Study type: In vivo/preclinical · Status: Evidence verified by machine against declared source
Sensory neurons regulate stimulus-dependent humoral immunity in mouse models of bacterial infection and asthma.
Nature communications · 2024
Study scale: Naïve n = 6, Naïve RTX: n = 5; Day 1: Veh: n = 4, RTX: n = 4; Day 8: Veh: n = 5, RTX: n = 5; Day 10: Veh: n = 13, RTX: n = 5; Day 11: Veh: n = 13, RTX: n = 5; Day 15: Veh: n = 5, RTX: n = 5.
Abstract only: Open source record
Product or molecular entity relationships
- VIP: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.
Public plain-language summary
Some fields are not published, because the text held for them did not answer their heading. The published text is limited to the declared source and preserves reported uncertainty. It does not establish efficacy, safety, suitability, or evidence strength.
Research question
Early investigations have shown that B cells respond to exogenous neuropeptides in vitro and can steer the predominant release of specific immunoglobulin33–37.
Study design
In vitro, some of these neurotransmitters appear to increase immunoglobulin release33–37.
Participants or experimental system
Here, using mouse models of Streptococcus pneumoniae infection and Alternaria alternata asthma, we show that sensory neurons are required for B cell recruitment and antibody production.
Study scale
Naïve n = 6, Naïve RTX: n = 5; Day 1: Veh: n = 4, RTX: n = 4; Day 8: Veh: n = 5, RTX: n = 5; Day 10: Veh: n = 13, RTX: n = 5; Day 11: Veh: n = 13, RTX: n = 5; Day 15: Veh: n = 5, RTX: n = 5.
Intervention or exposure
In response to asthma, sensory neurons release substance P. Administration of VIP into sensory neuron-depleted mice suppresses bacterial burden, while VIPR1 deficiency increases infection.
Comparator
We used an established model of sensory neuron chemical ablation with resiniferatoxin (RTX)2,44,45, we suppressed TRPV1-containing neurons similarly in the vagal (nodose/jugular) ganglion by >85% compared to TRPV1-DTR mice injected with the diphtheria toxin directly into the vagal ganglia as assessed by qPCR and TRPV1 immunohistochemistry (Supplementary Fig. 1).
Outcomes examined
Not published. The text held for this field did not answer this heading, so nothing is shown here and nothing is substituted for it.
Key findings
Meanwhile, during A. alternata-induced airway inflammation, sensory neuron depletion decreases B cell population sizes, IgE levels, and asthmatic characteristics.
Limitations and uncertainty
Given that many infectious diseases are recurring, prolonged, or stem from commensal microbes becoming invasive30,31, further inquiry into the neural influence on humoral immunity in response to infection is warranted.
Product relevance and evidence boundary
This record is a published study, held here with its citation and review status. It is not a statement that any catalog item is effective, safe, or suitable for any use, and nothing in it is a dose or a protocol.
Evidence verified by machine against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.