Toll-like receptors, triggering receptor expressed on myeloid cells family members and receptor for advanced glycation end-products in allergic airway inflammation

Abstract

Asthma is a chronic disorder of the airways characterized by cellular infiltration, airway hyper-responsive and airway inflammation. Innate immune cells are the first line of defense against endogenous and exogenous signals in the airways and as such possess a diverse array of pattern recognition receptors. Toll-like receptors are crucial sentinels which when activated, can either promote or ameliorate the inflammatory response in predisposed individuals. The recently discovered triggering receptor expressed on myeloid cells family members are emerging mediators of inflammation. These receptors are believed to modulate inflammatory responses by collaborating with classic PRRs. Endogenous signals like HMGB-1, signaling through the receptor for advanced glycation end products, also promotes inflammation, however, its contribution to inflammation in the airways is not well known. Here, we discuss the role of each receptor in airway inflammation and highlight potential synergistic mechanisms, which contribute to disease pathogenesis in allergic asthma.

Triggering receptor expressed on myeloid cells in the pathogenesis of periodontitis: potential novel treatment strategies

“…Toll-like Receptors (TLRs) are germ line encoded receptors of the innate immune response responsible for distinguishing between microorganisms and responding appropriately to specific microbes [30]. Synergism between TREM-1 and TLRs leads to an increased production of proinflammatory cytokines TNF-α and IL-1β, and inhibits the anti-inflammatory molecule IL-10 [31]. TREM-1 acts synergistically with TLR-2 to induce cytokine production, while TLR-2 can also upregulate TREM-1 via the MyD88-dependent pathway [32].…”

“…TREM-1 is able to positively modulate TLR-4 through regulation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway, which in turn modifies MyD88 and cluster of differentiation 14 (CD14) expressions [32]. TREM-1 can activate the NF-κB pathway leading to increased production of TNF-α, IL-2 and IL-1β [31,32]. …”

“…TLRs and NLRs) the result is a synergistically significant increase in cytokine and chemokine secretion when compared to either component alone [31]. …”

“…TREM-2 is thought to be a negative regulator of the inflammatory response; however, there has been very little study in regards to TREM-2 and periodontal diseases [31]. Chen, Wang, & Zhao [35] conducted the first experiments with TREM-2 and periodontal diseases.…”

Triggering receptor expressed on myeloid cells and 5’adenosine monophosphate-activated protein kinase in the inflammatory response: a potential therapeutic target

“…These receptors include G-protein coupled transmembrane receptors, Fc receptors, cytokine receptors, cell adhesion molecules and pattern recognition receptors like TLRs and C-type lectins [7],. Activation of these receptors results in inflammatory events like phagocytosis, degranulation, reactive oxygen species production, chemotaxis and cytokine release [8, 9]. Triggering Receptor Expressed on Myeloid cells (TREM) are a recently discovered cell surface receptor of immunoglobulin superfamily which has implications on inflammation associated with pathologies.…”