The chemical that brings eosinophils to the surface is eotaxin. It's part of the CC group. Eosinophils are white blood cells involved in the immune system, allergies and parasitic infections. Team members are epithelial cells from the lung and bronchi that make it when they are stimulated by interleukin-4 (again, suppressed by gamma interferon). Usually, it is applied to lure eosinophils to points of allergic irritation.
Eotaxin Family
- Interleukin-5 (IL-5)
- Eotaxin (Eotaxin-1, Eotaxin-2 and Eotaxin-3)
- Tumor necrosis factor (TNF)
- Interleukin-4 (IL-4)
These chemokine cousins are also involved in immunity: they can rub against special eosinophil receptors, which in turn send the cells wandering to a site of infection or inflammation. Excessive eosinophil activation or overproduction during physical conditions like asthma and allergic rhinitis can damage and inflame tissues.
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Diseases Associated with Eotaxin
There is a role for eotaxins in all sorts of disease but eosinophilia and inflammation are not different. Here are a few of the diseases linked to eosinophil chemoattractants:
| Allergic Diseases |
| It's also often the lungs that are invaded by eosinophils in allergic conditions, like allergic rhinitis and asthma. |
| Eosinophilic Esophagitis |
| It's a condition in which the eosinophils that live on the esophagus overpopulate and it's caused by food intolerance. |
| Urticaria |
| Eosinophilic and other immune cell-producing eczema-related skin disease. |
| Eosinophilic Pneumonia |
| A pneumonia of eosinophilia (drug-, infection- or allergic). |
| Autoimmune Diseases |
| Eosinophils could even be responsible for some autoimmune diseases (such as systemic lupus erythematosus). |
| Parasitic Infections |
| Eosinophils are the parasite-killers (pinworms, hookworms) and inflammation breeds more. |
Eotaxins Expressed on Bronchial Epithelial Cells
Bronchial Epithelial Cells
Of the airway's largest cells, perhaps most commonly bronchial epithelial cells, which close off the path and expel mucus to clean out bacteria and dust. But they are also involved in airway inflammation and can release multiple cytokines and chemokines to guide migration and activation of immune cells.
Eosinophils
Eosinophils are white blood cells that are mostly involved in allergy and anti-parasite immunity. A cold and other allergies swell eosinophil counts, swelling the airways.
Eosinophil Chemoattractant
Depending on the species, bronchial epithelial cells release chemokines (IL-5, eotaxin, etc. ), which can entice eosinophils to the site of airway inflammation, where they swarm and fire. Eosinophil chemoattractant is a strong eosinophil chemoattractant. Eotaxin does this through the receptor CCR3, which is found on the cells most involved in allergic inflammation: eosinophils, Th2 cells, mast cells and basophils.
Interactions
It's multimodal communication between bronchial epithelial cells and eosinophils. In the inflammatory phase, epithelial cell damage and cytokine increase can directly influence eosinophil function and inflame the airways even more. Eotaxin and IL-5 collaborate in getting eosinophils activated both at a system level by moving them out of the bone marrow, and on the ground level by activating their selective response to sites of inflammation. Mice lacking the eotaxin gene demonstrated that besides essential for eosinophil recruitment in pulmonary inflammation, eotaxin is also necessary for baseline eosinophil levels in intestinal mucosa.
Conclusion
Those potent chemokines eotaxin are eosinophils that migrate towards inflamed tissues. When chemokines like this are released by epithelial cells of the bronchioles, they are correlated with every allergy and inflammation from asthma to allergic rhinitis.
On occasion (allergens, viruses, bacterial infections, etc) bronchial epithelial cells could regulate eosinophil chemotactic molecules. This upregulation can come in all shapes and sizes: signaling (cytokines, chemical messengers, muscle reactions). When turned off, these chemokines will attract eosinophils into the airways by binding to receptors for the chemicals in question and causing local inflammation.
Data on eosinophil chemotactic factors in the bronchial epithelium, then, gave us insights into how conditions such as asthma might manifest, and new targets to target. The suppression of eosinophilic airway inflammation could be turned around, by shutting down chemokines or signals.
References
- Lilly, C. M., et al. Expression of eotaxin by human lung epithelial cells: induction by cytokines and inhibition by glucocorticoids. The Journal of clinical investigation. 1997, 99(7): 1767-1773.
- Papadopoulos, N.; et al. Rhinovirus infection up‐regulates eotaxin and eotaxin‐2 expression in bronchial epithelial cells. Clinical & Experimental Allergy. 2001, 31(7): 1060-1066.
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