One health: Subchronic exposure to low ambient hydrogen sulfide increases mortality of influenza A virus infection in mice.

The environment plays an important role in modulating susceptibility and severity of respiratory tract infections. Influenza is a significant zoonotic disease globally. Hydrogen sulfide (HS), a respiratory tract irritant and toxic gas, is ubiquitous in the environment.

Mouse Models for the Study of Borrelia burgdorferi Infection.

Lyme disease, a tickborne illness caused by Borrelia burgdorferi, is an emerging, significant public health concern. B. burgdorferi infections are challenging to study because of their complex life cycle that requires adaptation to both ticks and mammalian hosts for long-term survival and transmission.

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

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.

Secreted IgM modulates IL-10 expression in B cells.

IL-10 B cells are critical for immune homeostasis and restraining immune responses in infection, cancer, and inflammation; however, the signals that govern IL-10 B cell differentiation are ill-defined. Here we find that IL-10 B cells expand in mice lacking secreted IgM ((s)IgM) up to 10-fold relative to wildtype (WT) among all major B cell and regulatory B cell subsets. The IL-10 B cell increase is polyclonal and presents within 24 hours of birth.