Biomedical Laboratory Science

Saturday, August 26, 2017

The Theory of Disappearing Microbiota and the Epidemics of Chronic Diseases.

In the present era, medical scientists have been confounded by the increasing incidence of multiple diseases across the world, beginning first in developed countries, and gradually spreading to other areas as they develop. These include the rises in cases of obesity, asthma, hay fever, food allergies, inflammatory bowel disease, juvenile (type 1) diabetes and autism, among many others. Are these diseases, which affect different body systems, unrelated or can a unified theory explain the increased incidence of all of these?

I believe that the latter possibility is true, and that the central theory to explain why these diseases have arisen and by what mechanism is based on modern changes in early life events that are related to the human microbiome. According to this theory, the microbiome of humans and of other animals is not accidental, but has been selected over long time periods to optimize host reproductive success through interactions between the microbiota and host physiology. Early life is the crucial period during which the adult microbiome becomes established, and development of the host and of the microbiota occur together in a conjoined manner through a dynamic equilibrium that follows a well-choreographed path. In early life, the context is set for the important developmental decisions that are required for the immune system to distinguish between what is self and what is not self, for metabolic organs to partition how much energy to expend or to save, and for the brain to determine how to respond socially to a person who might be either a friend or a foe.




Figure 1: A model for the interaction of the inherited microbiota with
early life immunological development in past and present children.



Heterogeneity in Tuberculosis.

Infection with Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), results in a range of clinical presentations in humans. Most infections manifest as a clinically asymptomatic, contained state that is termed latent TB infection (LTBI); a smaller subset of infected individuals present with symptomatic, active TB. Within these two seemingly binary states, there is a spectrum of host outcomes that have varying symptoms, microbiologies, immune responses and pathologies. Recently, it has become apparent that there is diversity of infection even within a single individual. A good understanding of the heterogeneity that is intrinsic to TB — at both the population level and the individual level — is crucial to inform the development of intervention strategies that account for and target the unique, complex and independent nature of the local host–pathogen interactions that occur in this infection. In this Review, we draw on model systems and human data to discuss multiple facets of TB biology and their relationship to the overall heterogeneity observed in the human disease.



Figure 1: A classical tuberculosis granuloma. The hallmark tuberculosis
granuloma is a highly organized collection of immune cells that aggregate
around a central necrotic core.


Source: NATURE REVIEWS IMMUNOLOGY


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