↓ Skip to main content

The IL-23/IL-22/IL-18 axis in murine Campylobacter jejuni infection

Overview of attention for article published in Gut Pathogens, July 2016
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age
  • Above-average Attention Score compared to outputs of the same age and source (61st percentile)

Mentioned by

twitter
6 X users

Citations

dimensions_citation
18 Dimensions

Readers on

mendeley
21 Mendeley
Title
The IL-23/IL-22/IL-18 axis in murine Campylobacter jejuni infection
Published in
Gut Pathogens, July 2016
DOI 10.1186/s13099-016-0106-4
Pubmed ID
Authors

Markus M. Heimesaat, Ursula Grundmann, Marie E. Alutis, André Fischer, Ulf B. Göbel, Stefan Bereswill

Abstract

Human Campylobacter jejuni infections are worldwide on the rise. Information about the distinct molecular mechanisms underlying campylobacteriosis, however, are scarce. In the present study we investigated whether cytokines including IL-23, IL-22 and IL-18 sharing pivotal functions in host immunity were involved in mediating immunopathological responses upon C. jejuni infection. To address this, conventionally colonized IL-23p19(-/-), IL-22(-/-) and IL-18(-/-) mice were perorally infected with C. jejuni strain ATCC 43431. Respective gene-deficient, but not wildtype mice were susceptible to C. jejuni infection and could be readily colonized with highest pathogenic loads in the terminal ileum and colon at day 14 postinfection (p.i.). In IL-23p19(-/-), IL-22(-/-) and IL-18(-/-) mice viable C. jejuni were detected in MLNs, but did not translocate to spleen, liver, kidney and blood in the majority of cases. Susceptible IL-22(-/-), but neither IL-23p19(-/-), nor IL-18(-/-) mice harbored higher intestinal commensal E. coli loads when compared to resistant wildtype mice. Alike C. jejuni, commensal E. coli did not translocate from the intestinal to extra-intestinal tissue sites. Despite C. jejuni infection, mice lacking IL-23p19, IL-22 or IL-18 exhibited less apoptotic cells, but higher numbers of proliferating cells in their colonic epithelium as compared to wildtype mice at day 14 p.i. Less pronounced apoptosis was parallelled by lower abundance of neutrophils within the colonic mucosa and lamina propria of infected IL-23p19(-/-) and IL-22(-/-) as compared to wildtype control mice, whereas less distinct colonic TNF secretion could be measured in IL-22(-/-) and IL-18(-/-) than in wildtype mice at day 14 p.i. Notably, in infected IL-22(-/-) mice, colonic IL-23p19 mRNA levels were lower, whereas the other way round, colonic IL-22 expression rates were lower in IL-23p19(-/-) mice as compared to wildtype controls. Moreover, IL-18 mRNA was less distinctly expressed in large intestines of naive and infected IL-22(-/-) mice, but not vice versa, given that IL-22 mRNA levels did not differ between in IL-18(-/-) and wildtype mice. Cytokines belonging to the IL-23/IL-22/IL-18 axis mediate immunopathological responses upon murine C. jejuni infection in a differentially orchestrated manner. Future studies need to further unravel the underlying regulatory mechanisms orchestrating pathogenic-host interaction.

X Demographics

X Demographics

The data shown below were collected from the profiles of 6 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 21 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 19%
Other 3 14%
Student > Bachelor 3 14%
Researcher 2 10%
Professor 1 5%
Other 2 10%
Unknown 6 29%
Readers by discipline Count As %
Agricultural and Biological Sciences 4 19%
Medicine and Dentistry 4 19%
Immunology and Microbiology 2 10%
Biochemistry, Genetics and Molecular Biology 1 5%
Social Sciences 1 5%
Other 3 14%
Unknown 6 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 July 2016.
All research outputs
#12,767,578
of 22,880,230 outputs
Outputs from Gut Pathogens
#163
of 523 outputs
Outputs of similar age
#176,894
of 355,479 outputs
Outputs of similar age from Gut Pathogens
#6
of 18 outputs
Altmetric has tracked 22,880,230 research outputs across all sources so far. This one is in the 43rd percentile – i.e., 43% of other outputs scored the same or lower than it.
So far Altmetric has tracked 523 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.8. This one has gotten more attention than average, scoring higher than 67% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 355,479 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 49th percentile – i.e., 49% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 18 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 61% of its contemporaries.