Animal models are the cornerstone of basic research, providing simple, easy-to-study and ethical biological systems that help us better understand how the human body works. Immunologists tend to rely heavily on mice and rats for their research, owing to their similarity with human physiology, small body size, accelerated life spans, and ease of genetic modification. But it would be unwise of us to put all our eggs in one basket.
Though it may seem counterintuitive at first, many of our greatest scientific discoveries have arisen from studying animals with key physiological differences from humans. Though, broadly speaking, the way chickens and humans fight off pathogens are very similar, the variation between our immune organs and molecules provides easier ways to study the mechanistic underpinnings of the immune response. The chicken is the unlikely hero of immunological research – and not just through its contribution as tasty snacks to help fuel researchers through long days of experiments. It is precisely because of our differences that chickens have given rise to some of immunology’s most impactful breakthroughs, from fundamental adaptive immunity to vaccine development.
From Pasture to Pasteur: The Chicken’s Contribution to Vaccinology
Louis Pasteur is widely considered the father of immunology for his great contributions to our understanding of microbiology, microbial disease, and vaccination as both a preventative and prophylactic means of protection. Prompted by the rampant devastation of livestock by different infectious diseases, Pasteur started studying chicken cholera and its causative bacteria, Pasteurella multocida, in 1877. He isolated and began to grow the Pasteurella with the intention of injecting bacterial cultures into chickens, but accidentally left the samples out unattended on his laboratory bench for a month while on holiday. When he returned, he found that the bacteria had lost their virulence over time: chickens injected with these “attenuated” bacteria only developed mild symptoms, made full recoveries, and were also protected against new infections when subsequently injected with fresh, more virulent cultures.
We now know that this live, attenuated vaccine conferred protection by allowing the immune system to mount a response against the pathogen without the risk of severe dis-ease. After this “practice round”, the now-trained immune system can respond quickly and robustly when it encounters the same pathogen again. Pasteur and his colleagues applied this finding to other animal diseases, such as anthrax in cows or rabies in dogs, sheep, and eventually humans. These studies concluded that dead bacteria, which they inactivated with heat, could confer protection against future infection too. While newer versions of vaccines exist today, often using subunits of pathogens instead of whole organisms to train the immune system, vaccines for measles, mumps, and rubella, chickenpox, and influenza still use the same model of live-attenuated or inactivated pathogens that Pasteur discovered.
The impact of chickens on vaccinology doesn’t end there. Every year, in preparation for flu season, scientists use chicken eggs to grow candidate influenza viruses, which they then isolate for preparation into both live-attenuated and inactivated versions of a vaccine. The next time you get your flu shot – or any vaccine, for that matter – remember that you have chickens to thank.
What Came First: The Chicken or the Ig?
All multicellular organisms rely on the innate immune response as a rapid but non-specific first line of defense against pathogens, toxins, and other threats, but what happens when invaders slip through the cracks? In many vertebrates, this is when the adaptive immune response takes over. Adaptive im-munity offers a more sophisticated, targeted offense against specific pathogens that not only clears current infections but offers long lasting immunity against future infections too.
By 1948, there was some evidence to suggest that antibodies – otherwise known as immunoglobulins, which are proteins that specifically bind to and neutralize foreign antigens – were produced by plasma cells, but nobody knew where or how this occurred. It wasn’t until 1956 that Bruce Glick and Timothy Chang accidentally discovered that the bursa of Fabricius of chickens, a small and poorly characterized organ close to the cloaca, was critical for antibody production. While routinely injecting chickens with Salmonella bacteria to generate antibodies for a separate experiment, Glick and Chang saw that almost all bursectomized chickens died soon after they were exposed, and those that survived produced almost no antibodies against Salmonella at all. Chickens with intact bursas maintained high levels of Salmonella-specific antibodies and all remained healthy.
This observation laid the groundwork for Max Cooper’s research in the 1960s. After Jacques Miller found that removing the thymus from newborn mice severely reduced lymphocyte production and resulted in extreme immune deficiencies, most of Cooper’s contemporaries thought lymphocytes were generated in the thymus and then seeded the rest of the body, where they could then become antibody-generating plasma cells. Cooper disagreed: he thought thymus-derived lymphocytes and plasma cells might come from different sources instead of following one lineage path. So, he turned to the chicken (and its bursa) for answers. His experiments found that chickens without a thymus had very low lymphocyte counts, but could still produce normal levels of antibodies; however, chickens without a bursa produced no antibodies, but still had plenty of other lymphocytes. This was the first work that suggested there were two different arms of the adaptive immune system: one based in the bursa and one based in the thymus. Cooper’s further research found this was true in mammals as well, except mammalian antibody-producing cells are generated in the bone marrow instead of a bursa. We now refer to these two cell types as T cells, named after the thymus, and B cells, named not after the bone marrow, but after the bursa of Fabricius.
The main antibody isotype chickens produce is immunoglobulin Y (IgY), which is functionally similar to, but structurally distinct from, any of the antibodies that humans produce. As a result, IgY could be used to target mammalian structures without activating unwanted components of the mammalian immune system, which is a common struggle with many immune-based therapeutics today. Since IgY is easy to harvest from chicken eggs, it makes an excellent candidate for antibody-based diagnostic or therapeutic tools. Indeed, scientists are already studying IgY in the context of preventative and prophylactic antimicrobial treatment, cancer immunotherapy, and allergy therapies with promising results.
When it comes to immunology’s favourite model organisms, chickens still may not rule the roost. Nevertheless, immunologists remain deeply indebted to chickens for their contributions to the field, both as a model system to understand the mechanisms underlying the immune response and as tools for disease diagnosis, prevention, and treatment.
Victoria Sephton
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