The-Scientist explores a strange interaction that helped eliminate smallpox without us even noticing. The vaccine that helped eliminate this killer got an extra boost from local skin bacteria that got scraped in with the shot and bolstered the host’s immune response:
In the study, the researchers vaccinated three groups of mice with the vaccinia virus and compared their immune responses. The first group included seven-week-old specific-pathogen-free (SPF) mice (laboratory mice bred to lack specific microbes) treated with antibiotics, the second was SPF mice without antibiotic treatment, and the last group consisted of seven-to-nine-week-old old germ-free mice, which don’t contain any microbes. After six days, the researchers observed a lesion on the vaccination site in all groups, but of varying sizes. Untreated SPF mice had larger lesions than the other groups. Historically, observing the formation of this lesion indicated to clinicians that the vaccine worked—even though they didn’t understand the underlying mechanism. In the new study, the researchers found that the lesion is a consequence of the proliferation of several skin bacteria that infect the vaccination site.
The researchers measured the rodents’ local immune response to the vaccine, reporting that it was weaker in the antibiotic-treated SPF group and the germ-free mice. Following vaccination, their analysis showed that immune cells in the antibiotic-treated mice and the germ-free mice declined significantly. However, neutrophils persisted and even increased in number in the group without antibiotic treatment. “That was the really interesting thing,” says [Cambridge researcher Geoffrey] Smith. “That suggested that the bacteria, when they were present, were contributing to the immune response that we got from vaccination.”
Also, the researchers observed that even though the smallpox vaccination offered protection against the disease in all groups, SPF mice had three times more neutralizing antibodies than their germ-free counterparts.
You can read more from the Cambridge/University of Bern researchers here, in PLOS Pathogens.