Giving birth is one of the most exciting times in parents’ lives. And doctors do everything in their power to help deliver healthy babies. This often includes providing antibiotics to protect infants from contracting an infection during vaginal or cesarean deliveries.

Currently, antibiotics directed at a wide range of bacteria are prescribed to 4-10% of all newborns.* However, new research conducted by the Cincinnati Children’s Hospital Medical Center (CCHMC) and the California National Primate Research Center (CNPRC) reveals that antibiotic treatments in newborns can change the immune system’s response to lung infections like pneumonia. 

 Researchers studied a group of rhesus macaque infants and their reactions to antibiotics vs. a group that did not receive the medication. The result? The animals that received antibiotics showed a more severe reaction to pneumonia than the control group. 

 “Early life antibiotic use has been linked to chronic health conditions in children but we don’t understand the underlying biology of these effects. This important study is the first to provide experimental evidence of a potential negative effect of antibiotic treatment in infancy in a relevant animal model of childhood development,” said Dr. Lisa Miller, co-author on the study.

The researchers will continue their studies in other animals, including mice, to eventually test and screen human babies as part of preparing to help those more at risk of contracting pneumonia after receiving antibiotics during birth.

Researchers also have a clear message for parents: infants who need antibiotics should still get them. Antibiotics transform lethal infections into minor diseases and have saved countless lives. 

“The next step is to learn how to balance the benefits of antibiotic treatment with the impact on the immune system to avoid potential health risks in susceptible infants,” says Miller.

Cardiovascular disease is one of the leading causes of death in the United States, and it has many possible causes. One of the most well-known risk factors is hyperlipidemia, which presents as a high level of lipids, like triglycerides or cholesterol, in the blood. Scientists and doctors are still looking for effective ways to reduce cardiovascular risk from hyperlipidemia—and according to new research, fish oil may be part of the solution.

Recently, a team including Peter Havel, DVM, PhD, of UC Davis and the California National Primate Research Center (CNPRC) found that targeting a protein known as angiopoietin-like protein-3 (or ANGPTL3) could be helpful for managing cardiovascular disease.

In the study, the scientists gave 59 male rhesus macaques flavored, fructose-sweetened beverages daily in addition to their regular diet. A subset of macaques also received a whole fish oil supplement. The fructose supplementation allowed researchers to model symptoms of metabolic syndromes seen in humans, including insulin resistance and hyperlipidemia. This model also rapidly increased levels of triglycerides and certain lipoproteins in the blood, mirroring human risk factors for cardiovascular disease.

The results showed ANGPTL3 levels increased simultaneously with lipid levels in monkeys fed a high-sugar diet. It was also found that inhibiting the production of ANGPTL3 resulted in lower levels of several lipids and lipoproteins in circulation, which suggests the protein could be a helpful therapeutic target. What’s more, the researchers found that increases in the protein and lipids in the blood could be prevented if the animals were also provided with the fish oil supplement.

While the exact mechanisms remain unknown, Havel hopes to clarify in future studies exactly how components of fish oil influence ANGPTL3 production and circulating lipid levels. Understanding this could help scientists develop new interventions for the prevention and treatment of cardiovascular disease.

Heart health is incredibly important, which is why NPRC scientists are actively conducting research on cardiovascular diseases and treatments. Learn more about their breakthrough discoveries by visiting this link.

In 2018, wildfires tore across the state of California, leaving smoldering remains in their wake. These were some of the worst natural disasters on U.S. soil in recent years, and what’s worse, similar occurrences are becoming increasingly common.

If there’s any good to come from these phenomena, it’s that scientists are collecting data in the aftermath that could help reduce the effects of fires on humans and animals. This new research will add to the existing body of knowledge on the subject, including a study originally conducted in 2008 at the California National Primate Research Center (CNPRC). During the study, researchers found altered immunity and lung function in juvenile monkeys that were exposed as infants to wildfire smoke in 2008.

Lisa Miller, leader of the CNPRC Respiratory Diseases Unit, and her team recently tested lung function and blood samples from adult monkeys (now 10 years of age) that were originally exposed to the 2008 wildfire smoke. Their findings were consistent with the earlier study, suggesting that infant exposure to fine particles from fire leads to long term impairment of the respiratory and immune systems in adulthood. 

“The idea behind this is that if we detected any changes in the animals this information might translate as a biomarker that can be used for kids,” said Miller. “The ability of the animals to respond to a real pathogen was reduced. It was a surprise and somewhat disturbing.”

In 2018, smoke from the Butte County Camp Fire—which burned more than 700 square miles—reached the CNPRC, and about 2,000 animals and roughly 500 infant nonhuman primates were exposed for a period of more than 10 days. Because the fires came so close to the UC Davis campus where the CNPRC is located, researchers will once again be able to test the health effects of wildfire smoke on the center’s nonhuman primates. 

Examination of the results is still ongoing, but the additional data from this blaze will help Miller and team continue the search for causes, preventative measures and treatments for the damaging health effects of these massive wildfires.

Reviewed: June 2020

Feel that familiar tickle in your nose? You may be coming down with the common cold – a virus that has been afflicting humans for thousands of years.

One of the most ubiquitous illnesses, human rhinovirus (HRV) is responsible for more than 50% of cold-like illnesses and billions of dollars annually in medical visits and missed days of work. Yet, despite its prevalence and a nearly 60-year search, there is still no cure for the common cold.

But while most humans recover from the common cold in about seven days, a recent discovery of rhinovirus in chimpanzees resulted in a nearly 10% fatality rate. This is the first time scientists have seen rhinovirus cross the species barrier.

“It was completely unknown that rhinovirus could infect anything other than humans.” said Tony Goldberg, a professor in the University of Wisconsin-Madison’s School of Veterinary Medicine. “It was surprising to find it in chimpanzees, and it was equally surprising that it could kill healthy chimpanzees outright.”

The outbreak occurred in a chimpanzee community in Kibale National Park, Uganda. Of the 56 animals, five chimps between the ages of two and 57 died. A local veterinarian obtained a fecal sample from a deceased chimpanzee, allowing UW scientists to discover that the virus originated from a human cold host.

“We expected to see changes all over the genome,” said Ann Palmenberg, a UW-Madison professor of biochemistry. “But it is not a chimp-adapted virus.”

This discovery means that chimps are genetically predisposed to rhinovirus C, a particularly severe form of the common cold. This virus primarily affects young children with susceptible receptors, or “locks” that allows viruses to enter and infect cells.

“The virus found in Betty (a two-year old chimp) was one that looked like it came from a human, and the level of virus in the lung was comparable to what we see in children,” said James Gern, a Professor of Allergy and Immunology in the UW School of Medicine and Public Health. “There’s a species-wide susceptibility of chimps to this virus,” added Goldberg.

This discovery could have a major impact on scientist and zoologists alike. Goldberg suspects that rhinovirus C may have been overlooked for decades as a cause of chimpanzee death. Now, scientists are more motivated than ever to find a cure to the common cold — both for humans and their counterparts in the wild.

Reviewed August 2019

The California wildfires of 2017 are shining a spotlight on research originally conducted back in 2008 at the California National Primate Research Center (CNPRC) which found that exposure to high levels of wildfire smoke negatively affects development of both the immune system and lung function.

Because the fires came so close to the UC-Davis campus where the CNPRC is located, researchers could test the effect of wildfire smoke on the center’s 5,000 nonhuman primates. Since they live outside, they’re exposed to higher levels of smoke than humans. Additionally, the timing of the fire in early summer coincided with the end of the birthing season for rhesus macaques, allowing the researchers to study the effects of the smoke on newborns.

Lisa Miller, leader of the CNPRC Respiratory Diseases Unit, and her team tested lung function and took blood samples from monkeys that were two to three weeks old during the 10 days of peak smoke pollution.

The fine particles found in wildfire smoke can lodge deep in the lungs and are known to cause respiratory illness. This research, however, revealed that exposure in infancy can also impair the development of the immune system. A sample group of the nonhuman primates that had suffered smoke damage were exposed to an infectious disease. Compared to a control group, the immune systems of the doubly-exposed nonhuman primates weren’t as effective at combating the virus.

“The idea behind this is that if we detected any changes in the animals this information might translate as a biomarker that can be used for kids,” said Miller. “The ability of the animals to respond to a real pathogen was reduced. It was a surprise and somewhat disturbing.”

With renewed interest in this research, Miller and others are pressing forward with their work.

Reviewed August 2019

There’s no love lost between the cardiovascular system and the world’s population – after all, heart disease is the leading cause of death around the globe. While scientists have long attempted to create vascular models to explore potential causes, preventions, treatments and cures for vascular disease, understanding just how each medical condition arises has hampered potential discovery.

A recent study authored by University of Wisconsin-Madison professor and Wisconsin National Primate Research Center scientist Dr. Igor Slukvin and Akhilesh Kumar, assistant researcher in his lab, might change all of that. Now, scientists are poised to get a better look at the fundamental development of the cells that make up blood vessels and how they can be more reliably cultured in the laboratory dish.

The new scientific advancement provides a blueprint for how vasculature arises at the earliest stages of development, allowing scientists to study the cells that compose blood vessels and devise new models for studying blood vessel disease. Critically, the discovery of methods to generate the building-block cells could set the stage for engineering blood vessels in the laboratory for disease modeling, drug screening and therapeutic purposes.

“Now, investigators will have access to a plethora of new research identifying cell type alternatives for vascular engineering,” said Kumar, noting that the new Wisconsin study, paired with the ability of the progenitor stem cells to proliferate and differentiate to different cell types in culture, can potentially accelerate the time it takes to grow vascular grafts.

Previously, identifying different vascular cell types in living tissue was the easy part; distinguishing cell types from cells grown in culture was a different story. In the study, Kumar made an important revelation – cells that compose blood vessels arise from a common progenitor. The ability to trace the developmental path that gives rise to the cells that make up blood vessels provides science a potent pathway to devise new cellular therapies.

Immediate application of this scientific research includes creating laboratory models for vascular disease to inform a better basic understanding of what goes wrong in killers such as coronary artery disease and certain genetic diseases that affect vasculature. Moreover, these cells can be used in high-throughput drug screens, accelerating the pace of development of new drugs and repurposing old ones to treat vascular ailments. Creating new blood vessels from scratch is still far from reality, but the new Wisconsin study is an essential step toward that goal.

Reviewed August 2019

Gender disparity is not only a matter of wages and family roles. Pulmonary disease can affect women differently, and with a greater degree of severity, than men.

Scientists like Dr. Kent Pinkerton, a Core Scientist in the California National Primate Research Center (CNPRC) Respiratory Diseases Unit and for the Inhalation Exposure Core at UC Davis, are utilizing nonhuman primate research to examine gender-based differences in lung health and disease and the effects of climate change on lung health. Since the nonhuman primate lung has been shown to have similar architectural, morphological and developmental patterns to that of humans, it is the perfect model of lung development and aging processes.

Dr. Pinkerton and his colleagues thoroughly reviewed sociocultural implications of pulmonary disease attributable to numerous causes, including biomass burning and infectious diseases among women in low-to middle-income countries, as well as disparities in respiratory health among sexual minority women in high-income countries. The scientific team sought answers to many questions – 10, to be exact – addressing gender-based disparities in lung health as it relates to telomere length, stages of life, hormones, cumulative effects, and environmental toxins.

For example, women in low- to middle-income countries must combat with household air pollution (HAP) or indoor air pollution from the indoor burning of solid fuels. With limited access to fuels, households often use wood, charcoal, animal waste, coal or crop residue for cooking using either open fires or traditional unvented stoves. These cooking fires release soot into the household air and blacken the interior walls, resulting in air that exceeds World Health Organization (WHO) air quality standards by 10 to 100 fold.

HAP exposure is linked to  four million deaths worldwide each year, predominantly from COPD, cardiovascular disease, acute pneumonia in children under age five and lung cancer. Bearing responsibility for cooking and childcare, women especially suffer from HAP exposure-related diseases.

Thankfully, cleaner cooking solutions, like highly efficient cookstoves or effective, well-maintained chimneys, can reduce household exposures and improve the health of women and kids worldwide. However, with a need to reach hundreds of millions of households and to find the best solutions and mechanisms to implement such strategies, the problem is daunting.

Utilizing the CNPRC’s extensive capabilities and resources, and a myriad of research projects under way, Dr. Pinkerton is well positioned to understand the mechanisms underlying respiratory diseases and to develop new strategies to alleviate the detrimental health outcomes of pollutant exposures.

Reviewed August 2019

Wildfires can can destroy a community, but it’s the smoke that can suck the life out of your lungs.  

But what exactly is smoke? Simply put – it’s a collection of particles suspended in the air as a result of a fire. And smoke from wildfires is a particularly complex assortment, with a greater quantity and variety of particles than smoke from other types of fire. It’s this combination that make wildfire smoke especially toxic to the lungs according to Kent Pinkerton, a researcher at the California National Primate Research Center and a professor of pediatrics and veterinary medicine.

“Particles and gases that are generated from wildfires can create all sorts of conditions and symptoms, such as tightness or pain in the chest, wheezing, shortness of breath, and coughing, all of which would be triggered in certain individuals,” said Pinkerton. “We may also see burning and stinging of the nose, eyes and throat, even dizziness or lightheadedness. Typically, we see a rapid recovery from symptoms, but there can be those for whom the symptoms linger for a day or 2.”

Children, in particular, are accurately susceptible to the negative effects of wildfire smoke.

“Children are always active and energetic and they take in large quantities of air with a rapid respiration rate. Because of this, the effects of the smoke can be far greater for children than for adults,” he explained. “Their lungs have a smaller surface area for the particles to interact with. Each of those can affect children to cause wheezing, coughing, shortness of breath that may not be evident in adults who are breathing the same air.”

Household pets can experience the same symptoms, but they also have one natural advantage over humans – a sophisticated filtering system.

“For mammals like cats and dogs, they have a very similar lung structure to humans.  They can also feel those effects just like we do,” Pinkerton said. “They also have the ability to protect themselves— they are more likely to be nose breathers rather than breathing through their mouths, which provides a certain degree of protection through the filtration of particles that are in the air through the nasal cavity. They have a much more complicated structure in the nasal cavity that we do as humans.”

Whether it’s kids or pets, wildfire smoke can be devastating to a respiratory system. But thanks to the continuing work of Pinkerton and his team of researchers, future smoke victims will likely live longer, healthier lives.

Reviewed August 2019