The gastrointestinal tract is densely innervated by the peripheral nervous system and populated by the immune system.These two systems critically coordinate the sensations of and adaptations to dietary,microbial,and d...The gastrointestinal tract is densely innervated by the peripheral nervous system and populated by the immune system.These two systems critically coordinate the sensations of and adaptations to dietary,microbial,and damaging stimuli from the external and internal microenvironment during tissue homeostasis and inflammation.The brain receives and integrates ascending sensory signals from the gut and transduces descending signals back to the gut via autonomic neurons.Neurons regulate intestinal immune responses through the action of local axon reflexes or through neuronal circuits via the gut-brain axis.This neuroimmune crosstalk is critical for gut homeostatic maintenance and disease resolution.In this review,we discuss the roles of distinct types of gut-innervating neurons in the modulation of intestinal mucosal immunity.We will focus on the molecular mechanisms governing how different immune cells respond to neural signals in host defense and inflammation.We also discuss the therapeutic potential of strategies targeting neuroimmune crosstalk for intestinal diseases.展开更多
Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to me...Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to mediate pain and itch. Nociceptor and pruriceptor neurons respond to pathogen-associated molecular patterns, including Toll-like receptor ligands, N-formyl peptides, and bacterial toxins. Other pathogens are able to silence neuronal activity to produce analgesia during infection. Pain and itch could lead to neuronal modulation of the immune system or behavioral avoidance of future patho- gen exposure. Conversely, pathogens could modulate neuronal signaling to potentiate their pathogenesis and facilitate their spread to other hosts. Defining how pathogens modulate pain and itch has critical implications for sensory neurobiology and our understanding of host- microbe interactions.展开更多
基金The Chiu Lab is supported by NIH grants R01 DK127257 and R01 AI168005,Kenneth Rainin Foundation,Burroughs Wellcome Fund,Food Allergy Science Initiative,Chan-Zuckerberg Initiative,Fairbairn Lyme Initiative,Drako Family Foundation,and Jackson-Wijaya Research Fund.
文摘The gastrointestinal tract is densely innervated by the peripheral nervous system and populated by the immune system.These two systems critically coordinate the sensations of and adaptations to dietary,microbial,and damaging stimuli from the external and internal microenvironment during tissue homeostasis and inflammation.The brain receives and integrates ascending sensory signals from the gut and transduces descending signals back to the gut via autonomic neurons.Neurons regulate intestinal immune responses through the action of local axon reflexes or through neuronal circuits via the gut-brain axis.This neuroimmune crosstalk is critical for gut homeostatic maintenance and disease resolution.In this review,we discuss the roles of distinct types of gut-innervating neurons in the modulation of intestinal mucosal immunity.We will focus on the molecular mechanisms governing how different immune cells respond to neural signals in host defense and inflammation.We also discuss the therapeutic potential of strategies targeting neuroimmune crosstalk for intestinal diseases.
基金supported by funding from the National Institutes of Health(NCCIH DP2AT009499 and MAID K22AI114810),USA
文摘Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to mediate pain and itch. Nociceptor and pruriceptor neurons respond to pathogen-associated molecular patterns, including Toll-like receptor ligands, N-formyl peptides, and bacterial toxins. Other pathogens are able to silence neuronal activity to produce analgesia during infection. Pain and itch could lead to neuronal modulation of the immune system or behavioral avoidance of future patho- gen exposure. Conversely, pathogens could modulate neuronal signaling to potentiate their pathogenesis and facilitate their spread to other hosts. Defining how pathogens modulate pain and itch has critical implications for sensory neurobiology and our understanding of host- microbe interactions.
