# The role of IL-1 family of cytokines in tick-transmitted ehrlichiosis

> **NIH NIH R21** · UNIVERSITY OF TEXAS MED BR GALVESTON · 2020 · $197,500

## Abstract

Project Summary/Abstract
Infections transmitted by ticks have increased in incidence worldwide as a result of environmental changes.
Important aspects of the induced disease pathogenesis facilitate the identification of preventive and/or
therapeutic alternatives to more severe illnesses. In ehrlichiosis and other vector borne diseases there is a lack
of information regarding the initiation of infection, due to the difficulties associated with a model using the
natural mode of infection. Our previously developed tick transmission model allowed us to identify important
differences in mortality and bacterial distribution by using different routes of infection. However, limited
knowledge is available about the site of infection and host response to pathogen-tick interaction. This proposed
project will identify the immune pathways involved in early pathogenesis of tick borne ehrlichiosis. Our model
demonstrates severe inflammation and antigen persistence in the skin area of tick inoculation of bacteria.
Interestingly, different routes of infection induced different disease outcome and bacterial dissemination. Our
preliminary results identify significant expression of the IL-36 group of cytokines during initial ehrlichial
transmission at the site of tick feeding, which could potentially mediate inflammatory cells recruitment.
Therefore, the objective of our research is to determine the role of IL-36 in initiation of infection during tick
transmission of the ehrlichial pathogen. Our hypothesis is that activation of skin KCs by tick-transmitted
ehrlichiae results in IL-36 mediated inflammation, which facilitates establishment of infection in
recruited monocytes/macrophages (Mo/Mϕs). We will first demonstrate KCs as the primary source of the
IL-36 family of cytokines during ehrlichiae-tick transmission, and further identify the role of IL-36 to drive
inflammatory processes. Furthermore, we will demonstrate how the recruitment of monocytes/macrophages
by these inflammatory mechanisms facilitates infection and dissemination during early transmission. By
accomplishing the goals of this project we expect to demonstrate the importance of the early activation of IL-36
as a key mediator in the skin at site of ehrlichial infection as part of disease pathogenesis. Understanding the
key determinants underlying the establishment of infection will enable us to identify markers of susceptibility to,
and new therapeutic targets for, tick borne ehrlichiosis.

## Key facts

- **NIH application ID:** 9850507
- **Project number:** 5R21AI144328-02
- **Recipient organization:** UNIVERSITY OF TEXAS MED BR GALVESTON
- **Principal Investigator:** Bin Gong
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $197,500
- **Award type:** 5
- **Project period:** 2019-01-15 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9850507

## Citation

> US National Institutes of Health, RePORTER application 9850507, The role of IL-1 family of cytokines in tick-transmitted ehrlichiosis (5R21AI144328-02). Retrieved via AI Analytics 2026-06-11 from https://api.ai-analytics.org/grant/nih/9850507. Licensed CC0.

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