# B cells modulate lung antiviral inflammatory responses via the neurotransmitter acetylcholine

## TL;DR

B cells help control lung inflammation during viral infections by using acetylcholine, but this can also increase virus replication.

## Contribution

B cells producing acetylcholine are identified as regulators of early antiviral inflammation in the lungs.

## Key findings

- ChAT+ B cells interact with macrophages to reduce TNFα production in the lungs after infection.
- This interaction decreases inflammation but increases viral replication in mice.
- B cells are part of an early regulatory response to viral infections in lung tissue.

## Abstract

The rapid onset of innate immune defenses is critical for early control of viral replication in an infected host, yet it can also lead to irreversible tissue damage, especially in the respiratory tract. Intricate regulatory mechanisms must exist that modulate inflammation, while controlling the infection. Here, B cells expressing choline acetyl transferase (ChAT), an enzyme required for production of the metabolite and neurotransmitter acetylcholine (ACh) are identified as such regulators of the immediate early response to influenza A virus. Lung tissue ChAT + B cells are shown to interact with a7 nicotinic Ach receptor-expressing lung interstitial macrophages in mice within 24h of infection to control their production of TNFa, shifting the balance towards reduced inflammation at the cost of enhanced viral replication. Thus, innate-stimulated B cells are key participants of an immediate-early regulatory cascade that controls lung tissue damage after viral infection.