Consequently, say the researchers, the lung cells absorb the TB bacteria, giving the infecting bacteria a place to live for the long term.
"The bug sugarcoats itself and creates this magical interaction that allows it to slip by the immune system. We think that this is a beautiful example of the concept of host adaptation," said Larry Schlesinger, professor of internal medicine and director of the division of infectious diseases at Ohio State.
"TB has evolved in humans. We're the reservoir. It has had centuries to develop a sophisticated way to deal with its encounter with the human, and the lung is the special portal of entry," the researcher added.
Schlesinger presented the findings on TB's adaptation to the human respiratory system on September 26 at the First International Congress "Mycobacteria: A Challenge for the 21st Century" in Bogota, Colombia.
He said that at the point of infection in the lung, TB bacteria are eaten by a macrophage, also called an antigen-presenting cell. The macrophage activates specific molecules that make pieces of the bacteria visible to infection-fighting T cells.
The innate response kicks in to fight any pathogen, but an acquired immune response is required to activate T cells that are specifically designed to help macrophages kill TB bacteria, he added.
However, according to the researcher, the sugar coating delays activation of the acquired response, and thus the bacteria find comfort in the macrophages, causing a latent infection.
Schlesinger said that once the immune response fails to prompt macrophages to kill the TB bacteria, the bacteria eventually multiply so much that the infected cells burst and release the bugs into the lungs, leading to active infection.
He said that his lab had found that Mycobacterium tuberculosis had evolved over time to make itself particularly attractive to the macrophages in the lungs.
During the presentation, he also announced the discovery of two different strains of TB from ill patients that interact completely differently with macrophages.
He revealed that the two strains do not coat themselves with sugar, and, therefore, have a harder time finding their way into macrophages in the lungs.
Schlesinger said: "We believe that these strains haven't been living in humans for very long, so they don't know how to get into their niche and sleep into latency, which is the most commonly seen TB behaviour. But the few bacteria that do get into the lung macrophages grow like gangbusters, and we speculate that this is one reason for why they are a cause of TB outbreaks."
Schlesinger said that that discovery also indicated that the TB bacterium had evolved in relative isolation in different regions of the world.
"We feel that these isolates in different areas of the world interact with humans in a special way, and if these bugs then travel to a different part of the world and an abnormal encounter occurs, there can be outbreaks of TB as a result of the migration patterns of these strains," he said.