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Немецкие анализы на боррелиоз и сопутствующие инфекции

В России появилась возможность выполнять лабораторные анализы на боррелиоз и ко-инфекции в немецкой лаборатории ArminLabs

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Коинфекции Риккетсиозы

Тема в разделе "Виды коинфекций и их симптомы", создана пользователем Julia Göteborg, 15 апр 2016.

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    Бартонелла (Bartonella), ГЕМОБАРТОНЕЛЛА (Haemobartonella) - род паразитических палочкообразных или круглых микроорганизмов, обычно по-другому называемых риккетсиями. Их присутствие обнаруживается в эритроцитах крови и лимфатических клетках, а также в селезенке, печени и почках. Вид В. bacilliformis вызывает у человека бартонеллез.

    Bartonella bacilliformis (Ber) -- микроорганизм рода Bartonella (сем. Bartonellaceae, порядок Rickettsiales) палочковидной или кокковидной формы, обнаруживаемый в эритроцитах и клетках ретикулоэндотелиальной системы человека и обезьян вида резус; возбудитель бартонеллеза.
    Бартонелла
    ............................

    Rickettsia is a genus of nonmotile, gram-negative, nonspore-forming, highly pleomorphic bacteria that can present as cocci (0.1 μm in diameter), rods (1–4 μm long), or thread-like (10 μm long). The term rickettsia, named after Howard Taylor Ricketts, is often used interchangeably for any member of the Rickettsiales. Being obligate intracellular parasites, the Rickettsia survival depends on entry, growth, and replication within the cytoplasm of eukaryotic host cells (typically endothelial cells).[8] Rickettsia cannot live in artificial nutrient environments and is grown either in tissue or embryo cultures; typically, chicken embryos are used: a method developed by Ernest William Goodpasture and his colleagues at Vanderbilt University in the early 1930s.

    Rickettsia species are transmitted by numerous types of arthropod, including chigger, ticks, fleas, and lice, and are associated with both human and plant disease. Most notably, Rickettsia species are the pathogen responsible for: typhus, rickettsialpox, Boutonneuse fever, African tick bite fever, Rocky Mountain spotted fever, Flinders Island spotted fever and Queensland tick typhus (Australian tick typhus).[9] Despite the similar name, Rickettsia bacteria do not cause rickets, which is a result of vitamin D deficiency. The majority of Rickettsia bacteria are susceptible to antibiotics of the tetracycline group.

    The classification of Rickettsia into three groups (spotted fever, typhus, and scrub typhus) was based on serology. This grouping has since been confirmed by DNA sequencing. All three of these contain human pathogens. The scrub typhus group has been reclassified as a new genus – Orientia – but many medical textbooks still list this group under the rickettsial diseases.

    Rickettsia are more widespread than previously believed and are known to be associated with arthropods, leeches, and protists. Divisions have also been identified in the spotted fever group and this group likely should be divided into two clades.[10] Arthropod-inhabiting rickettsiae are generally associated with reproductive manipulation (such as parthenogenesis) to persist in host lineage [11]

    In March 2010, Swedish researchers reported a case of bacterial meningitis in a woman caused by Rickettsia helvetica previously thought to be harmless.[12]


    Митохондрия. Риккетсиозы.png

    Rickettsia - Wikipedia, the free encyclopedia

    Вы видите к чему принадлежат "наши" митохондрии - органеллы наших клеток, которые дышат аэробно, пока поступает достаточно кислорода, и производят энергию для нас? (Если плохо видно, откройте ссылку, схема оттуда) Наши клетки дышат митохондриями.
    Митохондрии принадлежат семейству Rickettsiaceae. Органеллы - это органеллы?
    Значит, лейкоциты как амебы (причем в точности), а органеллы клеток как облигатные внутриклеточные протеобактерии. Далее?
    Может и рассматривать их поведение как поведение амеб и бактерий?

    А рядышком с митохондриями - анаплазмы: анаплазма, эрлихия, неорикетсия, риккетсия - те, что считаются патогенными.
    Среди патогенных находится вольбрахия, которая якобы не патогенна (что странно в такой компании), и также еще не озвученная мидихлория.
    Получается, они все близкие родственники и похожи - "наши" митохондрии, анаплазмы и риккетсии, хм..



    A mitochondrion contains DNA, which is organized as several copies of a single, circular chromosome. This mitochondrial chromosome contains genes for redox proteins, such as those of the respiratory chain. The CoRR hypothesis proposes that this co-location is required for redox regulation. The mitochondrial genome codes for some RNAs of ribosomes, and the 22 tRNAs necessary for the translation of messenger RNAs into protein. The circular structure is also found in prokaryotes. The proto-mitochondrion was probably closely related to the Rickettsia.[20] However, the exact relationship of the ancestor of mitochondria to the alphaproteobacteria and whether the mitochondrion was formed at the same time or after the nucleus, remains controversial.[21]

    A recent study[22] by researchers of the University of Hawaii at Manoa and the Oregon State University indicates that the SAR11 clade of bacteria shares a relatively recent common ancestor with the mitochondria existing in most eukaryotic cells.
    Mitochondrion - Wikipedia, the free encyclopedia
     
    Последнее редактирование: 16 апр 2016
    Muss и Olena нравится это.
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    Ehrlichiosis is a tickborne[1] bacterial infection,[2] caused by bacteria of the family Anaplasmataceae, genera Ehrlichia and Anaplasma. These obligate intracellularbacteria infect and kill white blood cells.

    Signs and symptoms

    The most common symptoms include headache, muscle aches, and fatigue. @Влад A rash may occur, but is uncommon. Ehrlichiosis can also blunt the immune system by suppressing production of TNF-alpha, which may lead to opportunistic infections such as candidiasis.[citation needed]

    Most of the signs and symptoms of ehrlichiosis can likely be ascribed to the immune dysregulation that it causes.

    Late in infection, however, production of this substance[which?] can be upregulated by 30 fold, which is likely responsible for the "toxic shock-like" syndrome seen in some severe cases of ehrlichiosis. Some cases can present with purpura and in one such case the organisms were present in such overwhelming numbers that in 1991 Dr. Aileen Marty of the AFIP was able to demonstrate the bacteria in human tissues using standard stains, and later proved that the organisms were indeed Ehrlichia using immunoperoxidase stains.[8]

    Experiments in mouse models further supports this hypothesis, as mice lacking TNF-alpha I/II receptors are resistant to liver injury caused by ehrlichia infection.[9]

    3% of human monocytic ehrlichiosis cases result in death; however, these deaths occur "most commonly in immunosuppressed individuals who develop respiratory distress syndrome, hepatitis, or opportunistic nosocomial infections."[10]

    Ehrlichiosis - Wikipedia, the free encyclopedia

    .........................
    Neorickettsia is a genus of bacteria. Species or Strains in this genus are coccoid or pleomorphic cells that reside in cytoplasmicvacuoles within monocytes and macrophages of dogs, horses, bats, and humans.[1] @Olena

    Neorickettsia sennetsu causes Sennetsu ehrlichiosis,[2] Unlike most other closely related diseases, Neorickettsia sennetsu is transmitted by Trematodes from fish.[3] while Neorickettsia risticii causes Potomac Horse Fever
    Neorickettsia - Wikipedia, the free encyclopedia
    .........................

    Wolbachia(лат.) — род грамотрицательных плеоморфных бактерий из семейства Anaplasmataceae класса альфа-протобактерий, облигатные внутриклеточные симбионтычленистоногих и нематод-филярий. Обнаружены впервые в 1924году у обыкновенного комараМаршаллом Хертигом и Симеоном Буртом Вольбахом. Формальное описание было опубликовано в 1936году Хертигом, который назвал новый род в честь своего коллеги. Типовой и условно единственный вид— Wolbachiapipientis. По мнению ряда систематиков, Wolbachiapersica и Wolbachiamelophagi принадлежат другим ветвям протеобактерий (порядки Thiotrichales и Rhizobiales соответственно) и должны быть исключены из состава рода.
    Больше Wolbachia — Википедия


    Хорошо ли, когда хвост виляет собакой? (вольбахия и митохондрия)
    Проблемы Эволюции
     
    Последнее редактирование: 15 апр 2016
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    Midichloria is a genus of Gram-negative, non-sporeforming bacteria, with bacillus shape of ~0.45 µm in diameter and ~1.2 µm in length. First described in 2004 with the temporary name IricES1, Midichloria are symbionts of the hard tick Ixodes ricinus. They live in the cells of the ovary of the females of this tick species. These bacteria have been observed in the mitochondria of the host cells, a trait that has never been described in any other symbiont of animals. Midichloria bacteria seem to consume the mitochondria they parasitize, possibly using them as a source of energy and/or molecules to multiply. The interaction of these symbionts with their host is currently unknown, though the 100% prevalence in the females of the host tick seems to suggest a mutualistic association.

    Only one species, Midichloria mitochondrii, is described in this genus.[1] Molecular screenings, however, have detected the presence of related bacteria in other tick species, as well as in other blood-sucking arthropods, suggesting the possibility of horizontal transmission of these bacteria.

    It was given its own family, the Midichloriaceae in the Rickettsiales.[2] Some poorly studied candidate species belonging to this family may include Nicolleia massiliensis and the unclassified Montezuma strain.[3]

    Midichloria and the origin of mitochondria

    The Rickettsiales are widely regarded as being the closest relatives to mitochondria. Based on the fact that the Midichloria genes for the flagellum and for the cbb3 cytochrome oxidase were proven to be ancestral it was inferred that they were present in the bacterium that established the symbiosis with the ancestor of the eukaryotic cell to become the mitochondrion. The sequencing of the genome of Midichloria mitochondrii thus allowed an updated reconstruction of the free-living mitochondrial ancestor. It was a motile bacterium able to survive in microaerophilic conditions. Both these characteristics may have played an important role in the beginning of the symbiosis between the eukaryotic cell and the mitochondrion.
    Midichloria - Wikipedia, the free encyclopedia


    The Scientist Magazine
    Use the force, bacteria

    A couple of years ago, Australian postdoc Nate Lo was working at the University of Milan, looking for human pathogens in the tick species Ixodes ricinus, the main vector for Lyme disease. It was all routine until the day his PCR screening protocol revealed a novel 16S rRNA sequence. When his team took a tick apart to look for the new bug, they found it in the ovaries. And, when they looked closely at electron micrographs of infected ovarian tissues, they could see that the microbes were intracellular - living not in the cytoplasm of tick ova, but within their mitochondria.

    "We'd never seen anything like this before," Lo says, as he opens the image files on his laptop on a rainy afternoon in Sydney. "They seem to get in between the inner and outer mitochondrial membranes and eat the mitochondria up. In the end you've just got this empty sack."

    "It's a very novel observation," says Scott O'Neill, a specialist in invertebrate endosymbionts and head of the School of Integrative Science at the University of Queensland, who wasn't involved in the research. O'Neill, whose recent work has focused on the bacterium Wolbachia, says he wasn't aware of any other bacteria that live inside mitochondria. "It's pretty surprising to see a bacterial species living inside the mitochondrion, which itself was a bacterium," he says. "I think it is significant." Bill Ballard, a mitochondrial specialist from the University of New South Wales, agrees. "This is, as far as I know, the first [bacterium] that actually infects within the mitochondria," he says. "It's a pretty cool paper."

    Lo's newly found organism doesn't seem to have any negative effects on the ticks. "About half the mitochondria don't get infected," he says, "so perhaps they are only destroying old ones. We don't really know what's going on."

    Lo moved to his current post at the University of Sydney, and then wrote to scientists across Europe, Russia, North Africa, and the Middle East, asking them to send ticks for him to screen. Sure enough, he found his bugs, nestled into the ovaries of 100% of female ticks.

    Soon, Lo and his colleagues began looking for a name for their new genus, which proved easier said than done. The morphology of the organism didn't present any immediate clues, and there weren't any eminent tick bacterium researchers in whose honor it could be named.

    So Lo started surfing the Web, looking for ideas and finding nothing until one link took him to a page on the Wikipedia Web site describing midichlorians. He discovered that George Lucas had invented these creatures while dreaming up his Star Wars movies. The mysterious intracellular organisms apparently reside within the cells of almost all living things and communicate with the Force.

    Далее http://www.the-scientist.com/?articles.view/articleNo/24528/title/Use-the-force--bacteria/
     
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    Humans parasitized by the hard tick Ixodes ricinus are seropositive to Midichloria mitochondrii: is Midichloria a novel pathogen, or just a marker of tick bite?
    2012 Nov

    Abstract

    Midichloria mitochondrii is an intracellular bacterium found in the hard tick Ixodes ricinus. In this arthropod, M. mitochondrii is observed in the oocytes and in other cells of the ovary, where the symbiont is present in the cell cytoplasm and inside the mitochondria. No studies have so far investigated whether M. mitochondrii is present in the salivary glands of the tick and whether it is transmitted to vertebrates during the tick blood meal. To address the above issues, we developed a recombinant antigen of M. mitochondrii (to screen human sera) and antibodies against this antigen (for the staining of the symbiont). Using these reagents we show that (i) M. mitochondrii is present in the salivary glands of I. ricinus and that (ii) seropositivity against M. mitochondrii is highly prevalent in humans parasitized by I. ricinus (58%), while it is very low in healthy individuals (1.2%). These results provide evidence that M. mitochondrii is released with the tick saliva and raise the possibility that M. mitochondrii is infectious to vertebrates. Besides this, our study indicates that M. mitochondrii should be regarded as a package of antigens inoculated into the human host during the tick bite. This implies that the immunology of the response toward the saliva of I. ricinus is to be reconsidered on the basis of potential effects of M. mitochondrii and poses the basis for the development of novel markers for investigating the exposure of humans and animals to this tick species.

    Introduction

    Midichloria mitochondrii is an intracellular bacterium found in the hard tick Ixodes ricinus.1 In this arthropod, M. mitochondrii is abundant in diverse cell types of the ovary, including oocytes.2 No evidence has so far been published on the presence of this bacterium in the salivary glands of ticks. M. mitochondrii is peculiar in that it is observed not only in the cell cytoplasm, but also inside the mitochondria, within the intermembrane space of these organelles.1,2..

    ...There is circumstantial evidence that MALOs could be transmitted to terrestrial vertebrates during the tick bite:
    1. 16S rRNA gene sequences related with M. mitochondrii have been amplified from roe deer during a screening for tick-borne bacteria;10
    2. phylogeny of ticks and their respective MALOs are not congruent, with distantly related ticks harboring MALOs that are identical at the 16S rRNA gene level;3 this implies that MALOs could be transmitted horizontally among ticks, and a simple mechanism that could be hypothesized to explain horizontal transmission is the infection of an host parasitized by different tick species (or co-feeding with bacterial transmission without true infection);
    3. MALO 16S rRNA gene sequences have been amplified from human patients parasitized by ticks.11
    Based on the above information we designed a study to investigate whether M. mitochondrii is present in the salivary glands of the host tick I. ricinus and whether humans parasitized by I. ricinus develop antibodies against M. mitochondrii....

    Results and Discussion

    ...The antigen that we used for the above ELISA screening (rFliD) corresponds to a portion of a flagellar protein of M. mitochondrii. Thus, we did not expect any cross-reactivity towards antibodies generated during an infection caused by any other Rickettsiales. Indeed, M. mitochondrii is the sole member of the order Rickettsiales that has so far been shown to possess flagellar genes. However, I. ricinus is the main vector in Europe of the Lyme disease spirochetes (B. burgdorferi s.l.),17 bacteria that possess flagella, well known for their immunogenicity.18 One could thus argue that production of IgG antibodies in tick-exposed subjects had been induced by a Borrelia infection, and that these antibodies cross-reacted with rFliD from M. mitochondrii. Considering the numerous amino-acid differences between the FliD proteins of the two bacteria, we consider cross-reactivity rather unlikely.12 However, we decided to address this issue by screening all of the sera included in this study with a Western blot diagnostic kit for the detection of antibodies against B. burgdorferi s.l. Using this kit, positivity for B. burgdorferi s.l. was revealed in 32 out of the 80 samples of sera from the subjects exposed to tick bite; none of the healthy blood donors was positive to B. burgdorferi s.l. Among the 32 subjects positive to B. burgdorferi s.l., 11 were concurrently positive to M. mitochondrii; however, a total of 36 subjects positive to M. mitochondrii were negative to B. burgdorferi. Finally, 21 subjects were positive only to B. burgdorferi (Fig. 2). In summary, the above results show that a high proportion of the subjects positive to M. mitochondrii were not positive to B. burgdorferi (and vice-versa), indicating that the positivity to the former bacterium does not derive from the cross-reactivity with the latter...

    Conclusions

    Our work provides strong evidence for the transmission of M. mitochondrii to humans during the blood meal of I. ricinus. Based on the results here reported, we cannot conclude that M. mitochondrii replicates in the human host, determining a true infection. However, should we assume that M. mitochondrii does not replicate into the human host, we would have to conclude that the amount of bacteria (or bacterial antigens) inoculated is by itself sufficient for stimulating an antibody production. Overall, we are more prone to hypothesize that live M. mitochondrii bacteria (and not just proteins/DNA) can be inoculated into the vertebrate host, and that some replication can occur therein. At any case, our work shows that M. mitochondrii is to be regarded not only as an important symbiont of I. ricinus, but also as a package of antigens that ticks can inoculate into vertebrate hosts, and as a potential tick-borne microorganism that deserves further investigations. Among the 80 tick-exposed patients that we examined in this study, 47 were seropositive to M. mitochondrii, according to the defined threshold value.

    ... For sure, considering the high seroprevalence for M. mitochondrii that we determined in tick-exposed subjects, we would conclude that this bacterium does not cause overt pathology in humans, at least in the vast majority of the cases. On the other hand, the high seroprevalence that we recorded in tick-exposed subjects (associated with the extremely low seroprevalence in healthy blood donors) raises the possibility that M. mitochondrii plays a role in the immune response and immune-modulation determined by the I. ricinus saliva, which is important both for the success of the tick blood meal and for the establishment of the infection by the pathogens vectored by the tick.20,21 We emphasize that in the case of filarial nematodes, the discovery of Wolbachia bacterial endosymbionts in these parasites and of their immunological role led to a profound re-thinking of the immunology of filarial diseases.2224...

    Humans parasitized by the hard tick Ixodes ricinus are seropositive to Midichloria mitochondrii: is Midichloria a novel pathogen, or just a marker of tick bite?
     
    Последнее редактирование: 16 апр 2016
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    "Results for Lyme...

    "Just received my results back.. It would seem I tested negative for all the classic lyme disease tests including the SPOT test. I have however tested positive for the following:

    Midichloria mitochondrii - Positive
    D-lactate 4.74 (0.0 - 1.6)

    Has anyone else tested positive for these or know anything about them?"

    Results for Lyme...
     
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    New insights into Lyme disease

    Lyme borreliosis is transmitted through the bite of a tick that is infected by the bacterial spirochete Borrelia burgdorferi. Clinical manifestation of the disease can lead to heart conditions, neurological disorders, and inflammatory disorders. Oxidative stress has been implicated in the pathogenesis of many human diseases. The aim of this study was to investigate the mechanisms of oxidative stress and intracellular communication in Lyme borreliosis patients. Mitochondrial superoxide and cytosolic ionized calcium was measured in peripheral blood mononuclear cells (PBMCs) of Lyme borreliosis patients and healthy controls. Mitochondrial superoxide levels were significantly higher (p<0.0001) in Lyme borreliosis patients (n=32) as compared to healthy controls (n=30). Significantly low (p<0.0001) levels of cytosolic ionized calcium were also observed in Lyme borreliosis patients (n=11) when compared to healthy controls (n=11). These results indicate that there is an imbalance of reactive oxygen species and cytosolic calcium in Lyme borreliosis patients. The results further suggest that oxidative stress and interrupted intracellular communication may ultimately contribute to a condition of mitochondrial dysfunction in the immune cells of Lyme borreliosis patients.


    Introduction

    ...When an infected tick bites a host, B. burgdorferi is transmitted through the infected tick's saliva. Once transferred, B. burgdorferi stimulates the host's immune system to activate a localized inflammatory response [10]. Consequently the infection often presents itself by the presence of a “bulls-eye” rash called erythema migrans (EM) within 3–30 days post infection [11]. Once infected, B. burgdorferi disseminates and causes a variety of immunological and inflammatory reactions throughout the body...

    In order to combat an infection the host's immune cells will generate reactive oxygen species (ROS) through NADPH Oxidase (NOX; producing superoxide anion radical), and nitric oxide synthase (NOS; producing nitric oxide) [12]. The predominant generator of ROS within the cells is the mitochondria and it is believed that the major contributor to cellular oxidative damage is mitochondrial superoxide [13]. Upon the generation of superoxide (O2−•) and nitric oxide (NO), the reactive nitrogen species (RNS) peroxynitrite (ONOO−) can be formed. An example of this process is the neutrophil defense mechanism of oxidative burst which results in the mobilization of calcium and activation of NADPH oxidase leading to the subsequent generation of superoxide. Superoxide dismutase (SOD) then converts superoxide to hydrogen peroxide (H2O2), which is bactericidal [14]. These reactive species are normally kept in balance by endogenous antioxidant enzymes such as SOD and glutathione peroxidase which converts H2O2 to water [15]. However, if an imbalance occurs between ROS/RNS and the antioxidant enzymes, oxidative stress will ensue causing a toxic environment that can lead to damage of DNA, protein, and lipids [16]. In addition to creating a toxic environment for pathogens, ROS and RNS activate NF-κB. One of the major roles of the NF-κB pathway is generation of pro-inflammatory cytokines such as Interleukins 1 & 6, TNFα, and IFNγ [17]. Individuals infected by B. burgdorferi present with significantly increased levels of TNFα in their sera and synovial fluid [18,19]. This observation is similar to what is found in patients diagnosed with rheumatoid, suppurative, and reactive arthritis [19]. A number of studies have shown that in vitro stimulation of an infected individuals immune cells by either B. burgdorferi or associated proteins results in an induction of pro-inflammatory cytokines (IL-1β, IL-6, IL-17, IL-23, TNFα, and TGF β) [19–22]. Importantly, studies have shown that during an active Lyme infection or with in vitro stimulation with B. burgdorferi, both NOS and ROS are generated [22,23].

    However, the specific mechanisms of how these reactive species interact with and change intracellular communication of immune cells during an infection by B. burgdorferi are still unknown. In a previous study we addressed antigen specific T cell response to B. burgdorferi by measuring release of IFNγ [9]. The goal of this study was to explore the immune stimulated, inflammatory response to the oxidative stress state in PBMCs of Lyme borreliosis patients. To accomplish this we compared levels of mitochondrial superoxide and cytosolic ionized calcium in Lyme borreliosis patients with those in healthy controls.


    Results and discussion

    ...Dikalov also cites findings that by reducing mitochondrial ROS a resulting down regulation of NADPH oxidase occurred which ultimately broke the cycle causing oxidative stress in the cell [24]. As mentioned in the introduction, the cell has enzymatic antioxidants that serve this function. However, B. burgdorferi has been shown to passively absorb the host's cysteine [25]. Cysteine is one of the main amino acids required to synthesize glutathione (GSH), so depletion of cysteine concomitantly lowers the levels of glutathione in the host, in which GSH is a powerful antioxidant that plays a critical role in scavenging excess ROS and RNS (Fig. 3).

    Another integral molecule of cellular communication is ionized calcium (Ca2+I). Ionized calcium has a plethora of roles within the cell including maintenance of the cellular and mitochondrial membrane potentials, gene regulation, cell proliferation, and apoptosis. The level of Ca2+ in the cytosol is highly regulated and to maintain homeostasis reserves are stored in the endoplasmic reticulum or mitochondria [26]. This homeostasis can fluctuate in response to inflammation or infection. In regards to inflammation, rheumatoid arthritis patient’s PBMCs present with an approximate 22% decrease in resting cytosolic calcium when compared to un-afflicted patients [27]. However, an infection can stimulate neutrophils to activate NADPH oxidase which requires the mobilization of calcium. Since Lyme borreliosis is an infection that can lead to a severe inflammatory state, we assessed the levels of cytosolic Ca2+I in infected patient PBMCs compared with uninfected individuals (Table 1B). Our observations (Fig. 2) have shown a significant decrease in the levels of cytosolic Ca2+I in PBMCs of Lyme borreliosis patients when compared to healthy controls.

    ...A recent study has shown the effect of Lyme borreliosis on chemotaxis and migration of dendritic cells (DC) through interference of DC CD38 expression, resulting in an almost negligible level of CD38 protein [30]. These findings suggest that Borrelia may inhibit dendritic cell migration to lymph nodes through limiting calcium mobility and ultimately inhibiting further response by the host's immune cells to the site of infection [30]. This could possibly explain the significant decrease in levels of cytosolic Ca2+I we observed in Lyme borreliosis patient PBMCs (Fig. 3)

    Another possible effect of B. burgdorferi infection may be an alteration to the mitochondrial density of infected cells. Studies of other bacterial infections have shown that there is a similar outcome of oxidative stress and mitochondrial dysfunction in infected cells, but the mitochondrial density remains unchanged...


    ...In conclusion, our results have shown a significant rise in mitochondrial superoxide, indicative of a state of oxidative stress in the PBMCs of Lyme borreliosis patients. In these same patients we have presented evidence of a significant decrease in levels of cytosolic ionized calcium in PBMCs. Taken together, we hypothesize that these imbalances could cause oxidative stress, depolarization of the mitochondrial membrane, disruption of intracellular communication, and a release of pro-inflammatory cytokines [33]. All of which could ultimately contribute to a condition of mitochondrial dysfunction (Fig. 3). It is our intent to explore this mechanism in Lyme borreliosis patients further by expanding on our preliminary data and assessing additional markers for oxidative stress, intracellular communication, and the inflammatory pathways.

    New insights into Lyme disease
     
    Последнее редактирование: 17 апр 2016
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    Москва
    Хочу сдать анализы на коинфекции в германию. Все сдавать конечно дорого. Хочу услышать совет относительно того, что сдать.
    если сдавать на риккетсии и бартонеллы, какой выбрать анализ? Судя по посту это практически одно и тоже, в чем отличие и стоит ли сдавать на оба?
     

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