Akshaya Keerthi Saikumar
Manigandan V
Vishnu Raghuram
Shahana Parveen
Sugitharini V
Rohit Saluja
Elden Berla Thangam

Abstract

Introduction:

Monocytes play a major role in eliciting the immune response against infection. Also mast cells are found to play a critical role in mediating inflammatory immune response not only to allergic reaction but also to infection by inducing the production of inflammatory cytokines such as IL-1β, IL-6, IL-18 and IL-17. This study aims to investigate nod like receptor protein 3 (NLRP3) mediated production of Th1/Th17 cytokines in monocytes and mast cells.

Materials and Methods:

Mononuclear cells from peripheral and cord blood were stimulated with lipopolysaccharide (LPS), peptidoglycan (PGN) whereas human mast cell line-1 (HMC-1) cells were stimulated with histamine and LPS to analyse the activation of NLRP3 inflammosome components such as NLRP3, procaspase-1(p45), caspase-1(p10) nuclear factor-κB (NF-κB) and extracellular signal regulated kinase (ERK). The release of cytokines such as IL-1β, IL-6, IL-18 and IL-17 was quantified.

Results:

This study shows that stimulating the mononuclear and mast cells with LPS, PGN and LPS, histamine respectively induce the production of IL-1β, IL-6, IL-18 and IL-17 whereas the costimulation with gram positive and gram negative bacterial stimulants such as LPS and PGN showed synergistic response to cytokines whereas HMC- 1 cells when stimulated with histamine produces IL-1β, IL-6 and IL-17 but when co-stimulated with LPS level of cytokines were reduced. It is mediated through activation of NLRP3 inflammosome. Also these cells utilized NFκB and ERK pathway.

Conclusion:

The activation of NLRP3 inflammosome in innate immune cells leads to the production of IL-1β, IL-6, IL-18 and IL-17 cytokine. The signaling pathways NF-κB and ERK are found to have been involved in the activation of NLRP3 inflammosome complex during inflammatory conditions.

Keywords:

NLRP3 Inflammasome, innate immune cells, inflammation

VOLUME

7

,

ISSUE

Suppl 1
April 2019

Correspondence

Elden Berla Thangam

Email

berlathagam.e@ktr.srmuniv.ac.in

Received

Accepted

Published

Suggested Citation

DOI

License

This work is licensed under the Creative Commons Attribution-NonCommercial-Non-Derivatives 4.0 International License (CC BY-NC-ND 4.0). License