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This review elaborates the development of germfree and gnotobiotic animal models and their application in the scientific field to unravel mechanisms underlying host—microbe interactions and distinct diseases. Strictly germfree animals are raised in isolators and not colonized by any organism at all. The germfree state is continuously maintained by birth, raising, housing and breeding under strict sterile conditions. However, isolator raised germfree mice are exposed to a stressful environment and exert an underdeveloped immune system. To circumvent these physiological disadvantages depletion of the bacterial microbiota in conventionally raised and housed mice by antibiotic treatment has become an alternative approach. While fungi and parasites are not affected by antibiosis, the bacterial microbiota in these “secondary abiotic mice” have been shown to be virtually eradicated. Recolonization of isolator raised germfree animals or secondary abiotic mice results in a gnotobiotic state. Both, germfree and gnotobiotic mice have been successfully used to investigate biological functions of the conventional microbiota in health and disease. Particularly for the development of novel clinical applications germfree mice are widely used tools, as summarized in this review further focusing on the modulation of bacterial microbiota in laboratory mice to better mimic conditions in the human host.

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dissecting the molecular mechanisms of the interplay between pathogens, commensal microbiota, and host immunity during infection and inflammation [ 13 ]. To accomplish this, secondary abiotic mice were subjected to human FMT, and the human microbiota could

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opportunities to elucidate the molecular mechanisms underlying the interplay between pathogen(s), the human commensal gut microbiota, and host immune responses during intestinal inflammation. In the present study, we show that NAP exerts anti

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sepsis. Immune Dysfunction in Sepsis Cytokines play a critical role in the host immune response to infection. A coordinated cytokine response is essential for creating an appropriate host immune response and for its resolution

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U , Bereswill S , Heimesaat MM : Dissecting the interplay between intestinal microbiota and host immunity in health and disease: lessons learned from germfree and gnotobiotic animal models . Eur J Microbiol Immunol (Bp) 6 , 253

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Congenital human cytomegalovirus (CMV) infection is the leading infectious cause of mental retardation, sensorineural deafness and visual impairment. It is mainly related to a primary maternal infection. The placenta should be considered the most important site of both the protection of the fetus from CMV infection and the transmission of CMV from mother to fetus. The control of the passage of CMV across the placenta probably involves a cascade of regulatory events. Roles are played by factors relating to the host immune-selective pressures, such as local cytokines and maternal CMV-specific neutralizing antibodies. The presence of other pathogens at the maternal-fetal interface also influences the outcome of CMV infection. Further investigations are needed in which clinical CMV strains are applied in in vitro studies to unravel the molecular mechanism of the intrauterine transmission of CMV and to elucidate the complex regulation that leads to prevention of the in utero transmission of CMV in vivo.

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Patrinia scabra Bunge has long been used in clinic as a traditional Chinese medicine for treating leukemia and cancer and regulating host immune response. Despite their wide use in China, no report on system analysis on their chemical constituents is available so far. The current study was designed to profile the fingerprint of ethyl acetate extract of it, and in addition, to characterize the major fingerprint peaks and determine their quantity. Therefore, a detailed gradient high-performance liquid chromatography was described to separate more than 30 compounds with satisfactory resolution in P. scabra Bunge. Based on the chromatograms of 10 batches samples, a typical high-performance liquid chromatographic (HPLC) fingerprint was established with 23 chromatographic peaks being assigned as common fingerprint peaks. Furthermore, a quadrupole time of flight mass spectrometry (Q-TOF/MS) was coupled for the characterization of major compound. As (+)-nortrachelogenin was the most predominant compound in P. scabra Bunge, the quantification on it was also carried out with the method being validated. As a result, (+)-nortrachelogenin was found to be from 1.33 to 2.21 mg g−1 in this plant material. This rapid and effective analytical method could be employed for quality assessment of P. scabra Bunge, as well as pharmaceutical products containing this herbal material.

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Human immunodeficiency virus (HIV) infections cause severe CD4+ T cell depletion leading to chronic inflammation and immune activation, impaired barrier function, and microbial translocation. Even under effective antiretroviral therapy, these processes persist, leading to gut microbiome dysbiosis and disturbance of microbiome–host homeostasis. This systematic review aims at analyzing how gut microbiome and host immune system influence each other during HIV pathogenesis. An online search applying the PubMed database was conducted. The number of total results (n = 35) was narrowed down to 5 relevant studies focusing on the interaction between the host and gut microbiome, whereas strict exclusion criteria were applied, thereby assuring that no other comorbidities impacted study results. Our analyses revealed that gut microbiome diversity correlated positively with CD4+ T cell counts and negatively with microbial translocation markers. However, quantitative changes in bacterial richness did not consistently correlate with the numbers of metabolically active bacterial populations. Despite the reported increase in potentially pathogenic bacteria and, conversely, decrease in protective populations, the gut microbiota exhibited immune-modulating qualities given that mucosal inflammatory sequelae were dampened by decreasing pro-inflammatory and accelerating anti-inflammatory cytokine responses. Future research is needed to further elucidate these findings, to gain a deeper insight into host–microbiota interactions and to develop novel therapeutic strategies.

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Orvosi Hetilap
Authors: Olivér Rosero, Tibor Kovács, Péter Ónody, László Harsányi and Attila Szijártó

A gastrointestinalis traktus a táplálék feldolgozásában betöltött emésztő-, illetve felszívófunkcióján túl kiemelkedő jelentőséggel bír a béllumenben lévő patogénekkel szemben, megakadályozva azok keringésbe jutását, és fontos szerepet játszik az immunhomeosztázis fenntartásában. Bakteriális transzlokáció alatt a gyomor-bél rendszer életképes baktériumainak vagy bakteriális termékeinek különböző, extraintestinalis szövetekbe jutása értendő. A kóros jelenséget számos klinikai kórkép kapcsán azonosították. A bakteriális transzlokáció kialakulására prediszponáló, alapvető feltételek közé tartozik a bél mikroflórájának megváltozása, a nyálkahártya-integritás sérülése, valamint a gazdaszervezet immunhiányos állapota. A bakteriális transzlokáció fellépése megnövekedett szövődményekkel és mortalitási rátával párosul, ezért a jövőben fontos mérlegelendő szempontot kell képeznie a kockázati csoportba tartozó betegek terápiás algoritmusának felállítása során. Orv. Hetil., 2014, 155(8), 304–312.

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Host immune responses are pivotal for combating enteropathogenic infections. We here assessed the impact of the innate receptor nucleotide oligomerization domain protein 2 (NOD2) in murine Campylobacter jejuni-infection. Conventionally colonized IL-10−/− mice lacking NOD2 and IL-10−/− controls were perorally challenged with C. jejuni strain 81-176 and displayed comparable pathogenic colonization of intestines until day 14 postinfection (p.i.). Whereas overall intestinal microbiota compositions were comparable in naive mice, NOD2−/− IL-10−/− mice exhibited less fecal bifidobacteria and lactobacilli than IL-10−/− counterparts after infection. Interestingly, NOD2−/− IL-10−/− mice were clinically more compromised during the early phase of infection, whereas, conversely, IL-10−/− animals exhibited more frequently bloody feces lateron. While colonic apoptotic cell and T lymphocyte numbers were comparable in either C. jejuni-infected mice, B lymphocytes were lower in the colon of infected NOD2−/− IL-10−/− mice versus controls. At day 14 p.i., colonic TNF and IL-23p19 mRNA levels were upregulated in NOD2−/− IL-10−/− mice only. Translocation rates of intestinal commensals to mesenteric lymphnodes and extra-intestinal compartments including liver and kidney were comparable, whereas viable bacteria were more frequently detected in spleens derived from IL-10−/− as compared to NOD2−/− IL-10−/− mice. In conclusion, NOD2 is involved during C. jejuni infection in conventionally colonized IL-10−/− mice in a time-dependent manner.

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