These studies have enlightened the elicitor/receptor concept, formerly introduced to account for the specificity of the compatible and incompatible interactions. The present knowledge of R and Avr genes also allows to predict how such genes have evolved and how they could be used to improve disease resistance. At the beginning of the twenty first century, this remains a major challenge in view of the severe losses caused by pests and pathogens to most crops on the earth.

Fungal Proteins↗

PubMed2003

Novel bacteria degrading N-acylhomoserine lactones and their use as quenchers of quorum-sensing-regulated functions of plant-pathogenic bacteria.

Bacteria degrading the quorum-sensing (QS) signal molecule N-hexanoylhomoserine lactone were isolated from a tobacco rhizosphere. Twenty-five isolates degrading this homoserine lactone fell into six groups according to their genomic REP-PCR and rrs PCR-RFLP profiles. Representative strains from each group were identified as members of the genera Pseudomonas, Comamonas, Variovorax and Rhodococcus: all these isolates degraded N-acylhomoserine lactones other than the hexanoic acid derivative, albeit with different specificity and kinetics. One of these isolates, Rhodococcus erythropolis strain W2, was used to quench QS-regulated functions of other microbes. In vitro, W2 strongly interfered with violacein production by Chromobacterium violaceum, and transfer of pathogenicity in Agrobacterium tumefaciens. In planta, R. erythropolis W2 markedly reduced the pathogenicity of Pectobacterium carotovorum subsp. carotovorum in potato tubers. These series of results reveal the diversity of the QS-interfering bacteria in the rhizosphere and demonstrate the validity of targeting QS signal molecules to control pathogens with natural bacterial isolates.

4-Butyrolactone↗

PubMed1995

Pathogenic mechanisms of vessel damage in vasculitis syndromes.

The pathogenesis of vasculitis syndromes is via a diverse array of mechanisms that disrupt vessel integrity and produce clinical signs and symptoms of tissue ischemia. In many patients with vasculitis, it is not possible to directly classify the syndrome according to a particular schema, and attempts to define the pathogenic process mediating vessel damage by biopsy and laboratory tests may be useful to guide therapy. The continued use of new techniques to probe immune cell types and cytokines in vasculitis lesional tissues will further clarify molecular mechanisms of vascular damage, and it is hoped that they will lead to new and more effective therapeutic strategies targeted at the vasculitis syndromes.

Antibody Formation↗