Not only for Christmas: Prophylactic oral application of <i>trans</i>-cinnamaldehyde alleviates acute murine campylobacteriosis

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Abstract

The prevalence of Campylobacter jejuni infections is increasing worldwide and responsible for significant morbidities and socioeconomic expenses. The rise in antimicrobial resistance of C. jejuni underscores the urge for evaluating antibiotics-independent compounds as therapeutic and preventive treatment options of human campylobacteriosis. Given its well-known anti-microbial and immune-modulatory properties we here surveyed the disease-modifying effects of trans-cinnamaldehyde pretreatment in experimental campylobacteriosis. Therefore, secondary abiotic IL-10 ^−/− mice were orally challenged with trans-cinnamaldehyde starting 7 days prior C. jejuni infection. Whereas gastrointestinal colonization properties of the enteropathogens remained unaffected, trans-cinnamaldehyde pretreatment did not only improve clinical signs in infected mice, but also alleviated colonic epithelial cell apoptosis on day 6 post-infection. Furthermore, trans-cinnamaldehyde application resulted in less pronounced T cell responses in the colon that were accompanied by dampened proinflammatory mediator secretion in distinct intestinal compartments. Notably, the immune-modulatory effects of trans-cinnamaldehyde were not restricted to the intestinal tract but could also be observed in extra-intestinal organs such as the liver and kidneys. In conclusion, our preclinical placebo-controlled intervention study provides first evidence that due to its immune-modulatory effects, trans-cinnamaldehyde constitutes a promising prophylactic option to alleviate campylobacteriosis.

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A guide to histomorphological evaluation of intestinal inflammation in mouse models.

Ulrike Erben, Christoph Loddenkemper, Katja Doerfel … (2014)

Histomorphology remains a powerful routine evaluating intestinal inflammation in animal models. Emphasizing the focus of a given animal study, histopathology can overstate differences between established models. We aimed to systematize histopathological evaluation of intestinal inflammation in mouse models facilitating inter-study comparisons. Samples of all parts of the intestinal tract from well-established mouse models of intestinal inflammation were evaluated from hematoxylin/eosin-stained sections and specific observations confirmed by subsequent immunohistochemistry. Three main categories sufficiently reflected the severity of histopathology independent of the localization and the overall extent of an inflammation: (i) quality and dimension of inflammatory cell infiltrates, (ii) epithelial changes and (iii) overall mucosal architecture. Scoring schemata were defined along specified criteria for each of the three categories. The direction of the initial hit proved crucial for the comparability of histological changes. Chemical noxes, infection with intestinal parasites or other models where the barrier was disturbed from outside, the luminal side, showed high levels of similarity and distinct differences to changes in the intestinal balance resulting from inside events like altered cytokine responses or disruption of the immune cell homeostasis. With a high degree of generalisation and maximum scores from 4-8 suitable scoring schemata accounted specific histopathological hallmarks. Truly integrating demands and experiences of gastroenterologists, mouse researchers, microbiologists and pathologists we provide an easy-to-use guideline evaluating histomorphology in mouse models of intestinal inflammation. Standard criteria and definitions facilitate classification and rating of new relevant models, allow comparison in animal studies and transfer of functional findings to comparable histopathologies in human disease.

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Bactericidal activities of plant essential oils and some of their isolated constituents against Campylobacter jejuni, Escherichia coli, Listeria monocytogenes, and Salmonella enterica.

Mendel Friedman, Philip R Henika, Robert E. Mandrell (2002)

An improved method of sample preparation was used in a microplate assay to evaluate the bactericidal activity levels of 96 essential oils and 23 oil compounds against Campylobacter jejuni, Escherichia coli O157:H7, Listeria monocytogenes, and Salmonella enterica obtained from food and clinical sources. Bactericidal activity (BA50) was defined as the percentage of the sample in the assay mixture that resulted in a 50% decrease in CFU relative to a buffer control. Twenty-seven oils and 12 compounds were active against all four species of bacteria. The oils that were most active against C. jejuni (with BA50 values ranging from 0.003 to 0.009) were marigold, ginger root, jasmine, patchouli, gardenia, cedarwood, carrot seed, celery seed, mugwort, spikenard, and orange bitter oils; those that were most active against E. coli (with BA50 values ranging from 0.046 to 0.14) were oregano, thyme, cinnamon, palmarosa, bay leaf, clove bud, lemon grass, and allspice oils; those that were most active against L monocytogenes (with BA50 values ranging from 0.057 to 0.092) were gardenia, cedarwood, bay leaf, clove bud, oregano, cinnamon, allspice, thyme, and patchouli oils; and those that were most active against S. enterica (with BA50 values ranging from 0.045 to 0.14) were thyme, oregano, cinnamon, clove bud, allspice, bay leaf, palmarosa, and marjoram oils. The oil compounds that were most active against C. jejuni (with BA50 values ranging from 0.003 to 0.034) were cinnamaldehyde, estragole, carvacrol, benzaldehyde, citral, thymol, eugenol, perillaldehyde, carvone R, and geranyl acetate; those that were most active against E. coli (with BA50 values ranging from 0.057 to 0.28) were carvacrol, cinnamaldehyde, thymol, eugenol, salicylaldehyde, geraniol, isoeugenol, citral, perillaldehyde, and estragole; those that were most active against L monocytogenes (with BA50 values ranging from 0.019 to 0.43) were cinnamaldehyde, eugenol, thymol, carvacrol, citral, geraniol, perillaldehyde, carvone S, estragole, and salicylaldehyde; and those that were most active against S. enterica (with BA50 values ranging from 0.034 to 0.21) were thymol, cinnamaldehyde, carvacrol, eugenol, salicylaldehyde, geraniol, isoeugenol, terpineol, perillaldehyde, and estragole. The possible significance of these results with regard to food microbiology is discussed.

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Gram-negative bacteria aggravate murine small intestinal Th1-type immunopathology following oral infection with Toxoplasma gondii.

Markus M Heimesaat, Stefan Bereswill, André Fischer … (2006)

Oral infection of susceptible mice with Toxoplasma gondii results in Th1-type immunopathology in the ileum. We investigated gut flora changes during ileitis and determined contributions of gut bacteria to intestinal inflammation. Analysis of the intestinal microflora revealed that ileitis was accompanied by increasing bacterial load, decreasing species diversity, and bacterial translocation. Gram-negative bacteria identified as Escherichia coli and Bacteroides/Prevotella spp. accumulated in inflamed ileum at high concentrations. Prophylactic or therapeutic administration of ciprofloxacin and/or metronidazole ameliorated ileal immunopathology and reduced intestinal NO and IFN-gamma levels. Most strikingly, gnotobiotic mice in which cultivable gut bacteria were removed by quintuple antibiotic treatment did not develop ileitis after Toxoplasma gondii infection. A reduction in total numbers of lymphocytes was observed in the lamina propria of specific pathogen-free (SPF), but not gnotobiotic, mice upon development of ileitis. Relative numbers of CD4(+) T cells did not differ in naive vs infected gnotobiotic or SPF mice, but infected SPF mice showed a significant increase in the frequencies of activated CD4(+) T cells compared with gnotobiotic mice. Furthermore, recolonization with total gut flora, E. coli, or Bacteroides/Prevotella spp., but not Lactobacillus johnsonii, induced immunopathology in gnotobiotic mice. Animals recolonized with E. coli and/or total gut flora, but not L. johnsonii, showed elevated ileal NO and/or IFN-gamma levels. In conclusion, Gram-negative bacteria, i.e., E. coli, aggravate pathogen-induced intestinal Th1-type immunopathology. Thus, pathogen-induced acute ileitis may prove useful to study bacteria-host interactions in small intestinal inflammation and to test novel therapies based on modulation of gut flora.

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Author and article information

Contributors

Markus M. Heimesaat:

ORCID: 0000-0001-6399-651X

Journal

Journal ID (publisher-id): 1886

Title: European Journal of Microbiology and Immunology

Abbreviated Title: EuJMI

Publisher: Akadémiai Kiadó (Budapest )

ISSN (Print): 2062-509X

ISSN (Electronic): 2062-8633

Publication date (Electronic): 01 September 2023

Publication date (Print): 13 October 2023

Volume: 13

Issue: 2

Pages: 45-56

Affiliations

[1] Gastrointestinal Microbiology Research Group, Institute of Microbiology, Infectious Diseases and Immunology, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health , 12203 Berlin, Germany

Author notes

[* ]Corresponding author. Gastrointestinal Microbiology Research Group, Institute of Microbiology, Infectious Diseases and Immunology, Charité - Universitätsmedizin Berlin , Hindenburgdamm 30, D-12203 Berlin, Germany. Tel.: +49 30 450524318. E-mail: markus.heimesaat@ 123456charite.de

Author information

Markus M. Heimesaat https://orcid.org/0000-0001-6399-651X

Article

DOI: 10.1556/1886.2023.00024

PMC ID: 10578138

PubMed ID: 37656630

SO-VID: 8e24b2d9-6669-4a22-a422-c79afda20b16

License:

Open Access statement. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes – if any – are indicated.