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COVID-induced Lung Infection Linked To Heart Damage
Severe acute respiratory distress syndrome (ARDS) related to COVID-19 infections can damage the heart even when the virus itself doesn't affect heart tissue. The findings come from a study today in Circulation.
The study suggests that ARDS triggers widespread inflammation in the body, which leads to secondary cardiovascular complications.
Though clinicians and researchers have observed for 4 years that COVID-19 infections lead to an increased risk of stroke, heart attack, and inflammation in the chest, the mechanism of damage was not understood.
"This was a critical question and finding the answer opens up a whole new understanding of the link between this serious lung injury and the kind of inflammation that can lead to cardiovascular complications," said Michelle Olive, PhD, an associate director at the National Heart, Lung, and Blood Institute, in a press release from the institute. "The research also suggests that suppressing the inflammation through treatments might help minimize these complications."
Olive was not involved in the study.
The study was conducted by looking at the autopsy cardiac specimens from 21 patients with COVID-19 who died from SARS-CoV-2–associated ARDS, and 33 patients who died from other causes. The study authors also used mice with SARS-CoV-2–associated ARDS to look more closely at cardiac immune cell dynamics. They also induced ARDS in mice without SARS-CoV-2 to compare cardiac findings.
Sending 'shockwaves' through the bodyIn both human and mice, the authors found that ARDS triggered remodeling of cardiac resident macrophages, leading to greater inflammation and reducing cardiac function. Macrophages are immune cells, and typically keep tissue healthy, but they can turn inflammatory if they proliferate too quickly.
Though no cardiac tissue was directly damaged, the lung infection caused by COVID-19 increased cardiac macrophages, which in turn led to cardiac problems for both people and mice with SARS-CoV-2–induced ARDS. Specifically, researchers found a higher proportion of CCR2+ (C-C chemokine receptor type 2 positive) macrophages in humans who had COVID-19 compared to those who did not.
The mice experiment inducing ARDS without a virus also showed an increase in macrophages and cardiac damage. In a subsequent experiment, the authors found that treating mice exposed to the virus-induced ARDS with a tumor necrosis factor neutralizing antibody reduced both inflammation and the number of CCR2+ macrophages.
What this study shows is that after a COVID infection, the immune system can inflict remote damage on other organs.
"What this study shows is that after a COVID infection, the immune system can inflict remote damage on other organs by triggering serious inflammation throughout the body – and this is in addition to damage the virus itself has directly inflicted on the lung tissue," said Matthias Nahrendorf, MD, PhD, a senior author on the study and professor of radiology at Harvard Medical School.
"These findings can also be applied more generally, as our results suggest that any severe infection can send shockwaves through the whole body."
Promoting Respiratory Health Naturally: Expert Lists Dietary Practices For A Lung-Healthy Diet
Did you know your diet plays an important role in maintaining your respiratory health? A healthy diet can help to improve respiratory health by providing the body with the nutrients it needs to function properly. Similarly, certain foods can be harmful causing inflammation in the lungs and making it more difficult to breathe. We spoke to Dr Ganesh Chaudhary, Bachelor of Ayurvedic Medicine and Surgery (BAMS), PHC, Darbhanga, Bihar, who listed dietary practices to boost respiratory health.
According to the American Lung Association, your body receives nutrients from the foods you eat, including proteins, fats, and carbs. You might breathe more easily if you consume a diet higher in fat and lower in carbohydrates. For every unit of oxygen needed during the metabolism of carbohydrates, your body creates more carbon dioxide. The least amount is produced by your body when it metabolises fat.
Antioxidants are essential for combating oxidative stress and inflammation in the lungs. Therefore, include plenty of fruits and vegetables, such as berries, oranges, tomatoes, leafy greens, and bell peppers in your diet. "These foods are rich in vitamins C and E, as well as other antioxidants like beta-carotene, which help protect lung tissues from damage caused by harmful free radicals", said Dr Chaudhary.
Consume Omega-3 Fatty AcidsAnother ingredient to make part of the respiratory diet is omega-3 fatty acid, which is well known for its anti-inflammatory properties. Hence, include sources of omega-3s, such as fatty fish, seeds, and walnuts into your diet. Dr Chaudhary added, "These healthy fats help reduce inflammation in the airways, promoting better lung function and reducing the risk of conditions like asthma and Chronic Obstructive Pulmonary Disease (COPD)."
Also Read: Detox Your Lungs: Benefits Of Mullein Tea To Fight Air Pollution
Did you know proper hydration is essential for maintaining healthy respiratory function? This is because water helps keep the mucous membranes in the airways moist, facilitating easier breathing and reducing the risk of respiratory infections.
According to a 2018 study conducted in Korea on over a thousand adults, those who drank at least two cups of green tea daily had higher lung function than those who drank none at all.
Include Lean Protein SourcesProtein is crucial for maintaining respiratory muscle strength and supporting immune function. Start by including lean protein sources, such as poultry, fish, tofu, and low-fat dairy products. Dr Chaudhary added, "These foods provide essential nutrients like zinc, which plays a role in immune health, and amino acids necessary for muscle repair and function."
Also Read: Respiratory Health: Here Are Ways to Clear Chest Congestion And Mucus
Eat Foods Rich in Magnesium"Magnesium is a mineral that supports lung function by relaxing the muscles of the airways and reducing bronchial spasms. Hence, include magnesium-rich foods, such as leafy greens, nuts, seeds, whole grains, and legumes in your diet", added Dr Chaudhary. Ensuring an adequate intake of magnesium can help prevent asthma attacks and improve overall respiratory health.
Limit Processed Foods and Trans FatsProcessed foods and those high in trans fats can contribute to inflammation and impair lung function. Therefore, refrain from consuming fried foods, processed snacks, and baked goods made with hydrogenated oils. Instead, opt for whole, minimally processed foods to support respiratory health.
Moderate Salt Intake"Excessive salt intake can lead to fluid retention and worsen conditions like asthma and COPD by causing airway inflammation and constriction. Hence, limit your intake of high-sodium processed foods and try to use herbs, spices, and other flavourings to season your meals instead of salt", highlighted Dr Chaudhary. Opt for fresh, whole foods to help regulate salt intake and support respiratory health.
[Disclaimer: This article contains information provided by an expert and is for informational purposes only. Hence, we advise you to consult your expert before making any dietary changes, especially if you are dealing with any health issues.]
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Lungs Communicate With Brain To Report Infection, Change Behavior
Summary: Researchers unveiled a groundbreaking mechanism where the lungs directly inform the brain of infections, altering traditional views on sickness response. This study, conducted in mice, demonstrates that neurological pathways, rather than just immune responses, are responsible for symptoms of illness.
The findings suggest that treating respiratory infections and chronic lung conditions might require approaches that target both the nervous system and the pathogen.
Additionally, the study observed a gender difference in sickness behavior, potentially offering a scientific basis for the so-called "man flu," with males showing greater dependence on neuronal communications during illness.
Key Facts:
Source: University of Calgary
University of Calgary researchers have discovered the lungs communicate directly with the brain when there is an infection. Findings show the brain plays a critical role in triggering the symptoms of sickness, which may change the way we treat respiratory infections and chronic conditions.
"The lungs are using the same sensors and neurons in the pain pathway to let the brain know there's an infection," says Dr. Bryan Yipp, MD '05, MSc'05, clinician researcher at the Cumming School of Medicine and senior author on the study.
"The brain prompts the symptoms associated with sickness; that overall feeling of being unwell, feeling tired and loosing your appetite. The discovery indicates we may have to treat the nervous system as well as the infection."
Sickness was thought to be a consequence of the immune system kicking into action. Credit: Neuroscience News Prior to this study, conducted in mice, it was thought infections in the lungs and pneumonia induce inflammatory molecules that eventually made their way to the brain through the blood stream.
Sickness was thought to be a consequence of the immune system kicking into action. However, findings reveal that sickness results from nervous system activation in the lung.
Understanding the lung-brain dialogue is important for treatment because bacteria that cause lung infections can produce a biofilm, a coating to surround themselves so the nervous system can't see them. That allows the bug to hide out in the lungs for a long time, which may shed light across diverse serious lung infections that are less symptomatic.
For example, an unexplained anomaly Yipp witnessed in the intensive care unit (ICU) during COVID. The phenomenon, coined "happy hypoxia", was being recorded in ICUs throughout the world.
"We would have patients whose oxygen levels were extremely low and x-rays confirmed they may need to be put on life support. Yet, when I went to see the patient, they would say I feel fine," says Yipp.
"These people were experiencing limited sickness symptoms even though the virus was aggressively damaging their lungs."
Yipp says understanding the lung brain communication pathways may also have broad implications for people with chronic lung infections like cystic fibrosis (CF). Many people with CF have a biofilm bacterium in their lungs and are asymptomatic. They feel okay, but then have a flare where they can become very ill. The reason for the flare can't always be traced.
"It is possible the flare is also neurological that these people live asymptomatically because bacteria are hiding out," says Yipp.
The findings, published in Cell, are the work of an interdisciplinary team including experts in neurobiology, microbiology, immunology, and infectious disease.
"Physician specialties are usually based on individual organs, with pulmonologists caring for the lungs and neurologists caring for the brain. Our study shows the lung is altering the brain and the brain is altering the organ. This intersection of communication is a different way of thinking about disease," says Yipp.
"It's all connected to the brain and there are probably even more complex circuits that are happening. We can now think about targeting neurocircuitry along with antibiotics to deal with infections and the sickness they cause."
University of Calgary researchers Drs. Christophe Altier, PhD, Joe Harrison, PhD, and Deborah Kurrasch, PhD, along with Dr. Jaideep Bains, PhD, Krembil Research Institute, Toronto, are corresponding authors on the study.
The researchers add there was one more unique finding. Male mice were much sicker than the females even though they had the same bacterial infection. Researchers found that male sickness was more dependent on neuronal communications then females.
Yipp says this finding could lend credibility to the so-called "man flu", a colloquial term where men are thought to wildly exaggerate sickness due to respiratory infections. Turns out they may not be exaggerating, after all.
University of Calgary researchers have discovered the lungs communicate directly with the brain when there is an infection. Findings show the brain plays a critical role in triggering the symptoms of sickness, which may change the way we treat respiratory infections and chronic conditions.
"The lungs are using the same sensors and neurons in the pain pathway to let the brain know there's an infection," says Dr. Bryan Yipp, MD '05, MSc'05, clinician researcher at the Cumming School of Medicine and senior author on the study.
"The brain prompts the symptoms associated with sickness; that overall feeling of being unwell, feeling tired and loosing your appetite. The discovery indicates we may have to treat the nervous system as well as the infection."
Prior to this study, conducted in mice, it was thought infections in the lungs and pneumonia induce inflammatory molecules that eventually made their way to the brain through the blood stream. Sickness was thought to be a consequence of the immune system kicking into action. However, findings reveal that sickness results from nervous system activation in the lung.
Understanding the lung-brain dialogue is important for treatment because bacteria that cause lung infections can produce a biofilm, a coating to surround themselves so the nervous system can't see them. That allows the bug to hide out in the lungs for a long time, which may shed light across diverse serious lung infections that are less symptomatic.
For example, an unexplained anomaly Yipp witnessed in the intensive care unit (ICU) during COVID. The phenomenon, coined "happy hypoxia", was being recorded in ICUs throughout the world.
"We would have patients whose oxygen levels were extremely low and x-rays confirmed they may need to be put on life support. Yet, when I went to see the patient, they would say I feel fine," says Yipp.
"These people were experiencing limited sickness symptoms even though the virus was aggressively damaging their lungs."
Yipp says understanding the lung brain communication pathways may also have broad implications for people with chronic lung infections like cystic fibrosis (CF). Many people with CF have a biofilm bacterium in their lungs and are asymptomatic. They feel okay, but then have a flare where they can become very ill. The reason for the flare can't always be traced.
"It is possible the flare is also neurological that these people live asymptomatically because bacteria are hiding out," says Yipp.
The findings, published in Cell, are the work of an interdisciplinary team including experts in neurobiology, microbiology, immunology, and infectious disease.
"Physician specialties are usually based on individual organs, with pulmonologists caring for the lungs and neurologists caring for the brain. Our study shows the lung is altering the brain and the brain is altering the organ. This intersection of communication is a different way of thinking about disease," says Yipp.
"It's all connected to the brain and there are probably even more complex circuits that are happening. We can now think about targeting neurocircuitry along with antibiotics to deal with infections and the sickness they cause."
University of Calgary researchers Drs. Christophe Altier, PhD, Joe Harrison, PhD, and Deborah Kurrasch, PhD, along with Dr. Jaideep Bains, PhD, Krembil Research Institute, Toronto, are corresponding authors on the study.
The researchers add there was one more unique finding. Male mice were much sicker than the females even though they had the same bacterial infection. Researchers found that male sickness was more dependent on neuronal communications then females.
Yipp says this finding could lend credibility to the so-called "man flu", a colloquial term where men are thought to wildly exaggerate sickness due to respiratory infections. Turns out they may not be exaggerating, after all.
About this neuroscience research newsAuthor: Kelly JohnstonSource: University of CalgaryContact: Kelly Johnston – University of CalgaryImage: The image is credited to Neuroscience News
Original Research: Closed access."Biofilm exopolysaccharides alter sensory-neuron-mediated sickness during lung infection" by Bryan Yipp et al. Cell
Abstract
Biofilm exopolysaccharides alter sensory-neuron-mediated sickness during lung infection
HighlightsInfections of the lung cause observable sickness thought to be secondary to inflammation. Signs of sickness are crucial to alert others via behavioral-immune responses to limit contact with contagious individuals.
Gram-negative bacteria produce exopolysaccharide (EPS) that provides microbial protection; however, the impact of EPS on sickness remains uncertain.
Using genome-engineered Pseudomonas aeruginosa (P. aeruginosa) strains, we compared EPS-producers versus non-producers and a virulent Escherichia coli (E. coli) lung infection model in male and female mice. EPS-negative P. aeruginosa and virulent E. coli infection caused severe sickness, behavioral alterations, inflammation, and hypothermia mediated by TLR4 detection of the exposed lipopolysaccharide (LPS) in lung TRPV1+ sensory neurons.
However, inflammation did not account for sickness.
Stimulation of lung nociceptors induced acute stress responses in the paraventricular hypothalamic nuclei by activating corticotropin-releasing hormone neurons responsible for sickness behavior and hypothermia.
Thus, EPS-producing biofilm pathogens evade initiating a lung-brain sensory neuronal response that results in sickness.
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