CX3CR1 Contributes to Nasal Neutrophilia in Airways Allergy: Novel Role for IL-8 in Inducing CX3CR1Expression by Neutrophils

Image

CX3CR1 Contributes to Nasal Neutrophilia in Airways Allergy: Novel Role for IL-8 in Inducing CX3CR1Expression by Neutrophils

Background: CX3CR1 is involved in promotion of inflammation by recruiting inflammatory cells to the inflamed tissue. However, no reports studied their expression by neutrophils infiltrating the nasal tissue in chronic rhinosinusitis (CRS) patients with or without associated airways allergy.

Objectives: Our objectives were to evaluate the expression of CX3CR1 by neutrophil infiltrating the inflamed nasal tissue in patients suffering from CRS, and to study the receptor gene induction in activated human neutrophils.

Methods: Immunohistochemistry were conducted to evaluate CX3CR1 expression by neutrophil cells infiltrating the middle turbinate from patients operated for endoscopic sinus surgery. The gene expression and the receptor surface expression in resting versus activated neurophils by IL-8 were studied by Q-PCR and flow cytometry (FACS).

 Results: It is shown that CX3CR1 was significantly expressed by nasal infiltrating leukocytes when compared to control group. This expression was higher in patients with CRS and airway allergy than those with CRS and no airway allergy. Neutrophils contributed largely to the sub-epithelial layer inflammatory cells expressing CX3CR1. Both the gene and the surface expression of CX3CR1 were significantly induced in activated neutrophils by IL-8.

Conclusion: CX3CR1 expression by neutrophils is expressed in CRS and the receptor’s gene expression is induced in activated neutrophils by IL-8. These results further highlights and identifies an importance role for CX3CR1 in nasal inflammation.

To know more about the article: https://www.longdom.org/archive/imr-volume-14-issue-3-year-2018.html

A standard editorial manager system is utilized for manuscript submission, review, editorial processing and tracking which can be securely accessed by the authors, reviewers and editors for monitoring and tracking the article processing. Manuscripts can be uploaded online at Editorial Tracking System (https://www.longdom.org/submissions/immunome-research.html) or forwarded to the Editorial Office at: immunores@longdom.org

How we work:

  • After submission, an acknowledgement with manuscript number is sent to the corresponding author within 7 working days.
  • A 21 day window time frame is allotted for peer-review process wherein multiple experts are contacted.
  • Author proof is generated within 7 working days after the acceptance decision.

Benefits on Publication:

Open Access: Permanent free access to your article upon publication ensures extensive global reach and readership.

Easy Article Sharing: Our open access enables you to share your article directly with colleagues through email and on social media via a single link, permitting third party reuse with appropriate citation in addition to the retention of content copyright by the author.

Global Marketing: Through promotion in a targeted global email announcement or press release, your article will be seen by thousands of the top-most thought-leaders in your field.

Reprints: Distribute your work to colleagues and at conferences as we provide hard copy color reprints of your article on order.

Media Contact:
Stella M
Journal Manager
Immunome Research
Email: immunores@longdom.org