Essential Site Maintenance: Authorea-powered sites will be updated circa 15:00-17:00 Eastern on Tuesday 5 November.
There should be no interruption to normal services, but please contact us at [email protected] in case you face any issues.

loading page

Receptor for advanced glycation end-product (RAGE) modulates inflammation during feeding of tick, Haemaphysalis longicor
  • +7
  • * Anisuzzaman,
  • Md. Abdul Alim,
  • Makoto Matsubyashi,
  • Md. Shahadat Hossain,
  • Sharmin Shahid Labony,
  • Ireen Sultana Shanta,
  • Md. Haydar Ali,
  • Yasuhiko Yamamoto,
  • Takeshi Hatta,
  • Naotoshi Tsuji
* Anisuzzaman
Bangladesh Agricultural University

Corresponding Author:[email protected]

Author Profile
Md. Abdul Alim
Bangladesh Agricultural University
Author Profile
Makoto Matsubyashi
Osaka Koritsu Daigaku Jui Gakubu Juigaku Kenkyuka
Author Profile
Md. Shahadat Hossain
Bangladesh Agricultural University
Author Profile
Sharmin Shahid Labony
Bangladesh Agricultural University
Author Profile
Ireen Sultana Shanta
International Centre for Diarrhoeal Disease Research Bangladesh
Author Profile
Md. Haydar Ali
Bangladesh Agricultural University
Author Profile
Yasuhiko Yamamoto
Kanazawa Daigaku Daigakuin Iyaku Hokengaku Sogo Kenkyuka Iyaku Hoken Gakuiki Igakurui
Author Profile
Takeshi Hatta
Kitasato Daigaku Igakubu
Author Profile
Naotoshi Tsuji
Kitasato Daigaku Igakubu
Author Profile

Abstract

Abstract Ticks are notorious blood-sucking ectoparasites affecting both humans and animals, and serve as a unique vector of various deadly diseases. Here, we have shown the roles of the receptor for advanced glycation end-products (RAGE) during repeated infestations by the tick, Haemaphysalis longicornis using RAGE-/- mice. In primary infestation, a large blood pool developed which was flooded with numerous RBC, especially during the rapid feeding phase of the tick both in wild type (wt) and RAGE-/- mice. Very few inflammatory cells were detected around the zones of hemorrhage in the primary infestations. However, number of inflammatory cells gradually increased in the subsequent tick infestations and at the 3 rd infestations number of inflammatory cells reached to the highest level (350.3±16.8 cells/focus), and the site of attachment was totally occupied by the inflammatory cells in wild type (wt) mice whereas very few cells were detected at the ticks’ biting sites in RAGE-/- mice. RAGE was highly expressed in the 3 rd infestation in wt mice. In the 3 rd infestation, infiltration of innate lymphoid cells type 2 (ILC2s), expression of S100A8 and S100B significantly increased at the biting sites of ticks in wt, but not in RAGE -/- mice. Also, peripheral eosinophil counts significantly increased in wt but not in RAGE -/- mice. Taken together, our study revealed that RAGE-mediated inflammation and eosinophils played crucial roles in the tick induced inflammatory reactions.
24 Oct 2023Submitted to Parasite Immunology
24 Oct 2023Submission Checks Completed
24 Oct 2023Assigned to Editor
24 Oct 2023Review(s) Completed, Editorial Evaluation Pending
25 Oct 2023Reviewer(s) Assigned
07 May 2024Editorial Decision: Accept