Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts

ABSTRACT The age structure of human populations is exceptional among animal species. Unlike with most species, human juvenility is extremely extended, and death is not coincident with the end of the reproductive period. We examine the age structure of early humans with models that reveal an extraord...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Martin J. Blaser, Glenn F. Webb
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2014
Materias:	Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/fc20f1fa9a024d3da35f05ebe78629de
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:fc20f1fa9a024d3da35f05ebe78629de
record_format	dspace
spelling	oai:doaj.org-article:fc20f1fa9a024d3da35f05ebe78629de2021-11-15T15:47:03ZHost Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts10.1128/mBio.02262-142150-7511https://doaj.org/article/fc20f1fa9a024d3da35f05ebe78629de2014-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mBio.02262-14https://doaj.org/toc/2150-7511ABSTRACT The age structure of human populations is exceptional among animal species. Unlike with most species, human juvenility is extremely extended, and death is not coincident with the end of the reproductive period. We examine the age structure of early humans with models that reveal an extraordinary balance of human fertility and mortality. We hypothesize that the age structure of early humans was maintained by mechanisms incorporating the programmed death of senescent individuals, including by means of interactions with their indigenous microorganisms. First, before and during reproductive life, there was selection for microbes that preserve host function through regulation of energy homeostasis, promotion of fecundity, and defense against competing high-grade pathogens. Second, we hypothesize that after reproductive life, there was selection for organisms that contribute to host demise. While deleterious to the individual, the presence of such interplay may be salutary for the overall host population in terms of resource utilization, resistance to periodic diminutions in the food supply, and epidemics due to high-grade pathogens. We provide deterministic mathematical models based on age-structured populations that illustrate the dynamics of such relationships and explore the relevant parameter values within which population viability is maintained. We argue that the age structure of early humans was robust in its balance of the juvenile, reproductive-age, and senescent classes. These concepts are relevant to issues in modern human longevity, including inflammation-induced neoplasia and degenerative diseases of the elderly, which are a legacy of human evolution. IMPORTANCE The extended longevity of modern humans is a very recent societal artifact, although it is inherent in human evolution. The age structure of early humans was balanced by fertility and mortality, with an exceptionally prolonged juvenility. We examined the role of indigenous microbes in early humans as fundamental contributors to this age structure. We hypothesize that the human microbiome evolved mechanisms specific to the mortality of senescent individuals among early humans because their mortality contributed to the stability of the general population. The hypothesis that we present provides new bases for modern medical problems, such as inflammation-induced neoplasia and degenerative diseases of the elderly. We postulate that these mechanisms evolved because they contributed to the stability of early human populations, but their legacy is now a burden on human longevity in the changed modern world.Martin J. BlaserGlenn F. WebbAmerican Society for MicrobiologyarticleMicrobiologyQR1-502ENmBio, Vol 5, Iss 6 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Microbiology QR1-502
spellingShingle	Microbiology QR1-502 Martin J. Blaser Glenn F. Webb Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts
description	ABSTRACT The age structure of human populations is exceptional among animal species. Unlike with most species, human juvenility is extremely extended, and death is not coincident with the end of the reproductive period. We examine the age structure of early humans with models that reveal an extraordinary balance of human fertility and mortality. We hypothesize that the age structure of early humans was maintained by mechanisms incorporating the programmed death of senescent individuals, including by means of interactions with their indigenous microorganisms. First, before and during reproductive life, there was selection for microbes that preserve host function through regulation of energy homeostasis, promotion of fecundity, and defense against competing high-grade pathogens. Second, we hypothesize that after reproductive life, there was selection for organisms that contribute to host demise. While deleterious to the individual, the presence of such interplay may be salutary for the overall host population in terms of resource utilization, resistance to periodic diminutions in the food supply, and epidemics due to high-grade pathogens. We provide deterministic mathematical models based on age-structured populations that illustrate the dynamics of such relationships and explore the relevant parameter values within which population viability is maintained. We argue that the age structure of early humans was robust in its balance of the juvenile, reproductive-age, and senescent classes. These concepts are relevant to issues in modern human longevity, including inflammation-induced neoplasia and degenerative diseases of the elderly, which are a legacy of human evolution. IMPORTANCE The extended longevity of modern humans is a very recent societal artifact, although it is inherent in human evolution. The age structure of early humans was balanced by fertility and mortality, with an exceptionally prolonged juvenility. We examined the role of indigenous microbes in early humans as fundamental contributors to this age structure. We hypothesize that the human microbiome evolved mechanisms specific to the mortality of senescent individuals among early humans because their mortality contributed to the stability of the general population. The hypothesis that we present provides new bases for modern medical problems, such as inflammation-induced neoplasia and degenerative diseases of the elderly. We postulate that these mechanisms evolved because they contributed to the stability of early human populations, but their legacy is now a burden on human longevity in the changed modern world.
format	article
author	Martin J. Blaser Glenn F. Webb
author_facet	Martin J. Blaser Glenn F. Webb
author_sort	Martin J. Blaser
title	Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts
title_short	Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts
title_full	Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts
title_fullStr	Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts
title_full_unstemmed	Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts
title_sort	host demise as a beneficial function of indigenous microbiota in human hosts
publisher	American Society for Microbiology
publishDate	2014
url	https://doaj.org/article/fc20f1fa9a024d3da35f05ebe78629de
work_keys_str_mv	AT martinjblaser hostdemiseasabeneficialfunctionofindigenousmicrobiotainhumanhosts AT glennfwebb hostdemiseasabeneficialfunctionofindigenousmicrobiotainhumanhosts
_version_	1718427560779448320

Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts

Ejemplares similares