Interleukins (ILs) are a major subclass of cytokines acting as molecular messengers playing role in immune system responses via a cascade of signaling pathways. Belonging to the cytokine family, the ILs play a crucial role in the theranostics of various diseases. Their abnormal expression leads to the development of various diseases such as cancer, neurodegenerative diseases, allergies, asthma, autoimmune diseases, and other physiological abnormalities. This paves the path of exploring the ILs for the development of sensitive and efficient biosensors and promoting them for clinical testing in a wide array of diseases. Further, detecting the level of ILs is very important for their early diagnosis and their progression within the body, and simultaneously their possible immunotherapeutic approaches. To achieve this goal, multidisciplinary scientific approaches involving immunology, electrochemistry, nanotechnology, photometry, etc. are already being put into action. The advancements in nanoscience and nanotechnology are aiding the development of highly sensitive biosensors for ILs detection. This review focuses on giving a detailed description of all the presently discovered ILs and their role in various diseases. Simultaneously, it also discusses the various electrochemical biosensors that can be employed for the detection of ILs in body fluids. Moreover, the role of nanomaterials in electrochemical biosensing is also discussed in this review.

Review—Interleukins Profiling for Biosensing Applications: Possibilities and the Future of Disease Detection

Intestinal ischemia/reperfusion (I/R) injury is a grave condition with high morbidity and mortality. We previously confirmed that intestinal I/R induces intestinal flora disorders and changes in metabolites, but the role of different metabolites in intestinal I/R injury is currently unclear. Based on targeted metabolic sequencing, pravastatin (PA) was determined to be a metabolite of the gut microbiota. Further, intestinal I/R model mice were established through superior mesenteric artery obstruction. In addition, a co-culture model of small intestinal organoids and type II innate lymphoid cells (ILC2s) was subjected to hypoxia/reoxygenation (H/R) to simulate an intestinal I/R model. Moreover, correlation analysis between the PA level in preoperative feces of patients undergoing cardiopulmonary bypass and the indices of postoperative intestinal I/R injury was carried out. IL-33-deficient mice, ILC2-deleted mice, and anti-IL-13 neutralizing antibodies were also used to explore the potential mechanism through which PA attenuates intestinal I/R injury. We demonstrated that PA levels in the preoperative stool of patients undergoing cardiopulmonary bypass were negatively correlated with the indices of postoperative intestinal I/R injury. Furthermore, PA alleviated intestinal I/R injury and improved the survival of mice. We further showed that PA promotes IL-13 release from ILC2s by activating IL-33/ST2 signaling to attenuate intestinal I/R injury. In addition, IL-13 promoted the self-renewal of intestinal stem cells by activating Notch1 and Wnt signals. Overall, results indicated that the gut microbial metabolite PA can attenuate intestinal I/R injury by promoting the release of IL-13 from ILC2s via IL-33/ST2 signaling, revealing a novel mechanism of and therapeutic strategy for intestinal I/R injury.

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Gut Microbial Metabolite Pravastatin Attenuates Intestinal Ischemia/Reperfusion Injury Through Promoting IL-13 Release From Type II Innate Lymphoid Cells via IL-33/ST2 Signaling.

The dual function of ILC2: From host protection to pathogenic players in type 2 asthma.

Viral infections are often studied in model mammalian organisms under specific pathogen-free conditions. However, in nature, coinfections are common, and infection with one organism can alter host ...

https://www.tandfonline.com/doi/pdf/10.1080/19490976.2021.1961202

Helminth-virus interactions: determinants of coinfection outcomes.

IL-33: A central cytokine in helminth infections.

Parasitic helminths are sensed by the immune system via tissue-derived alarmins that promote the initiation of the appropriate type 2 immune responses. Here we establish the nuclear alarmin cytokine IL-33 as a non-redundant trigger of specifically IL-9-driven and mast cell-mediated immunity to the intestinal parasite Strongyloides ratti. Blockade of endogenous IL-33 using a helminth-derived IL-33 inhibitor elevated intestinal parasite burdens in the context of reduced mast cell activation while stabilization of endogenous IL-33 or application of recombinant IL-33 reciprocally reduced intestinal parasite burdens and increased mast cell activation. Using gene-deficient mice, we show that application of IL-33 triggered rapid mast cell-mediated expulsion of parasites directly in the intestine, independent of the adaptive immune system, basophils, eosinophils or Gr-1+ cells but dependent on functional IL-9 receptor and innate lymphoid cells (ILC). Thereby we connect the described axis of IL-33-mediated ILC2 expansion to the rapid initiation of IL-9-mediated and mast cell-driven intestinal anti-helminth immunity.

/pdf/il-33-facilitates-rapid-expulsion-of-the-parasitic-nematode-4rldxb73d5.pdf

IL-33 facilitates rapid expulsion of the parasitic nematode Strongyloides ratti from the intestine via ILC2- and IL-9-driven mast cell activation.

https://research.birmingham.ac.uk/portal/files/120778025/1_s2.0_S1931312821000834_main.pdf

Henry J. McSorley

Papers

IL-33 facilitates rapid expulsion of the parasitic nematode Strongyloides ratti from the intestine via ILC2- and IL-9-driven mast cell activation.

Il4ra-independent vaginal eosinophil accumulation following helminth infection exacerbates epithelial ulcerative pathology of HSV-2 infection

IL-33: A central cytokine in helminth infections.

The devil's in the detail: cell-specific role of PPARγ in ILC2 activation by IL-33.