Study identifies key driver of inflammation, opening door to potential new treatments

by Johns Hopkins University School of Medicine

edited by Andrew Zinin

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Researchers at Johns Hopkins Medicine have uncovered a critical biological mechanism that helps explain how inflammation is triggered and sustained in a wide range of diseases—highlighting a promising avenue for future therapeutic development.

The study, published in PLOS One, identified human resistin as a central driver of immune system activation. Researchers found that this protein plays a key role in turning on a powerful inflammatory pathway known as the NLRP3 inflammasome, which has been linked to numerous health conditions, including cardiovascular disease, diabetes and autoimmune disorders.

"Chronic inflammation plays a role in everything from heart disease to autoimmune disorders, yet the underlying triggers have remained unclear," said Roger Anthony Johns, MD, professor of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine. "By identifying a key molecule that drives inflammatory responses, we're getting closer to understanding how we might interrupt this process, opening the door to developing more targeted therapies in the future."

Inflammation is a natural part of the body's defense system, but when it becomes chronic, it can contribute to serious diseases. Until now, researchers did not fully understand how certain inflammatory signals were activated and amplified. The study findings show that human resistin acts as a "switch," both preparing and activating immune cells called macrophages. Specifically, the protein triggers a cascade of molecular events that ultimately leads to the release of inflammatory molecules such as IL-1β and IL-18, which can drive tissue damage and disease progression.

Researchers also examined lung tissue from patients with pulmonary hypertension, a serious condition characterized by high blood pressure in the lungs, and found increased activity of resistin and the inflammasome pathway in these patients, suggesting the mechanism plays a role in disease severity.

"Seeing this heightened activity in patient lung tissue reinforces that this pathway isn't just something we observe in the lab—it's directly relevant to human disease," Johns said. "It suggests that resistin may play a meaningful role in the severity of pulmonary hypertension and highlights both resistin and the inflammasome as potential targets we could one day modulate to improve outcomes."

The study also demonstrated that blocking resistin with a targeted antibody reduced activation of this inflammatory pathway—hinting at a potential new therapeutic strategy.

"By identifying human resistin as a key regulator of inflammation, the findings open the door to developing drugs that could interrupt this pathway and reduce harmful immune responses," Johns said. "This work provides new insight into how inflammation is driven at the cellular level, highlighting the potential for therapies that target resistin to treat a range of inflammatory diseases."

While additional research is needed, the findings represent an important step toward a better understanding of how inflammation is triggered and sustained in the body. By uncovering the role of human resistin in this process, researchers have laid the groundwork for future investigations aimed at developing targeted therapies to reduce harmful inflammation and improve outcomes for patients.

Publication details

Udeshika Kariyawasam et al, Human resistin is critical to activation of the NLRP3 inflammasome in macrophages, PLOS One (2026). DOI: 10.1371/journal.pone.0337682

Journal information: PLoS ONE

Key medical concepts

Interleukin-1betaInterleukin-18Pulmonary Hypertension

Clinical categories

Allergy and immunology Provided by Johns Hopkins University School of Medicine Who's behind this story?

Andrew Zinin

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