Abstract
Mast cells (MCs) are engaged in the processes of host defense, primarily via the presence of receptors responsible for the detection of pathogen-associated molecular patterns (PAMPs). Since BDs are exclusively host defense molecules, and MCs can elicit the antimicrobial response, this study is aimed at determining whether BDs might be involved in MC pathogen defense. We found that defensin BD-2 significantly augments the mRNA and protein expression of Toll-like receptors (TLRs) and retinoic acid-inducible gene-I-like receptor (RLR) essential for the detection of viral molecules, i.e., TLR3, TLR7, TLR9, and RIG-I in mature tissue rat peritoneal MCs (PMCs). We established that BD-2 might stimulate PMCs to release proinflammatory and immunoregulatory mediators and to induce a migratory response. Presented data on IgE-coated PMC upon BD-2 treatment suggest that in the case of allergies, there is an enhanced MC immune response and cell influx to the site of the ongoing infection. In conclusion, our data highlight that BD-2 might strongly influence MC features and activity, mainly by strengthening their role in the inflammatory mechanisms and controlling the activity of cells participating in antimicrobial processes.
Highlights
One of the critical components of the innate immune response is a family of small, multifunctional molecules known as antimicrobial peptides (AMPs)
We determined whether stimulation with BD-2 influences TLR3, TLR7, TLR9, and RIG-I mRNA expressions in mature rat peritoneal MCs (PMCs)
Our findings demonstrate that the expression of TLR3, TLR7, TLR9, and RIG-I is enhanced by treatment with BD-2 in in vivo differentiated PMCs
Summary
One of the critical components of the innate immune response is a family of small, multifunctional molecules known as antimicrobial peptides (AMPs). The β-defensins (BDs) are expressed by the skin and mucosal epithelial cell lining, i.e., the urinary tract, kidney, or trachea. They can be expressed in monocytes, macrophages, and dendritic cells. While BDs mainly serve as potent microbicidal agents, they exhibit immunomodulatory properties. They appear to be essential chemokines, inducing the production and release of diverse immunoregulatory mediators by inflammatory cells; they are distinguished as active agents in inflammatory processes. BDs modulate mechanisms of adaptive immunity, and they supply a link between the innate and adaptive immune response as they can recruit immature memory T cells and dendritic cells to sites of infection and/or inflammation [5, 6]
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