Mapping of &lt;i&gt;CARD4&lt;/i&gt; gene to pig chromosome 18 (Brief report) (Kartierung des &lt;i&gt;CARD4&lt;/i&gt; Gens auf dem Schweinechromosom Nr. 18)

Abstract. The caspase recruitment domain family, member 4 gene (CARD4) is a member of the CATERPILLER (caspase recruitment domain, transcription enhancer, r (purine)-binding, pyrin, lots of leucine repeats) family. In humans, CARD4 has been shown to be involved in the innate immune system responsible for cytosolic recognition of bacteria. This gene also contributes to the inflammation processes seen in asthma (HYSI et al., 2005) and intestinal bacterial infections (KIM et al., 2004). The human CARD4 gene is located on chromosome 7. It contains 14 exons and spans approximately 4.4 kb. The objective of this study was to determine the chromosomal location of CARD4 in the pig by linkage and RH mapping.

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Changes in the microbiota cause genetically modified Anopheles to spread in a population

Science ◽

10.1126/science.aak9691 ◽

2017 ◽

Vol 357 (6358) ◽

pp. 1396-1399 ◽

Cited By ~ 30

Author(s):

Andrew Pike ◽

Yuemei Dong ◽

Nahid Borhani Dizaji ◽

Anthony Gacita ◽

Emmanuel F. Mongodin ◽

...

Keyword(s):

Immune System ◽

Innate Immune System ◽

Bacterial Infections ◽

Genetically Modified ◽

Reproductive Organs ◽

Innate Immune ◽

Wild Type ◽

Immune Genes ◽

Cage Population ◽

Genetically Modified Mosquitoes

The mosquito’s innate immune system controls both Plasmodium and bacterial infections. We investigated the competitiveness of mosquitoes genetically modified to alter expression of their own anti-Plasmodium immune genes in a mixed-cage population with wild-type mosquitoes. We observed that genetically modified mosquitoes with increased immune activity in the midgut tissue did not have an observed fitness disadvantage and showed reduced microbial loads in both the midgut and reproductive organs. These changes result in a mating preference of genetically modified males for wild-type females, whereas wild-type males prefer genetically modified females. These changes foster the spread of the genetic modification in a mosquito cage population.

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Deficiency in Hematopoietic Phosphatase Ptpn6/Shp1 Hyperactivates the Innate Immune System and Impairs Control of Bacterial Infections in Zebrafish Embryos

The Journal of Immunology ◽

10.4049/jimmunol.1200551 ◽

2013 ◽

Vol 190 (4) ◽

pp. 1631-1645 ◽

Cited By ~ 23

Author(s):

Zakia Kanwal ◽

Anna Zakrzewska ◽

Jeroen den Hertog ◽

Herman P. Spaink ◽

Marcel J. M. Schaaf ◽

...

Keyword(s):

Immune System ◽

Innate Immune System ◽

Bacterial Infections ◽

Innate Immune ◽

Zebrafish Embryos

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Synergistic elimination of bacteria by phage and the innate immune system

10.1101/057927 ◽

2016 ◽

Author(s):

Chung Yin (Joey) Leung ◽

Joshua S. Weitz

Keyword(s):

Immune Response ◽

Immune System ◽

Numerical Simulations ◽

Innate Immune System ◽

Bacterial Infections ◽

Phage Therapy ◽

Innate Immune ◽

Host Immune System ◽

Burn Wound

AbstractPhage therapy has been viewed as a potential treatment for bacterial infections for over a century. Yet, the year 2016 marks the first phase I/II human trial of a phage therapeutic - to treat burn wound patients in Europe. The slow progress in realizing clinical therapeutics is matched by a similar dearth in principled understanding of phage therapy. Theoretical models and in vitro experiments find that combining phage and bacteria often leads to coexistence of both phage and bacteria or phage elimination altogether. Both outcomes stand in contrast to the stated goals of phage therapy. A potential resolution to the gap between models, experiments, and therapeutic use of phage is the hypothesis that the combined effect of phage and host immune system can synergistically eliminate bacterial pathogens. Here, we propose a phage therapy model that considers the nonlinear dynamics arising from interactions between bacteria, phage and the host innate immune system. The model builds upon earlier efforts by incorporating a maximum capacity of the immune response and density-dependent immune evasion by bacteria. We analytically identify a synergistic regime in this model in which phage and the innate immune response jointly contribute to the elimination of the target bacteria. Crucially, we find that in this synergistic regime, neither phage alone nor the innate immune system alone can eliminate the bacteria. We confirm these findings using numerical simulations in biologically plausible scenarios. We utilize our numerical simulations to explore the synergistic effect and its significance for guiding the use of phage therapy in clinically relevant applications.

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Bacterial glycans and their interactions with lectins in the innate immune system

Biochemical Society Transactions ◽

10.1042/bst20170410 ◽

2019 ◽

Vol 47 (6) ◽

pp. 1569-1579 ◽

Cited By ~ 4

Author(s):

Mariano Prado Acosta ◽

Bernd Lepenies

Keyword(s):

Innate Immunity ◽

Immune System ◽

Immune Responses ◽

Innate Immune System ◽

Bacterial Infections ◽

Innate Immune ◽

Immune Recognition ◽

Lectin Receptors ◽

Bacterial Surfaces ◽

Bacterial Glycosylation

Bacterial surfaces are rich in glycoconjugates that are mainly present in their outer layers and are of great importance for their interaction with the host innate immune system. The innate immune system is the first barrier against infection and recognizes pathogens via conserved pattern recognition receptors (PRRs). Lectins expressed by innate immune cells represent an important class of PRRs characterized by their ability to recognize carbohydrates. Among lectins in innate immunity, there are three major classes including the galectins, siglecs, and C-type lectin receptors. These lectins may contribute to initial recognition of bacterial glycans, thus providing an early defence mechanism against bacterial infections, but they may also be exploited by bacteria to escape immune responses. In this review, we will first exemplify bacterial glycosylation systems; we will then describe modes of recognition of bacterial glycans by lectins in innate immunity and, finally, we will briefly highlight how bacteria have found ways to exploit these interactions to evade immune recognition.

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