Interactions between the immune and the nervous systems occur under physiological and pathophysiological conditions. Nociceptors, the nervous system’s pain-sensing neurons, express an extensive array of ion channels and receptors that allow them to sense (potentially) noxious stimuli. Of note, the expression of receptors specific for immune-derived mediators and pattern recognition receptors for pathogen-associated molecular patterns (PAMPs) allow nociceptors to identify cues from the immune system and microbial pathogens, respectively. Nociceptor activation, in turn, leads to the release of neuropeptides and modulation of the immune system resulting in oedema and inflammation, which further contributes to pain signalling. During a microbial infection, for example, pain can arise from both direct microbial recognition through nociceptors and the accompanying inflammatory immune response. Moreover, excessive activation of the immune system to exogenous agents can lead to an aberrant nociceptive signalling. Thus, perturbations in the microbiota, impairment of host-microbiome interfaces, and/or abnormal immune responses to antigens (food, chemicals, irritants, etc.) may result in the development of chronic pain.
Chronic pain represents an important and unmet medical challenge worldwide. Growing evidence in the bidirectional crosstalk between the nervous and the immune systems has increased the interest on this communication in the context of pain signalling. However, the understanding of the cellular and molecular pathways is only in its infancy. Remarkably, pain often persists despite proper control of the inflammation—such as in rheumatoid arthritis or inflammatory bowel disease—or occurs in the absence of gross tissue abnormalities—such as in irritable bowel syndrome. Therefore, more research into the pathophysiological crosstalk between the immune system and nociceptors is of great scientific interest.
In this Research Topic, we aim to implement the understanding of the cellular and molecular mechanisms mediating the interaction between the immune and nervous systems in the context of (chronic) pain. Thus, we seek to integrate studies evaluating how exogenous compounds (food, chemicals), microbes and microbial products, or environmental agents, can modulate the immune response leading to the activation of nociceptive neurons. Moreover, we aim to further our insights into the metabolites involved in the communication between non-neuronal cells and sensory neurons in pain signalling. We particularly welcome the submission of Original Research and Review/Mini-Review articles covering, but not limited to, the following topics:
• Cellular and molecular pathways leading to the activation of the immune system and subsequent generation of nociceptive signals in response to exogenous triggers.
• Novel molecular pathways leading to the activation of the nociceptors and subsequent onset of neurogenic inflammation.
• Molecular mechanisms of microbial strains and related metabolites in the initiation of immune responses and the development of pain.
• Molecular pathways involved in the communication between non-neuronal cells and nociceptors.
• Immunogenic microbial triggers and mechanisms in the development of pain and neurogenic inflammation.
• Molecular profiling of immunogenic food compounds (endogenous or exogenous) or environmental compounds and their association with pain onset.
• Cellular and molecular mechanisms of food-associated immunogenic compounds (endogenous or exogenous) in the development of pain.
• Immunological mechanisms of compounds underlying the alleviation of pain.
• Immunological mechanisms of microbial compounds with analgesic properties.
Interactions between the immune and the nervous systems occur under physiological and pathophysiological conditions. Nociceptors, the nervous system’s pain-sensing neurons, express an extensive array of ion channels and receptors that allow them to sense (potentially) noxious stimuli. Of note, the expression of receptors specific for immune-derived mediators and pattern recognition receptors for pathogen-associated molecular patterns (PAMPs) allow nociceptors to identify cues from the immune system and microbial pathogens, respectively. Nociceptor activation, in turn, leads to the release of neuropeptides and modulation of the immune system resulting in oedema and inflammation, which further contributes to pain signalling. During a microbial infection, for example, pain can arise from both direct microbial recognition through nociceptors and the accompanying inflammatory immune response. Moreover, excessive activation of the immune system to exogenous agents can lead to an aberrant nociceptive signalling. Thus, perturbations in the microbiota, impairment of host-microbiome interfaces, and/or abnormal immune responses to antigens (food, chemicals, irritants, etc.) may result in the development of chronic pain.
Chronic pain represents an important and unmet medical challenge worldwide. Growing evidence in the bidirectional crosstalk between the nervous and the immune systems has increased the interest on this communication in the context of pain signalling. However, the understanding of the cellular and molecular pathways is only in its infancy. Remarkably, pain often persists despite proper control of the inflammation—such as in rheumatoid arthritis or inflammatory bowel disease—or occurs in the absence of gross tissue abnormalities—such as in irritable bowel syndrome. Therefore, more research into the pathophysiological crosstalk between the immune system and nociceptors is of great scientific interest.
In this Research Topic, we aim to implement the understanding of the cellular and molecular mechanisms mediating the interaction between the immune and nervous systems in the context of (chronic) pain. Thus, we seek to integrate studies evaluating how exogenous compounds (food, chemicals), microbes and microbial products, or environmental agents, can modulate the immune response leading to the activation of nociceptive neurons. Moreover, we aim to further our insights into the metabolites involved in the communication between non-neuronal cells and sensory neurons in pain signalling. We particularly welcome the submission of Original Research and Review/Mini-Review articles covering, but not limited to, the following topics:
• Cellular and molecular pathways leading to the activation of the immune system and subsequent generation of nociceptive signals in response to exogenous triggers.
• Novel molecular pathways leading to the activation of the nociceptors and subsequent onset of neurogenic inflammation.
• Molecular mechanisms of microbial strains and related metabolites in the initiation of immune responses and the development of pain.
• Molecular pathways involved in the communication between non-neuronal cells and nociceptors.
• Immunogenic microbial triggers and mechanisms in the development of pain and neurogenic inflammation.
• Molecular profiling of immunogenic food compounds (endogenous or exogenous) or environmental compounds and their association with pain onset.
• Cellular and molecular mechanisms of food-associated immunogenic compounds (endogenous or exogenous) in the development of pain.
• Immunological mechanisms of compounds underlying the alleviation of pain.
• Immunological mechanisms of microbial compounds with analgesic properties.
