Protective bubble around lungs symbolizing defense against RSV, with CHI3L1 protein visualized.

Breathe Easier: How to Protect Your Lungs from RSV

Theo Raines in Health & Wellness November 2025 • 4 min read.

"New research uncovers a key protein, CHI3L1, that worsens RSV-induced airway inflammation, offering potential targets for future treatments."

Respiratory Syncytial Virus (RSV) is a common culprit behind bronchiolitis, especially in infants and young children. While most kids recover, RSV can lead to serious lower respiratory tract illnesses (LRTIs), sometimes requiring hospitalization. For some, early RSV infections might even pave the way for recurrent wheezing and asthma later in life, making effective treatments a top priority.

Current treatments for RSV primarily focus on supportive care, like managing fluids and breathing difficulties. Researchers are constantly seeking ways to prevent and treat RSV more effectively. Understanding how RSV evades our natural defenses is key to developing new strategies to keep our little ones breathing easy.

Now, new research sheds light on a specific protein, Chitinase 3-like 1 (CHI3L1), and its role in RSV-induced airway inflammation. By understanding this protein's actions, scientists hope to develop targeted therapies that can alleviate the severity of RSV infections, particularly in those most vulnerable.

CHI3L1: The Unexpected Culprit Behind RSV Lung Inflammation?

Protective bubble around lungs symbolizing defense against RSV, with CHI3L1 protein visualized.

Researchers have been investigating the role of CHI3L1, a protein also known as YKL-40 in humans and breast regression protein (BRP)-39 in mice, in the development of asthma. Interestingly, CHI3L1 levels are elevated in asthma patients and seem to correlate with the severity of the disease. In mice, BRP-39 has been identified as a key player in allergic responses and tissue remodeling.

To understand how CHI3L1 might be involved in RSV infections, researchers measured YKL-40 levels in nasopharyngeal aspirates (NPA) from hospitalized children with acute respiratory symptoms. They also studied wild-type mice and BRP-39 knockout mice (lacking the CHI3L1 equivalent) infected with live RSV. Analyzing lung tissue and fluid samples, they assessed lung inflammation, airway reactivity, and the expression of various cytokines.

Here's what the researchers discovered:

YKL-40 and IL-13 levels were higher in the NPAs of children with RSV compared to those without.
RSV infection in mice led to increased expression of BRP-39 and Th2 cytokines, especially IL-13.
Mice lacking BRP-39 experienced less airway inflammation from RSV compared to normal mice.
BRP-39 appears to regulate M2 macrophage activation in RSV-infected mice.
Blocking CHI3L1 with an antibody reduced airway inflammation and Th2 cytokine production in RSV-infected mice.

These findings suggest that CHI3L1 contributes to the airway inflammation triggered by RSV. By exacerbating Th2 inflammation, particularly IL-13 production, CHI3L1 appears to worsen the effects of RSV infection in the lungs.

What Does This Mean for Future RSV Treatments?

This research opens the door for new therapies that target CHI3L1 to reduce RSV-induced lung inflammation. By understanding the role of CHI3L1 in RSV infections, scientists can potentially develop treatments to lessen the severity of the illness, particularly in vulnerable populations like infants and young children. Future research will focus on how to translate these findings into effective and safe treatments that can help everyone breathe a little easier during RSV season.

About this Article -

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Everything You Need To Know

What is Respiratory Syncytial Virus (RSV), and why is it a concern?

Respiratory Syncytial Virus, or RSV, is a very common virus that often causes bronchiolitis, especially in young children and infants. While most children recover without issue, RSV can sometimes lead to serious lower respiratory tract illnesses requiring hospitalization. In some cases, early RSV infections may even contribute to recurrent wheezing and potentially asthma later in life, which is why effective treatments are so important. Current treatments are mainly supportive, focusing on managing symptoms like breathing difficulties.

What is CHI3L1, and how does it relate to RSV infections?

CHI3L1, also known as YKL-40 in humans and BRP-39 in mice, is a protein that appears to play a significant role in RSV-induced airway inflammation. Research indicates that CHI3L1 levels are elevated in patients with asthma, correlating with the severity of the disease. Studies in mice have identified BRP-39 as a key factor in allergic responses and tissue remodeling. In the context of RSV, CHI3L1 seems to worsen lung inflammation by exacerbating Th2 inflammation, particularly the production of IL-13.

How could blocking CHI3L1 help in treating RSV?

The research indicates that blocking CHI3L1 with an antibody can reduce airway inflammation and Th2 cytokine production in RSV-infected mice. This suggests that targeting CHI3L1 could be a viable strategy for developing new therapies to lessen the severity of RSV infections, especially in vulnerable populations such as infants and young children. By understanding the specific role of CHI3L1 in RSV infections, scientists can work towards creating treatments that alleviate lung inflammation and improve breathing.

What is IL-13, and what role does it play in RSV-induced lung inflammation?

IL-13 is a Th2 cytokine. The study showed RSV infection in mice led to increased expression of BRP-39 and Th2 cytokines, especially IL-13. By exacerbating Th2 inflammation, particularly IL-13 production, CHI3L1 appears to worsen the effects of RSV infection in the lungs. In simpler terms, IL-13 is like a messenger that tells the immune system to cause inflammation, and CHI3L1 makes this message stronger, leading to more inflammation in the lungs during an RSV infection.

What are M2 macrophages, and how does CHI3L1 affect them during an RSV infection?

M2 macrophages are a type of immune cell that plays a role in tissue repair and the resolution of inflammation. In the context of RSV infection, BRP-39, the mouse equivalent of CHI3L1, appears to regulate M2 macrophage activation. This means that CHI3L1 influences how these immune cells behave during an RSV infection, potentially affecting the balance between inflammation and recovery in the lungs. Further research is needed to fully understand the implications of this regulation.