Hosts rely on the availability of nutrients for growth, and for defense against pathogens. At the same time, changes in host nutrition can alter the dynamics of pathogens that rely on their host for reproduction. For primary producer hosts, enhanced nutrient loads may increase host biomass or pathogen reproduction, promoting faster density-dependent pathogen transmission. However, the effect of elevated nutrients may be reduced if hosts allocate a growth-limiting nutrient to pathogen defense. In canonical disease models, transmission is not a function of nutrient availability. Yet, including nutrient availability is necessary to mechanistically understand the response of infection to changes in the environment. Here, we explore the implications of nutrient-mediated pathogen infectivity and host immunity on infection outcomes. We developed a stoichiometric disease model that explicitly integrates the contrasting dependencies of pathogen infectivity and host immunity on nitrogen (N) and parameterized it for an algal-host system. Our findings reveal dynamic shifts in host biomass build-up, pathogen prevalence, and the force of infection along N supply gradients with N-mediated host infectivity and immunity, compared with a model in which the transmission rate was fixed. We show contrasting responses in pathogen performance with increasing N supply between N-mediated infectivity and N-mediated immunity, revealing an optimum for pathogen transmission at intermediate N supply. This was caused by N limitation of the pathogen at a low N supply and by pathogen suppression via enhanced host immunity at a high N supply. By integrating both nutrient-mediated pathogen infectivity and host immunity into a stoichiometric model, we provide a theoretical framework that is a first step in reconciling the contrasting role nutrients can have on host-pathogen dynamics.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/ecy.4170 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The mechanism of action of indole-3-propionic acid on bone metabolism.
Food Funct
January 2025
Acupuncture and Tuina School, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China.
Indole-3-propionic acid (IPA), a metabolite produced by gut microbiota through tryptophan metabolism, has recently been identified as playing a pivotal role in bone metabolism. IPA promotes osteoblast differentiation by upregulating mitochondrial transcription factor A (Tfam), contributing to increased bone density and supporting bone repair. Simultaneously, it inhibits the formation and activity of osteoclasts, reducing bone resorption, possibly through modulation of the nuclear factor-κB (NF-κB) pathway and downregulation of osteoclast-associated factors, thereby maintaining bone structural integrity.
View Article and Find Full Text PDFMultiorgan proteomic analysis of infected animal models predict potential host factors for chikungunya virus.
MedComm (2020)
January 2025
Chikungunya virus (CHIKV) is a mosquito-borne alphavirus that is primarily known for causing severe joint and muscle symptoms, but its pathological effects have extended beyond these tissues. In this study, we conducted a comprehensive proteomic analysis across various organs in rodent and nonhuman primate models to investigate CHIKV's impact on organs beyond joints and muscles and to identify key host factors involved in its pathogenesis. Our findings reveal significant species-specific similarities and differences in immune responses and metabolic regulation, with proteins like Interferon-Stimulated Gene 15 (ISG15) and Retinoic Acid-Inducible Gene I (RIG-I) playing crucial roles in the anti-CHIKV defense.
View Article and Find Full Text PDFα-Lipoic acid increases phagocytosis of some lactic acid bacteria via modulation of CD36 expression.
Biosci Microbiota Food Health
August 2024
Local Brand R&D, SSP Co., Ltd., Opera City Tower, 3-20-2 Nishi Shinjuku, Shinjuku-ku, Tokyo 163-1488, Japan.
Phagocytosis by immunocompetent cells is a key role in the biological defense mechanism and is the starting point of the reaction that leads from innate to acquired immunity. Several studies have demonstrated that some lactic acid bacteria strains activate the innate and acquired immune systems of the host. However, further investigation of the mechanism and improvement of usefulness is needed because the effect differs depending on the type and strain of lactic acid bacteria.
View Article and Find Full Text PDF, the most common non-viral sexually transmitted parasite, causes more than 270 million infections annually. The infection's outcome varies greatly depending on different factors that include variation in human immune responses, the vaginal microbiome, and the inherent virulence of the strain. Although the pathogenicity of the different strains depends, at least partially, on differential gene expression of virulence genes; the regulatory mechanisms governing this transcriptional control remain incompletely understood.
View Article and Find Full Text PDFUltraviolet (UV)-induced DNA mutations produce genetic drivers of cutaneous melanoma initiation and numerous neoantigens that can trigger anti-tumor immune responses in the host. Consequently, melanoma cells must rapidly evolve to evade immune detection by simultaneously modulating cell-autonomous epigenetic mechanisms and tumor-microenvironment interactions. Angiogenesis has been implicated in this process; although an increase of vasculature initiates the immune response in normal tissue, solid tumors manage to somehow enhance blood flow while preventing immune cell infiltration.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!