Willi von Bellden (German Edition)

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The possibility of subjugation to German influence with all of its liability for external strife. The answer is one which future events will determine. In this book the author has tried to tell what forces and influences are sharpening each of the three horns. There are bandits, disloyal Mexicans, ambitious officials, patriotic citizens, honest business men, Teutonic intriguers, spies, propagandists, diplomats, millionaires, army officers and I.

Is it any wonder, then, that Mexico finds herself in such a Dilemma? Mexico has always been a home and workshop for foreigners. Several thousand years ago the Chinese settled in that country and, judging from the relics which are found to-day, in and about Mexico City, Chinese civilisation flourished there for a few hundred years. After the Chinese civilisation disappeared the Aztec and pre-Aztec Indians dominated the land. A few hundred years ago the Spaniards landed and Mexico passed through a period of conquest which ended with the execution of the Austrian, Emperor Maximilian.

And to-day, in Monterey is preserved the rifle which was used at this execution, preserved even by the Rebels during the revolutions. A few decades ago English, French and American capitalists went to Mexico to develop the wonderfully rich resources, and Mexico under President Porfirio Diaz became a great, internationally respected nation. The revolution which overthrew Diaz drove thousands of these foreigners from the country, and the immigration of Germans and Austrians, which had started earlier, increased until to-day the Teuton strength is so great that Mexican politics is interwoven with German intrigue.

Where a few years ago The Mexican Herald , an English language newspaper, had a wide circulation and commanded the respect and attention of all foreigners, there is to-day a Deutsche Zeitung von Mexico. Germany is active in Mexico, honestly and dishonestly. Most of the things which the Germans are doing there, both against the United States and against Mexico itself, are done at the direction of Berlin.

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Who would have expected Mexico to think of invading the United States to "get back" American territory until it was suggested to the German Minister in Mexico City by Dr. Alfred Zimmermann, former Secretary of State? What honest, intelligent Mexican favours war with the United States when there is nothing to gain for Mexico except flattery from Berlin? What capable Mexican business man, or government official, favours labour riots at Tampico to cut off the oil supply which is bringing millions of dollars to the Mexican Treasury?

What is there for Mexico to gain if the oil wells and mines are destroyed?

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    Written in the nineteenth century, this work comprises of translations of medieval Persian Chronicles. Hitherto, the underlying mechanism of ColIb-release or secretion triggered by the SOS response is not known. In conclusion, we reason that increased cirA expression and consequential high susceptibility of E. Interestingly, several other colicins parasitize siderophore outer membrane receptors, which are all under control of the Fur-regulon. This suggests that increased sensitivity to colicin-mediated killing under iron depletion may also apply for other colicins binding to TonB-dependent outer-membrane transporters.

    Previously, it was shown that killing of susceptible bacteria by pyocin, a bacteriocin produced by Pseudomomas spp. Pyocin binds the ferri-pyoverdine receptor FpvA, which is controlled by Fur. In summary, physiological changes of the murine intestine upon Salmonella -induced colitis are likely to provide the environmental cues required for upregulation of both, ColIb and its receptor CirA.

    Yet, we cannot rule out that other physiological parameters altered in the inflamed gut also contribute to the observed phenotype. So far, it is unclear if expression of other types of colicins as well as other Enterobacteriaceae -derived bacteriocins microcins, pyocins, klebicins would be upregulated in the inflamed gut. The majority of these bacteriocins is only under control of the SOS response and repressed by LexA and not regulated in a Fur-dependent fashion.

    Thus, it remains to be shown if the principle of colicin-colicin-receptor upregulation in the inflamed gut also applies to other bacteriocins and their respective receptors. Supposedly, colicins play a major role in mediating bacterial population dynamics [54]. In contrast, a number of other studies reported that high bacteriocidal activity against closely related, sensitive strains observed in vitro could not be recapitulated in in vivo experiments see below.

    Our data presented in this paper might explain this puzzling observation: we suggest that the fitness benefit of colicin production strongly depends on the environmental conditions prevailing in the gut. Under normal conditions, colicin expression and expression of their cognate receptors may not be stimulated enough to induce colicin-dependent inhibition of the sensitive strain. In the absence of gut inflammation, S. Tm did not benefit from ColIb in competition with E. Likewise, competition experiments in germfree mice with a colicin-producing E.

    The underlying reasons for the absence of an overt fitness-benefit of colicin production were attributed to colicin inactivation by intestinal proteases [33] , acquisition of colicin-resistances [55] or absent colicin activity under anaerobic conditions [35] , [36]. Our study suggests that absence of inflammatory conditions might be an additional explanation. Colicin production is a common trait in E. Many experimental and theoretical studies have addressed the ecological consequences of colicin production in bacterial populations [58] , [59]. In general, it is assumed, that colicins afford a competitive advantage to the strain producing it.

    However, the producer pays a fitness cost due to the higher metabolic load of colicin synthesis as well as lethality of production e. In recA negative strains decreased frequencies of colicin producers were observed, suggesting that the rate of colicin production is regulated by the SOS response [60]. Nevertheless, colicin expression needs to be tightly controlled to ensure, that the fraction of producers is kept at low rates under conditions, when colicin is not required.

    Those conditions include the lack of stress, nutrient starvation but also the absence of any direct competitors. Thus, we assume that colicin production of a bacterial population should be confined to environmental niches which are characterized by high density and diversity of competing E. Thus, the intestinal mucus layer is one highly competitive environment for E. In contrast, we identify inflammation-induced blooms as an alternative niche for colicin-dependent Enterobacterial competition Figure 8.

    Enterobacterial blooms can contain multiple closely-related species at high concentrations which likely compete for the same resources. Under this highly competitive situation, the chances are increased that colicin-sensitive competitors are present at high numbers. Thus, the bacteria may benefit hugely from colicin production under this environmental condition. Moreover, the population size of the colicin-producer is large enough to tolerate loss of a fraction of the population due to suicidal colicin production.

    In summary, the results presented here provide evidence that intestinal inflammation drives colicin-dependent competition by bacteria of the Enterobacteriaceae family. These findings shed new light on the role of colicins as important fitness factors providing a competitive advantage for growth in Enterobacterial blooms.

    The permit no. Low-complexity microbiota LCM mice were generated by associating germfree mice with members of the Altered Schaedler flora [65] as described previously [66]. Tm or mixtures of S. Histology of the cecum was done at necropsy. Cecum tissue was embedded in O.

    Sakura, Torrance and flash frozen. The parameters submucosal edema, PMN infiltration, loss of goblet cells and epithelial damage were scored according to the severity of inflammatory symptoms yielding a total score of 0—13 points. For infections, E. Tm strains were grown as described [67].

    Briefly, cultures in LB supplemented with 0. Bacterial strains and plasmids used in this study are listed in Table 1. The P2 plasmid was cured from S. For generation of pM, the cib promoter from E. Four microliters of the Gibson assembly mix were transformed into chemically competent E. Constructs were verified using colony PCR, restriction analysis and sequencing. For annotation of transcription factor binding sites Fur and LexA regulon , all known transcription factor binding sites of each family one were taken from RegulonDB version 8.

    The nucleotide sequences of the cib S. FQ and cirA promoter regions E. For expression of ColIb-His, we used E. For expression of cirA -His we used E. At OD between 0. ColIb-His was eluted with 5 mM Imidazole. Control and immune serum were received from bleedings day 61, 90 and post immunization. For measuring colicin production and -sensitivity, the colicin-producing strain was grown o.

    The plate was overlaid with the tester strain in top-agar 0. Growth of the tester strain was analyzed after 24 h. Formation of an inhibition zone halo around the producer indicated production of colicin and sensitivity of the tester strain. Starter cultures of E. Following supplements were used: 0.

    Luciferase assays were performed as described [75]. For luciferase assay from bacteria extracted from cecum content, the cecum content was harvested from infected mice and shortly stored on ice. A defined volume i. The samples were then thawn and processed as described above. Only values above detection limit control cecum content were considered. The relative luminescence units rlu per cfu luciferase-reporter strain were calculated. Starter culture of 3 ml LB, grown for 12 h was used for inoculation of 3 ml LB with supplements grown for 4 h.

    Total protein was quantified in the lysate using protein assay reagent BioRad. Proteins were separated by SDS gel electrophoresis [76]. Proteins were transferred onto a nitrocellulose membrane GE Healthcare at mA for 2 h. The membrane was blocked in PBS 0. For detection of E. P-values less than 0.

    Halo-assay to confirm phenotypes of ColIb production and susceptibility. Tm wt was spotted on LB agar plates containing mitomycin C and incubated o.

    Article excerpt

    B Plasmid-based complementation of the ColIb-deficient S. Tm mutant S. Ec MG was cultivated in LB medium o. The experiments were done in triplicates and the diameter of the ColIb inhibition zone halo was measured after 24 hours. The detection limit dotted line is the average size of the S. Tm wt colony. Nucleotide sequence of S. Tm wt cib imm and its respective promoter regions. Fur- and LexA repressor binding sites were annotated to the cib and imm sequence region of S.

    Tm wt as described in the materials and methods section. Nucleotide sequence of Ec MG cirA and its promoter region. Fur-repressor binding site was annotated to the cirA sequence region of Ec MG as described in the materials and methods section. Overnight cultures of indicated S. Tm DnaK was detected as loading control A. ColIb dependent competition of complemented S. Plasmid-based reconstitution of cib and cirA to the mutant strains leads to an over-complementation apparent by ColIb-dependent killing of E. Primers used in this study. All PCR primer sequences used in the study are listed.

    Abstract The host's immune system plays a key role in modulating growth of pathogens and the intestinal microbiota in the gut. Author Summary Colicins are bacterial protein toxins which show potent activity against sensitive strains in vitro. Competing interests: The authors declare no competing financial interests. Introduction Enteric Salmonella enterica serovar Typhimurium S. Results ColIb affords S.

    Tm a growth advantage over colicin-sensitive E. Download: PPT. Figure 1. Colicin-dependent competition of S. Figure 2. Regulation of S. Figure 3. Expression of S. Figure 4. Figure 5. Induction of cirA expression increases sensitivity to ColIb of E. ColIb-dependent competition of S.

    Figure 6. ColIb dependent competition of S. Inflammation-induced Enterobacterial blooms foster cib and cirA expression in vivo The in vitro co-culture experiments of S. Figure 7. Tm ColIb and the E. Figure 8. Model for the role of colicins for bacterial competition in inflammation-induced blooms. Colicin-dependent bacterial competition is enhanced in the inflamed gut Supposedly, colicins play a major role in mediating bacterial population dynamics [54].

    Implications for the evolution of colicin-dependent competition Colicin production is a common trait in E. Construction of bacterial mutants and plasmids Bacterial strains and plasmids used in this study are listed in Table 1. Identification of regulator binding sites For annotation of transcription factor binding sites Fur and LexA regulon , all known transcription factor binding sites of each family one were taken from RegulonDB version 8.

    Colicin killing-assay For measuring colicin production and -sensitivity, the colicin-producing strain was grown o. Luciferase assay Luciferase assays were performed as described [75]. Supporting Information. Figure S1.

    Willi von Bellden (German Edition) Willi von Bellden (German Edition)
    Willi von Bellden (German Edition) Willi von Bellden (German Edition)
    Willi von Bellden (German Edition) Willi von Bellden (German Edition)
    Willi von Bellden (German Edition) Willi von Bellden (German Edition)
    Willi von Bellden (German Edition) Willi von Bellden (German Edition)
    Willi von Bellden (German Edition) Willi von Bellden (German Edition)
    Willi von Bellden (German Edition) Willi von Bellden (German Edition)
    Willi von Bellden (German Edition) Willi von Bellden (German Edition)
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