On the control of acute rodent malaria infections by innate immunity

Does specific immunity, innate immunity or resource (red blood cell) limitation control the first peak of the blood-stage parasite in acute rodent malaria infections? Since mice deficient in specific immunity exhibit similar initial dynamics as wild-type mice it is generally viewed that the initial control of parasite is due to either limitation of resources (RBC) or innate immune responses. There are conflicting views on the roles of these two mechanisms as there is experimental evidence supporting both these hypotheses. While mathematical models based on RBC limitation are capable of describing the dynamics of primary infections, it was not clear whether a model incorporating the key features of innate immunity would be able to do the same. We examine the conditions under which a model incorporating parasite and innate immunity can describe data from acute <i>Plasmodium chabaudi</i> infections in mice. We find that innate immune response must decay slowly if the parasite density is to fall rather than equilibrate. Further, we show that within this framework the differences in the dynamics of two parasite strains are best ascribed to differences in susceptibility to innate immunity, rather than differences in the strains' growth rates or their propensity to elicit innate immunity. We suggest that further work is required to determine if innate immunity or resource limitation control acute malaria infections in mice

The evolution of resistance through costly acquired immunity

We examine the evolutionary dynamics of resistance to parasites through acquired immunity. Resistance can be achieved through the innate mechanisms of avoidance of infection and reduced pathogenicity once infected, through recovery from infection and through remaining immune to infection: acquired immunity. We assume that each of these mechanisms is costly to the host and find that the evolutionary dynamics of innate immunity in hosts that also have acquired immunity are quantitatively the same as in hosts that possess only innate immunity. However, compared with resistance through avoidance or recovery, there is less likely to be polymorphism in the length of acquired immunity within populations. Long-lived organisms that can recover at intermediate rates faced with fast-transmitting pathogens that cause intermediate pathogenicity (mortality of infected individuals) are most likely to evolve long-lived acquired immunity. Our work emphasizes that because whether or not acquired immunity is beneficial depends on the characteristics of the disease, organisms may be selected to only develop acquired immunity to some of the diseases that they encounter

Innate immunity and neuroinflammation

Copyright © 2013 Abhishek Shastri et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Inflammation of central nervous system (CNS) is usually associated with trauma and infection. Neuroinflammation occurs in close relation to trauma, infection, and neurodegenerative diseases. Low-level neuroinflammation is considered to have beneficial effects whereas chronic neuroinflammation can be harmful. Innate immune system consisting of pattern-recognition receptors, macrophages, and complement system plays a key role in CNS homeostasis following injury and infection. Here, we discuss how innate immune components can also contribute to neuroinflammation and neurodegeneration

libtissue - implementing innate immunity

In a previous paper the authors argued the case for incorporating ideas from innate immunity into articficial immune systems (AISs) and presented an outline for a conceptual framework for such systems. A number of key general properties observed in the biological innate and adaptive immune systems were hughlighted, and how such properties might be instantiated in artificial systems was discussed in detail. The next logical step is to take these ideas and build a software system with which AISs with these properties can be implemented and experimentally evaluated. This paper reports on the results of that step - the libtissue system.Comment: 8 pages, 4 tables, 5 figures, Workshop on Artificial Immune Systems and Immune System Modelling (AISB06), Bristol, U

In vivo detection of lamellocytes in Drosophila melanogaster.

Drosophila has recently become a powerful model organism for studies of innate immunity. The cellular elements of innate immunity in Drosophila, the hemocytes, have been characterized by morphological criteria, molecular markers, and cell-type-specific immunological markers. Here we suggest that an MiET1 GFP-reporter element insertion in the untranslated region of a gene (l1-atilla) - expressed in a subset of hemocytes, the lamellocytes - allows in vivo investigations of lamellocyte differentiation and facilitates genetic screens

Integrative Genomics Reveals the Genetics and Evolution of the Honey Bee’s Social Immune System

Social organisms combat pathogens through individual innate immune responses or through social immunity—behaviors among individuals that limit pathogen transmission within groups. Although we have a relatively detailed understanding of the genetics and evolution of the innate immune system of animals, we know little about social immunity. Addressing this knowledge gap is crucial for understanding how life-history traits influence immunity, and identifying if trade-offs exist between innate and social immunity. Hygienic behavior in the Western honey bee, Apis mellifera, provides an excellent model for investigating the genetics and evolution of social immunity in animals. This heritable, colony-level behavior is performed by nurse bees when they detect and remove infected or dead brood from the colony. We sequenced 125 haploid genomes from two artificially selected highly hygienic populations and a baseline unselected population. Genomic contrasts allowed us to identify a minimum of 73 genes tentatively associated with hygienic behavior. Many genes were within previously discovered QTLs associated with hygienic behavior and were predictive of hygienic behavior within the unselected population. These genes were often involved in neuronal development and sensory perception in solitary insects. We found that genes associated with hygienic behavior have evidence of positive selection within honey bees (Apis), supporting the hypothesis that social immunity contributes to fitness. Our results indicate that genes influencing developmental neurobiology and behavior in solitary insects may have been co-opted to give rise to a novel and adaptive social immune phenotype in honey bees.York University Librarie

'Towards a Conceptual Framework for Innate Immunity'

Innate immunity now occupies a central role in immunology. However, artificial immune system models have largely been inspired by adaptive not innate immunity. This paper reviews the biological principles and properties of innate immunity and, adopting a conceptual framework, asks how these can be incorporated into artificial models. The aim is to outline a meta-framework for models of innate immunity

Hypercytokinemia: Increased or decreased innate immunity?

The adipose tissue is an active endocrine organ which secretes proinflammatory cytokines and chemokines resulting into raised serum levels. Hypercytokinemia has been interpreted as raised level of innate immunity and its evolution is interpreted as a response to increased chances of infection under starvation conditions in which the thrifty phenotype evolved. If starvation and infection challenges co-occurred during hunter gatherer life, thrifty genotype and infection resistant genotype may have co-evolved. An inherent weakness of this explanation is that in obesity or insulin resistance there is no evidence of increased resistance to infections. The raised levels of inflammatory cytokines have not been demonstrated to combat infections or enhance wound healing. We suggest that the raised chemokine levels actually decrease peripheral innate immunity. The normal movement of monocyte-macrophages and neutrophils from blood vessels to injured tissue is under a chemokine gradient. A gradient results from the difference between the basal levels of chemokines and those secreted by the injured tissue. Increase in the basal level is expected to weaken the gradient thereby decreasing extravasation and infiltration. Using diffusion kinetics we show that a small rise in basal levels can cause substantial reduction in cell infiltration. This interpretation is consistent with the behavioural switch hypothesis proposed by Watve and Yajnik which suggests that obesity and insulin resistance mark a transition from “soldier” to “diplomat” lifestyle. Hypercytokinemia may have evolved as a mechanism of disinvestment in peripheral innate immunity since the diplomat lifestyle is less injury prone. We evaluate the two alternative hypotheses by available evidence