The appendix‐mucosal immunity and tolerance in the gut: consequences for the syndromes of appendicitis and its epidemiology

Costa, Alan de

doi:10.1111/ans.17522

Cited by 8 publications

(7 citation statements)

References 71 publications

(232 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Eosinophil infiltration, mast cell degranulation, and muscle oedema are features of hypersensitivity type I reaction that are common in AA [ 4 ]. The Th2 cells, through IL production, are responsible for a type I hypersensitivity reaction, with eosinophils being involved via IL-5, which controls the recruitment and function of eosinophils in target tissues [ 18 , 30 , 31 ]. Eosinophils are implicated in the initiation and maintenance of type 2 immune responses [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

IL-5 Serum and Appendicular Lavage Fluid Concentrations Correlate with Eosinophilic Infiltration in the Appendicular Wall Supporting a Role for a Hypersensitivity Type I Reaction in Acute Appendicitis

Carvalho

Carolino

Coelho

et al. 2022

IJMS

View full text Add to dashboard Cite

Appendicitis is the most common abdominal surgical emergency, but its aetiology is not fully understood. We and others have proposed that allergic responses play significant roles in its pathophysiology. Eosinophils and Interleukin (IL)-5 are involved in a hypersensitivity type I reaction. Eosinophil infiltration is common in the allergic target organ and is dependent on IL-5. In the presence of an allergic component, it is expected that the eosinophil count and IL-5 local and systemic concentrations become elevated. To address this hypothesis, we designed a prospective study that included 65 patients with acute appendicitis (grouped as acute phlegmonous or gangrenous according to the histological definition) and 18 patients with the clinical diagnosis of acute appendicitis, but with normal histological findings (control group) were enrolled. Eosinophil blood counts and appendicular wall eosinophil infiltration were determined. IL-5 levels in blood and appendicular lavage fluid were evaluated. Appendicular lavage fluid was collected by a new methodology developed and standardized by our group. Appendicular wall eosinophil infiltration was higher in acute phlegmonous appendicitis than in gangrenous appendicitis (p = 0.000). IL-5 blood levels were similar in both pathologic and control groups (p > 0.05). In the appendicular lavage fluid, the higher levels of IL-5 were observed in the phlegmonous appendicitis group (p = 0.056). We found a positive correlation between the appendicular wall eosinophilic infiltration and the IL-5 concentrations, in both the blood and the appendicular lavage fluid, supporting the IL-5 reliance in eosinophil local infiltration. We observed the highest presence of eosinophils at phlegmonous appendicitis walls. In conclusion, the present data are compatible with a hypersensitivity type I allergic reaction in the target organ, the appendix, during the phlegmonous phase of appendicitis.

show abstract

Section: Discussionmentioning

confidence: 99%

IL-5 Serum and Appendicular Lavage Fluid Concentrations Correlate with Eosinophilic Infiltration in the Appendicular Wall Supporting a Role for a Hypersensitivity Type I Reaction in Acute Appendicitis

Carvalho

Carolino

Coelho

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…Th2 cells secrete Th2 cytokines, such as IL-4, IL-5, IL-9 and IL-13, and stimulate B cells to produce antibodies, in particular IgE in the course of humoral-mediated immunity [61,65,66] (Figure 1).…”

Section: T-lymphocytes: Il-4 Il-5 Il-9 and Il-13mentioning

confidence: 99%

Compilation of Evidence Supporting the Role of a T Helper 2 Reaction in the Pathogenesis of Acute Appendicitis

Carvalho,

Barreira,

Henriques

et al. 2024

IJMS

View full text Add to dashboard Cite

Despite being the most common abdominal surgical emergency, the cause of acute appendicitis (AA) remains unclear, since in recent decades little progress has been made regarding its etiology. Obstruction of the appendicular lumen has been traditionally presented as the initial event of AA; however, this is often the exception rather than the rule, as experimental data suggest that obstruction is not an important causal factor in AA, despite possibly occurring as a consequence of the inflammatory process. Type I hypersensitivity reaction has been extensively studied, involving Th2 lymphocytes, and cytokines such as IL-4, IL-5, IL-9 and IL-13, which have well-defined functions, such as a positive-feedback effect on Th0 for differentiating into Th2 cells, recruitment of eosinophils and the release of eosinophilic proteins and the production of IgE with the activation of mast cells, with the release of proteins from their granules. Cytotoxic activity and tissue damage will be responsible for the clinical manifestation of the allergy. AA histological features are similar to those found in allergic reactions like asthma. The intestine has all the components for an allergic immune response. It has contact with hundreds of antigens daily, most of them harmless, but some can potentially induce an allergic response. In recent years, researchers have been trying to assess if allergy is a component of AA, with their latest advances in the understanding of AA as a Th2 reaction shown by the authors of this article.

show abstract

“…Increase in the expression would be explained by an alteration of the intestinal microflora that occurs along the pathogenesis of appendicitis. Moreover, the CD51 cells also produce anti-self antibodies and an anti-inflammatory molecule such as IL-10 which means the increase of the expression was process to prevent inflammation currently occurring [27].…”

Section: Recovery Process In Appendicitismentioning

confidence: 99%

Endothelial Dysfunction in Appendicitis

Fikri¹,

Alnaz²,

Alnaz³

2023

Endothelial Dysfunction - A Novel Paradigm

View full text Add to dashboard Cite

In an inflammation, including appendicitis, vascular adequacy is required to supply anti-inflammatory substances and nutrition due to inflamed tissue remodeling. Normal tissue has balanced tissue regeneration and tissue destruction from apoptosis. While in inflammation, inflammatory substances tend to cause tissue destruction and lead to necrosis. This requires the tissue to increase cell regeneration to maintain tissue homeostasis in the appendix, induced mainly by oxygenation, nutrition, growth factors, and mainly anti-inflammatory substances that are obtained with vascular adequacy. This process needs active vascularization that can be achieved with neovascularization to ensure good vascularization to the tissue lacking from vascular damage. The ability of neovascularization is mainly related to growth factors acting in the endothelium and inducing neovascularization process. This mechanism is impaired in the process of inflammation by inflammatory substances causing endothelial dysfunction. As stated that vascular adequacy is related to growth factors such as vascular endothelial growth factors (VEGF) that may differ from one person to another, external and internal factors plays role in affecting individualized difference in adapting to inflammatory process, the expression of the VEGF may be a novel distinction to cut-off requirements of inflammation process in appendicitis would be self-limiting or continue to cause tissue necrosis and perforating appendicitis that urges surgical treatment to encounter the unstoppable inflammatory process in the appendix.

show abstract

The appendix‐mucosal immunity and tolerance in the gut: consequences for the syndromes of appendicitis and its epidemiology

Cited by 8 publications

References 71 publications

IL-5 Serum and Appendicular Lavage Fluid Concentrations Correlate with Eosinophilic Infiltration in the Appendicular Wall Supporting a Role for a Hypersensitivity Type I Reaction in Acute Appendicitis

IL-5 Serum and Appendicular Lavage Fluid Concentrations Correlate with Eosinophilic Infiltration in the Appendicular Wall Supporting a Role for a Hypersensitivity Type I Reaction in Acute Appendicitis

Compilation of Evidence Supporting the Role of a T Helper 2 Reaction in the Pathogenesis of Acute Appendicitis

Endothelial Dysfunction in Appendicitis

Contact Info

Product

Resources

About