Commentary style article edited 1

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Commentary Style Article: Mucosal Immunology

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Title: Commentary Style Article: Mucosal Immunology
Abstract
An expansive scope of microbial pathogens is competent for getting into the
gastrointestinal tract, resulting in infectious diarrhea and colitis. The equation between different
cytokines is required to exterminate the microbial risk and prevent complex infections. The
present research proposed IL-33 as a crucial controller of the immune response to the intestinal
pathogen Citrobacter rodentium (CR). The study found that the inadequacy of the IL-33 alarming
roadmap elongates bacterial-induced colitis. Improving this route significantly deepens the
inflammatory response and makes the mice sensitive to structural infection. Spontaneously, IL33 intervenes in its noxious application by advancing gut permeability and hindering the
activation of protective T helper 17 cells at the point of infection hence damaging the protection
of the host techniques against the enteric pathogen.
Background
Infectious diarrhea and colitis resulting from pathogenic intestinal microbes express a
tremendous health challenge in the developing and developed world. Subsequently, absolute
knowledge of the contagious technique and the innate immunological response is needed to
connect and treat these infectious conditions. Citrobacter rodentium (CR) is defined as a noninvasive that effaces intestinal pathogen, infects intestinal epithelial cells (IECs), and brings
about infectious colitis in mice. Hence, it is ordinarily applied to imitate the human pathogenic
Escherichia coli infections and to perform research by studying the host-pathogen interplays.
Comparatively, with other enter pathogens, CR extracts an intense Th1 and Th17 immune
response along the colon that is crucial for evacuating infection. Th1 cells generate interferon-y

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(IFN- γ) and tumor necrosis element – α (TNF- α), advancing macrophage and cytotoxic T-cell
action. Th17 cells are activated by IL-1 β and IL-6, converting growth element –β and delivering
IL-17A, IL17A, and IL-22, which is essential for the host protection and bacterial evacuation by
activating the building of antimicrobial peptides and advancing the continuity of restrictive
intestinal duties. Whereas a suitable cytokine production is needed to ascend an effective
immune response against the microbial pathogens, too much of the release of specific cytokines
can brace the inflammatory methodology and expand the risk brought by the complexity of
infections. The IL-33, a member part of the IL-1 cytokine family, has maintained a high interest
in intestinal inflammation (Chen et al., 2019).
Study summary
With the study results, it can be reflected concerning a transitory structure of IL-33/IL17A consequences in the host return to instinct pathogens. IL-33 is highly plenty in the intestine
in stable conditions, and the communication of IL-33 or ST2 reinforces the above tissue
impairment. On the contrary, Th17 cells are fitting to the elastic immune response that begins in
the final phase of infection. Because IL-33 treatment has no damage to the immune response
final phase of CR infection, IL-17A probably reflects the authority to equalize the initial
pathogenic capability of IL-33 inside the gut. Nevertheless, other examinations are required to
improve the reciprocal management of intestinal IL-33 and IL-17A quantities during bacterial
infection.
The study summary holds its findings with an extension of the expanded spectrum of
operations of IL-33 alongside emphasizing on particular responsibility of the gut as an organ
vital with systemic immune regulatory qualities. Determining the essential and diverse duties of

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the IL-33/ST2 axis in the time of infections could aid in the development of therapeutic
involvements for the scope of infectious intestinal conditions.
Discussion
The intestinal epithelium describes one of the initial arrangements of defense against
encroaching pathogens. Indeed, it is of essence that permutation around the epithelium systems
and integrity limit is considered undesirable to any organism. Mainly, the study has
demonstrated that CR defines a non-invasive pathogen, and the condition is usually restricted to
the distal part of the colon. Accordingly, there was a view on harmful bacterial distribution
through the peripheral system alongside an intensified inflammatory structure of cytokine in
mice with CR infection. The IL-33 did respectively the treatment. The study agrees with other
studies by Sedhom and partners in which the findings showed that IL-33 proportionately
prohibits the communication of stiff protein connected in vitro and in vivo (Knoop et al., 2018).
More so, IL-33 treatment greatly intensifies intestinal penetrability in vivo, allowing for bacterial
relocation that expands the system and swells in the colon. Accordingly, for the CR infection, the
up-regulation of the antimicrobial REG3Y found in the colon was disfigured by corollary IL-33
application. Essentially, the IL-33-treated CR-infected animals were exposed to intestinal CR
hindrances. Notably, the researchers of (XIAO AND COLLEAGUES) in the recent presentation
had demonstrated that a stable state communication of REG3y in IECs of //33-/- mice are smaller
than in WT mice 24 (Naydenova et al., 2019).
Notably, IL-33 deficient mice have been published to demonstrate dysbiotic or own a
more significant application of pro-inflammatory bacteria channel of CR infection damage on
bacterial evacuation alongside the initiation of a guarding Th17 response. In the model system,
IL-33 treatment of infected mice vigorously expanded the density experienced in colonic Tregs;

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nevertheless, too much inflammation in the colon remained discovered. Directly to this result,
the exhaustibility of Foxp3+Tregs in CR-infected mice prepared with IL-33 failed to reclaim the
phenotype and improve pathology. In effect, it intimated that the harmful impacts of IL-33 are
not self-reliant on the increase of Tregs in the model.

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References
Chen, M. L., Takeda, K., & Sundrud, M. S. (2019). Emerging roles of bile acids in mucosal
immunity and inflammation. Mucosal immunology, 12(4), 851-861.
Knoop, K. A., & Newberry, R. D. (2018). Goblet cells: multifaceted players in immunity at
mucosal surfaces. Mucosal immunology, 11(6), 1551-1557.
Naydenova, K., Velikova, T., & Dimitrov, V. (2019). Interactions of allergic rhinitis and
bronchial asthma at mucosal immunology level. AIMS Allergy and Immunology, 3(1), 112.

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Summary figure and legend

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