IL-10: The Small Protein Playing a Large Role in Preventing Pulmonary Fibrosis

Recent research from the University of Illinois at Chicago has shed light on the significant role of the small protein IL-10 in safeguarding lung health. Historically, scientists believed our lungs were sterile, free of germs. However, current understanding confirms that lungs harbor allergens, bacteria, and viruses like influenza and SARS-CoV-2, which we inhale regularly. When these infectious agents or allergens lead to inflammation, they can cause chronic lung diseases such as pulmonary fibrosis.

The study highlights that IL-10, produced by lung interstitial macrophages—specialized immune cells residing in lung tissue—is crucial in controlling inflammation. These macrophages generate IL-10, which signals immune cells to reduce inflammatory responses. In mouse models lacking IL-10 signaling, spontaneous lung inflammation was observed, revealing the protein’s vital role in maintaining immune balance.

The absence of IL-10 signaling also allowed certain bacteria, including Delftia acidovorans and Rhodococcus erythropolis, to trigger lung inflammation, demonstrating how microbial imbalances can exacerbate lung conditions. Researchers emphasize that understanding the micro-operations within the lung environment, especially the interaction between microorganisms and immune signaling, is essential for developing treatments for pulmonary diseases like pulmonary fibrosis, bronchiolitis, and COPD.

This discovery underscores the potential of targeting IL-10 pathways to prevent or treat chronic lung diseases, offering new hope for managing these conditions more effectively.