Cellular stress or tissue injury-induced damage-associated molecular patterns (DAMPs) will initiate innate immune responses via interacting with pattern recognition receptors (PRRs). The recognition of DAMPs promotes sterile inflammation, which is essential for tissue healing and rehabilitation, but it is also involved in the pathogenesis of various inflammatory diseases.
PRRs can be generally classified into cytoplasmic receptors (e.g., nucleotide oligomerization domain (NOD)-like receptors, retinoic acid-inducible gene-I (RIG-I)-like receptors, and absent in melanoma-2 (AIM2)-like receptors) and cell surface-expressed receptors (e.g., C-type lectin-like receptors, scavenger receptors, and Toll-like receptors). Additionally, soluble PRRs or PRMs (pattern recognition molecules) presenting in the blood and mucosal secretions, like collectins and complement components, are also crucial participants in the host innate immune response. Studies on the function of DAMP-sensing PRRs will help us understand the mechanism of sterile inflammation and the disease development associated with dysregulated inflammation.
Digestive tract inflammation is a complex biological response of digestive tissues to harmful stimuli, like pathogens, toxic components, and damaged cells. Notably, digestive tract inflammation has been reported to affect local and distant innate immune activation. The primary focus of this Research Topic is the regulation of DAMP-sensing PRRs-initiated innate immune signaling during digestive tract inflammation. Indeed, distinct DAMP-sensing PRRs may cooperate to orchestrate the initiation, amplification, and resolution of inflammatory responses. It is of interest to reveal the crosstalk between the receptors and downstream effectors during the activation of multiple signaling pathways. It is noteworthy that endogenous pro-inflammatory molecules, consisting of peptides, lipids, and metabolites, are proposed to function as danger signals. Further investigation about the ligand-receptor interaction will broaden our understanding of DAMP sensing in digestive tract inflammatory responses.
We welcome manuscripts that cover, but are not limited to, the following subtopics:
• Role of different DAMP-sensing PRRs in digestive tract inflammatory diseases.
• DAMP-sensing PRRs in digestive tract cancer-related inflammation.
• Metabolite mediators of digestive tract inflammation and immunity.
• The interaction mechanism and function between DAMP-sensing PRRs and their ligands.
• The crosstalk of local digestive tract inflammatory response with distant innate immune activation.
Cellular stress or tissue injury-induced damage-associated molecular patterns (DAMPs) will initiate innate immune responses via interacting with pattern recognition receptors (PRRs). The recognition of DAMPs promotes sterile inflammation, which is essential for tissue healing and rehabilitation, but it is also involved in the pathogenesis of various inflammatory diseases.
PRRs can be generally classified into cytoplasmic receptors (e.g., nucleotide oligomerization domain (NOD)-like receptors, retinoic acid-inducible gene-I (RIG-I)-like receptors, and absent in melanoma-2 (AIM2)-like receptors) and cell surface-expressed receptors (e.g., C-type lectin-like receptors, scavenger receptors, and Toll-like receptors). Additionally, soluble PRRs or PRMs (pattern recognition molecules) presenting in the blood and mucosal secretions, like collectins and complement components, are also crucial participants in the host innate immune response. Studies on the function of DAMP-sensing PRRs will help us understand the mechanism of sterile inflammation and the disease development associated with dysregulated inflammation.
Digestive tract inflammation is a complex biological response of digestive tissues to harmful stimuli, like pathogens, toxic components, and damaged cells. Notably, digestive tract inflammation has been reported to affect local and distant innate immune activation. The primary focus of this Research Topic is the regulation of DAMP-sensing PRRs-initiated innate immune signaling during digestive tract inflammation. Indeed, distinct DAMP-sensing PRRs may cooperate to orchestrate the initiation, amplification, and resolution of inflammatory responses. It is of interest to reveal the crosstalk between the receptors and downstream effectors during the activation of multiple signaling pathways. It is noteworthy that endogenous pro-inflammatory molecules, consisting of peptides, lipids, and metabolites, are proposed to function as danger signals. Further investigation about the ligand-receptor interaction will broaden our understanding of DAMP sensing in digestive tract inflammatory responses.
We welcome manuscripts that cover, but are not limited to, the following subtopics:
• Role of different DAMP-sensing PRRs in digestive tract inflammatory diseases.
• DAMP-sensing PRRs in digestive tract cancer-related inflammation.
• Metabolite mediators of digestive tract inflammation and immunity.
• The interaction mechanism and function between DAMP-sensing PRRs and their ligands.
• The crosstalk of local digestive tract inflammatory response with distant innate immune activation.
