Category: News

Inflammation is part of your body’s natural healing process after infection or injury. But when inflammation persists for months or years, it can begin damaging healthy tissues instead of protecting them.

Chronic inflammation has long been associated with autoimmune and inflammatory diseases such as lupus, rheumatoid arthritis, and psoriasis. Research increasingly shows that it can also affect the blood vessels and the heart, increasing the risk of heart attacks, strokes, heart failure, or other cardiovascular complications.

Recognizing these connections between chronic inflammation and heart disease, UT Southwestern has launched its first Cardio-Rheumatology and Cardio-Dermatology Program. This program focuses on the connections among inflammation, autoimmune diseases, and cardiovascular health.

Having an autoimmune disease doesn’t automatically mean you’ll develop heart disease. But it may mean you and your care team should be more intentional about cardiovascular prevention and screening.

By bringing together specialists in cardiology, rheumatology, dermatology, imaging, and primary care, we can identify inflammation-associated cardiovascular risks sooner and help patients act before serious heart disease occurs.

How can inflammation affect the heart?

Inflammation doesn’t replace traditional cardiovascular disease risk factors such as high blood pressure, high cholesterol, diabetes, smoking, obesity, or family history. Rather, it’s one more layer of risk that deserves attention.

Inflammatory proteins can influence plaque growth, blood clotting, and how stiff our vessels are. Chronic inflammation can irritate the inner lining of blood vessels, making it easier for cholesterol and immune cells to accumulate and form plaque. Over time, that process contributes to atherosclerosis, or hardening of the arteries, which can lead to heart attacks and strokes.

Inflammation can also affect different parts of the cardiovascular system and may be associated with conditions or symptoms such as:

• Pericarditis, which is inflammation of the sac surrounding the heart.
• Myocarditis, which is inflammation of the heart muscle.
• Coronary microvascular disease, which involves the heart’s smallest blood vessels.
• Vascular inflammation, which affects arteries throughout the body.
• Symptoms such as chest pain, shortness of breath, fatigue, palpitations, or reduced exercise tolerance.

Who should see a cardio-rheumatology or cardio-dermatology specialist?

Our clinics are designed for people at the intersection of cardiovascular risk and inflammatory disease or symptoms, even when the source of inflammation is unclear.

Inflammatory conditions can cause vague symptoms such as chest discomfort, shortness of breath, or unusual fatigue. Standard heart disease risk calculators are useful for estimating risk based on traditional factors. But they may not fully capture the effects of chronic inflammation, disease activity, or some treatments on the heart and blood vessels.

Getting a consultation with us may be helpful if you have unexplained cardiovascular symptoms and a condition associated with autoimmune or chronic inflammation, such as:

• Ankylosing spondylitis
• Inflammatory bowel disease
• Lupus
• Psoriasis
• Hidradenitis Suppurativa
• Recurrent pericarditis
• Rheumatoid arthritis
• Systemic sclerosis (scleroderma)
• Vasculitis

Depending on your health history and symptoms, we may use advanced cardiovascular imaging to understand what’s happening to your heart and blood vessels. For example, noninvasive coronary artery calcium scoring can help measure the amount of calcified plaque in the coronary arteries and refine cardiovascular risk. Other imaging technologies include coronary CT, cardiac MRI, and PET imaging to help us create a more personalized prevention strategy.

How do we treat inflammation-related cardiovascular risk?

Heart-healthy habits and treatment of traditional risk factors remain the foundation of prevention. That includes managing blood pressure, cholesterol, and diabetes; avoiding tobacco; exercising regularly; getting enough sleep; and maintaining a healthy weight.

In some patients, inflammation is a treatable contributor to cardiovascular risk. But not every anti-inflammatory therapy prevents heart attacks or strokes, and standard prevention remains essential. Advances in cardiology, rheumatology, and dermatology are helping us develop more precise strategies for people with autoimmune or inflammatory diseases.

Medications can be highly effective for many patients, but some have side effects that may outweigh the benefits in certain cases. Treatment decisions require collaboration between patients and our specialist team to balance the personal benefits and risks.

Heart disease: Targeting inflammation as a risk factor

Low-dose colchicine, an anti-inflammatory medication frequently used for acute gout flare-ups, can reduce the risk of future cardiovascular events in selected patients with established atherosclerotic disease or multiple cardiovascular risk factors. Colchicine is also a first-line treatment for pericarditis. It is not appropriate for everyone, including some people with severe kidney or liver disease or people taking medications that interact with colchicine.

For recurrent pericarditis, therapies that block inflammatory pathways such as interleukin-1 (IL-1) can help reduce flare-ups and reduce the use of steroid medications long term. Researchers are also studying therapies that target interleukin-6 (IL-6), another important inflammatory pathway linked to heart failure and cardiovascular disease.

Rheumatologic diseases: More precise control of autoimmune inflammation

Rheumatology has led the way in immune-targeted therapies for decades. Today, patients with conditions such as rheumatoid arthritis, lupus, and vasculitis have access to treatments that target specific immune pathways rather than broadly suppressing the immune system.

Examples include biologic therapies that block tumor necrosis factor (TNF), interleukin-6, B cells, or other components of the immune response. Early studies are also exploring CAR T-cell therapy for severe autoimmune diseases. This approach remains investigational but illustrates the shift toward increasingly personalized treatment.

Dermatologic diseases: Looking beyond the skin

Psoriasis is more than a skin condition. We now know it is a systemic inflammatory disease. Moderate to severe psoriasis is associated with an increased risk of cardiovascular disease.

Several highly effective biologic therapies are available for psoriasis, including medications that target inflammatory pathways such as IL-17 and IL-23. These treatments can significantly improve skin symptoms and quality of life for many patients. Whether these medicines directly prevent heart attacks or strokes is still being studied.

The future of cardiovascular inflammation care

One of the most exciting aspects of this field is that we’re still learning. My goal, and that of my colleagues, is to move the field forward so we can better identify patients who are at risk before heart disease develops and understand which treatments provide the greatest benefit.

Challenge: Measuring inflammation

While we can measure inflammation in the body, it’s often difficult to determine whether it is specifically affecting the heart and blood vessels. For example, blood tests such as high-sensitivity C-reactive protein (hs-CRP) can show that inflammation is present somewhere in the body, but they cannot identify the source or prove that it is coming from the heart or blood vessels. Elevated levels may reflect arthritis, psoriasis, an infection, or another inflammatory condition.

Researchers are studying whether advanced imaging can help distinguish general inflammation from inflammation affecting plaque or blood vessels and whether that information improves treatment decisions.

Related: First-time stroke prevention: What women should know

Challenge: Risk prediction

Most cardiovascular risk calculators were developed using data from the general population and don’t fully account for the inflammatory burden, disease activity, medication exposures, or other factors that influence risk in patients with autoimmune diseases

As a result, a patient may appear to be at low risk on paper even when disease activity, inflammation, or medication exposure adds risk that the calculator does not capture. The future is likely to involve more personalized risk assessment that combines traditional risk factors with disease-specific information and, when appropriate, biomarkers and advanced imaging.

Rather than relying on a risk calculator alone, we can use the broader clinical picture to identify which patients with lupus, rheumatoid arthritis, psoriasis, and other inflammatory conditions may benefit from earlier evaluation or prevention.

Patients with autoimmune or inflammatory diseases should not have to wait until they have heart complications to learn about their cardiovascular risk. Our ultimate goal is to provide people with precise prevention strategies – matching the right patient with the right tests and therapy at the right time.

Source: Internal Medicine – Cardiology, UT Southwestern Medical Center

Low back pain is the single leading cause of disability worldwide, according to the World Health Organization. For people with chronic low back pain (cLBP) lasting more than 12 weeks, a sudden pain flare triggered by movement can often worsen the condition. Pain signals originate in the brain, but scientists still don’t fully understand the specific neural circuitry that sparks this movement-based pain.

Now, researchers at UC San Diego School of Medicine have found that the brain region’s Default Mode Network (DMN) is turned on when cLBP patients experience sudden pain brought on by movement. The DMN is also referred to as the “self network” because it is associated with interconnected regions of the frontal, parietal and temporal lobes of the brain that become active when we are thinking about ourselves and our identity or reflecting on internal thoughts and feelings — rather than focusing on the outside world.

The study, published on October 6, 2026 in the British Journal of Anaesthesia, could help explain why typical symptom-based treatments are often ineffective and suggests that targeting the brain’s DMN may be a better approach to managing cLBP.

The researchers had 114 cLBP patients perform a “leg raise test” — a standard way to trigger a back pain flare — while they measured blood flow in the brain using a specialized functional MRI technique called arterial spin labeling. As a control, they also tested how the patients’ brains responded to a harmless but painful heat stimulus on the calf, comparable to accidentally touching a hot stove.

They found that movement-evoked pain activated the DMN, providing the first evidence that the experience of chronic pain is not merely a sensation, but is deeply embedded in the sense of self. In addition:

• Participants who suffered from more severe chronic back pain had stronger connections between the DMN and the primary somatosensory cortex, the area of the brain that processes sensations from the back.
• The more intense the pain was during the leg raise test, the more activity was observed in the brain’s sensory and motor regions.
• An increase in heart rate during the leg raise test was a reliable indicator of how intense the pain flare was.

In contrast, when the participants were subjected to the painful heat, their DMN shut down, which is the brain’s usual response to acute pain. This allows the brain to focus entirely on the external threat rather than on the self, according to corresponding author Fadel Zeidan, PhD, professor in the Department of anesthesiology, endowed professor at the Sanford Institute for Empathy and Compassion and director of the Pain Health and Mindfulness Laboratory at UC San Diego School of Medicine.

“In every pain study, when you’re experiencing pain, the DMN deactivates,” said Zeidan. “What we show for the first time ever is that when you have a pain flare, it turns on instead. You start to identify the experience with who you are.”

In essence, in cLBP the brain is maladaptively coupling the physical pain with a deep, internal sense of self.

“The moment-to-moment experience is contaminated not only by the feeling of pain, but by the anticipation of it and recovery from it. It’s contaminated by past experiences like embarrassment about not being able to participate in normal activities and fear of movement when trying to avoid the pain.”

The researchers think that because pain flares evoked by movement in cLBP patients activate different brain networks than typical acute pain, this might be why standard pain treatments like opiates often fail for this type of pain.

“Current pain medicine is fixated on ridding patients of their pain symptoms, but that’s not the source of chronic pain. These data suggest that a chronic pain flare also encompasses one’s identity.”

Recent research by Zeidan’s team points to a different route to treatment by using mindfulness meditation and the psychedelic compound psilocybin, helping patients separate the physical experience of chronic pain from their identity, resulting in reductions to pain intensity. These preliminary findings are promising, but more research is needed to validate these early studies.

“These types of mind-body and psychedelic medicine approaches target the whole person,” Zeidan said. “Mindfulness is a meditation technique that’s about cultivating non-judgmental awareness of the present moment that dramatically reduces pain in a very unique way. Psilocybin seemingly resets the pain system that integrates trauma, past experiences and future worries to facilitate a restart, if you will. They’re not a silver bullet — you’re not necessarily getting rid of the pain, but you’re changing the relationship you have with that pain so it doesn’t contaminate your everyday life.”

Zeidan’s lab is currently conducting several neuroimaging-based clinical trials to further understand how approaches that target self-referential brain processes like mindfulness meditation and psychedelics can rewire the brain to alter the subjective experience of chronic pain.

For most people, a peanut butter sandwich poses no threat. But for the roughly 1.6 million children in the United States with peanut allergy, exposure can trigger a life-threatening reaction. Why some individuals are susceptible while others are not has remained one of the most pressing unsolved questions in allergy research. A new study from the UNC School of Medicine points to an unexpected answer: the gut lining itself may be primed for allergy before a child ever encounters a peanut.

Published September 30 in Cellular and Molecular Gastroenterology and Hepatology (CMGH), the study was led by graduate student Katelyn (Katie) Clough in a collaboration between the labs of Dr. Shehzad Z. Sheikh, MD, PhD and Dr. Erin C. Steinbach, MD, PhD, in the Center for Gastrointestinal Biology and Disease (CGIBD) and Division of Rheumatology, Allergy & Immunology at UNC, respectively. Using single-cell RNA sequencing, the team constructed a high-resolution map of every cell type in the small intestinal lining of a peanut allergy-susceptible mouse model and found a striking defect in a specialized cell population called Paneth cells. The finding was then confirmed in pediatric patients with peanut allergy.

A Missing Protein at the Front Line of Gut Defense

Paneth cells are the gut’s antimicrobial sentinels, residing deep in the intestinal crypts and secreting protective proteins that regulate the local microbiome and help maintain the integrity of the gut barrier. The study found that in allergy-susceptible mice, Paneth cells completely lack expression of lysozyme 1 (Lyz1) a key antimicrobial enzyme. The reason is genetic: the allergy-susceptible CC027 mouse strain inherits its chromosome 10 from a wild mouse species, CAST/EiJ, which simply does not carry the Lyz1 gene.

This is not merely a mouse curiosity. When the team examined small intestinal biopsies from pediatric patients with peanut allergy, they observed a significant decrease in LYZ-positive crypts compared to patients without peanut allergy suggesting that Paneth cell lysozyme deficiency is a biologically relevant feature of human peanut allergy susceptibility.

“What struck me most was that these Paneth cell changes were present in allergen-naïve mice the animals had never been exposed to peanut,” said Clough. “This tells us the gut is already in an altered state before any allergic challenge. The barrier defect may come first, and allergy follows.”

Charting the Gut Epithelium, Cell by Cell

To build the cell atlas, the team isolated and sequenced the RNA of thousands of individual intestinal epithelial cells from allergy-susceptible CC027 mice and allergy-resistant C3H/HeJ mice, identifying 13 distinct cell populations, including absorptive enterocytes, stem cells, goblet cells, enteroendocrine cells, tuft cells, and Paneth cells. Beyond the lysozyme finding, the atlas revealed a coordinated pattern of epithelial remodeling in allergy-susceptible animals that was present before any allergen exposure:

A novel population of interferon-responsive absorptive enterocytes (AE-IFN) was significantly depleted in allergy-susceptible mice, suggesting impaired epithelial antiviral and immune surveillance programs.

Goblet cells which form a protective mucus barrier were expanded, while enteroendocrine cells, which regulate gut permeability signaling, were reduced.

Tuft cells, key initiators of type 2 allergic immune responses, were increased and showed elevated expression of allergic immune receptors including IL-4Rα.

Paneth cells exhibited signs of cellular stress under electron microscopy, including dilated endoplasmic reticulum and dysmorphic secretory granules, consistent with secretory dysfunction, in addition to decreased production of the antimicrobial protein lysozyme-1.

From a Missing Gene to a Skewed Microbiome

The consequences of lysozyme deficiency extend beyond the Paneth cell. Lysozyme is a critical regulator of the gut microbiome, selectively eliminating bacteria that can promote allergic immune responses. Comparing the microbial profiles of Lyz1-deficient mice with allergy-susceptible CC027 mice, the team found that both share enrichment of the same bacterial genera including Ruminococcus and Akkermansia, suggesting that the loss of lysozyme drives a microbiome composition that promotes type 2 (allergic) immune skewing, goblet and tuft cell expansion, and ultimately increased intestinal permeability.

“This study repositions the intestinal epithelium as a possible primary driver of allergic susceptibility, not a passive bystander,” said Steinbach, an Assistant Professor in the Division of Rheumatology, Allergy & Immunology. “A genetic loss of a single antimicrobial protein in Paneth cells cascades into microbiome changes, immune skewing, and a gut barrier primed for allergy. That is a mechanistic chain in which we can potentially intervene.”

Why It Matter for Patients and Families

Peanut allergy affects approximately 2 percent of children in the United States and is responsible for the majority of fatal food-induced anaphylaxis cases. Current management relies on strict avoidance and emergency epinephrine use. Oral immunotherapy offers desensitization for some patients, but achieving sustained tolerance remains elusive. Understanding the epithelial and microbial underpinnings of susceptibility opens new avenues for prevention in that identifying high-risk individuals early, or correcting the gut barrier before allergen exposure, could prevent allergy from developing in the first place.

“My son has a life-threatening peanut allergy and our family, like most other families living with peanut allergy, every meal is a calculation,” said Sheikh, Professor of Medicine and Genetics. “This research gives us a new framework for asking why the gut becomes susceptible in the first place and ultimately for designing interventions that could protect children before their first allergic reaction.”

The team plans to expand these findings in a larger pediatric patient cohort and to use human intestinal organoid models to explore whether correcting lysozyme deficiency or microbiome composition can restore barrier function in peanut allergy-susceptible backgrounds.

The study was supported by the Helmsley Charitable Trust, the National Institute of Allergy and Infectious Diseases (NIAID), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the UNC Thurston Arthritis Research Center, the American Academy of Allergy, Asthma & Immunology Foundation, the UNC CGIBD, and additional NIH sources including National Institute of Environmental Health Sciences (NIEHS). Single-cell library preparation was performed by the UNC CGIBD Advanced Analytics Core Facility and bioinformatics analyses by the UNC Bioinformatics and Analytics Research Collaborative (BARC).

Source: University of North Carolina School of Medicine