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Journal articles on the topic 'Innate defense'

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Author: Grafiati

Published: 25 May 2024

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1

Yuan, Qian, and W. Allan Walker. "Innate Immunity of the Gut: Mucosal Defense in Health and Disease." Journal of Pediatric Gastroenterology and Nutrition 38, no. 5 (May 2004): 463–73. http://dx.doi.org/10.1002/j.1536-4801.2004.tb12203.x.

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ABSTRACTThe intestine is an important immune organ consisting of a complex cellular network, secreted peptides and proteins and other host defenses. Innate immunity plays a central role in intestinal immune defense against invading pathogens. It also serves as a bridge to the activation of the adaptive immune system. Pattern recognition molecules of microorganisms are an essential component for identifying invading pathogens. Toll‐like receptors (TLRs), CARD15/NOD2 and scavenger receptors all serve as the pattern recognition receptors in the innate immune defense system. Secreted bactericidal peptides or defensins produced by the intestinal epithelia represent another crucial element of innate mucosal immune defense. Mutations in pattern recognition receptors and dysfunction of secretory bactericidal peptides may impair host immune defenses leading to an invasion of pathogens resulting in chronic inflammation of the gut. This review updates our current understanding of innate immunity of the gastrointestinal tract.

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2

Drummond, R. A., S. L. Gaffen, A. G. Hise, and G. D. Brown. "Innate Defense against Fungal Pathogens." Cold Spring Harbor Perspectives in Medicine 5, no. 6 (November 10, 2014): a019620. http://dx.doi.org/10.1101/cshperspect.a019620.

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3

Darby, Creg, and Scott J. Hultgren. "Innate defense evicts bacterial squatters." Nature Immunology 3, no. 7 (July 2002): 602–4. http://dx.doi.org/10.1038/ni0702-602.

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4

Schoggins, John W., and Glenn Randall. "Lipids in Innate Antiviral Defense." Cell Host & Microbe 14, no. 4 (October 2013): 379–85. http://dx.doi.org/10.1016/j.chom.2013.09.010.

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5

Sollinger, Hans W. "Innate Alloimmunity. Part 1: Innate Immunity and Host Defense." Transplantation 90, no. 1 (July 2010): 1. http://dx.doi.org/10.1097/tp.0b013e3181e1704b.

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6

Ma’at, Suprapto. "Toll-like Receptor (TLR) dan Imunitas Natura." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 15, no. 3 (March 16, 2018): 111. http://dx.doi.org/10.24293/ijcpml.v15i3.978.

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In all living species, the first line of defence against microbial aggressions is constituted by innate immunity. Toll-like receptors(TLRs) are a family of pattern recognition receptors that are activated by specific components of microbes and certain host molecules.They constitute the first line of defense against many pathogens and play a crucial role in the function of the innate immune system.Recognition of pathogen-associated molecular pattern (PAMP) by TLR, alone or heterodimerization with other TLR or non-TLR receptors,induces signals responsible for the activation of genes important for an effective host defense, especially proinflammatory cytokines, orinitiates signal transduction pathways, which trigger expression of genes. These gene products control innate immune responses andfurther instruct development of antigen-specific acquired immunity.

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7

ZASLOFF, MICHAEL. "Vernix, the Newborn, and Innate Defense." Pediatric Research 53, no. 2 (February 2003): 203–4. http://dx.doi.org/10.1203/00006450-200302000-00001.

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8

Weindl, G., J. Wagener, and M. Schaller. "Epithelial Cells and Innate Antifungal Defense." Journal of Dental Research 89, no. 7 (April 15, 2010): 666–75. http://dx.doi.org/10.1177/0022034510368784.

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9

Kanneganti, Thirumala-Devi, Mohamed Lamkanfi, and Amal O. Amer. "Innate Immune Pathways in Host Defense." Mediators of Inflammation 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/708972.

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10

Fritz, J. H., S. E. Girardin, and D. J. Philpott. "Innate Immune Defense Through RNA Interference." Science Signaling 2006, no. 339 (June 6, 2006): pe27. http://dx.doi.org/10.1126/stke.3392006pe27.

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11

Duncan, Henry F., and Paul R. Cooper. "Pulp Innate Immune Defense: Translational Opportunities." Journal of Endodontics 46, no. 9 (September 2020): S10—S18. http://dx.doi.org/10.1016/j.joen.2020.06.019.

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12

Bhushan, Sudhanshu, Hans-Christian Schuppe, Svetlin Tchatalbachev, Monika Fijak, Wolfgang Weidner, Trinad Chakraborty, and Andreas Meinhardt. "Testicular innate immune defense against bacteria." Molecular and Cellular Endocrinology 306, no. 1-2 (July 10, 2009): 37–44. http://dx.doi.org/10.1016/j.mce.2008.10.017.

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13

Kraus, Dirk, and Andreas Peschel. "Staphylococcus aureusevasion of innate antimicrobial defense." Future Microbiology 3, no. 4 (August 2008): 437–51. http://dx.doi.org/10.2217/17460913.3.4.437.

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14

Zhang, Ping, Warren R. Summer, Gregory J. Bagby, and Steve Nelson. "Innate immunity and pulmonary host defense." Immunological Reviews 173, no. 1 (February 2000): 39–51. http://dx.doi.org/10.1034/j.1600-065x.2000.917306.x.

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15

Valdivia-Arenas, M. A., A. Amer, L. N. Henning, M. D. Wewers, and L. S. Schlesinger. "Lung infections and innate host defense." Drug Discovery Today: Disease Mechanisms 4, no. 2 (June 2007): 73–81. http://dx.doi.org/10.1016/j.ddmec.2007.10.003.

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16

Bier, Ethan, and Victor Nizet. "Hedgehog: Linking Uracil to Innate Defense." Cell Host & Microbe 17, no. 2 (February 2015): 146–48. http://dx.doi.org/10.1016/j.chom.2015.01.010.

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17

Kim, Yi Sak, Prashanta Silwal, Soo Yeon Kim, Tamotsu Yoshimori, and Eun-Kyeong Jo. "Autophagy-activating strategies to promote innate defense against mycobacteria." Experimental & Molecular Medicine 51, no. 12 (December 2019): 1–10. http://dx.doi.org/10.1038/s12276-019-0290-7.

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AbstractMycobacterium tuberculosis (Mtb) is a major causal pathogen of human tuberculosis (TB), which is a serious health burden worldwide. The demand for the development of an innovative therapeutic strategy to treat TB is high due to drug-resistant forms of TB. Autophagy is a cell-autonomous host defense mechanism by which intracytoplasmic cargos can be delivered and then destroyed in lysosomes. Previous studies have reported that autophagy-activating agents and small molecules may be beneficial in restricting intracellular Mtb infection, even with multidrug-resistant Mtb strains. Recent studies have revealed the essential roles of host nuclear receptors (NRs) in the activation of the host defense through antibacterial autophagy against Mtb infection. In particular, we discuss the function of estrogen-related receptor (ERR) α and peroxisome proliferator-activated receptor (PPAR) α in autophagy regulation to improve host defenses against Mtb infection. Despite promising findings relating to the antitubercular effects of various agents, our understanding of the molecular mechanism by which autophagy-activating agents suppress intracellular Mtb in vitro and in vivo is lacking. An improved understanding of the antibacterial autophagic mechanisms in the innate host defense will eventually lead to the development of new therapeutic strategies for human TB.

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18

Cartner, Samuel C., J. Russell Lindsey, Julie Gibbs-Erwin, Gail H. Cassell, and Jerry W. Simecka. "Roles of Innate and Adaptive Immunity in Respiratory Mycoplasmosis." Infection and Immunity 66, no. 8 (August 1, 1998): 3485–91. http://dx.doi.org/10.1128/iai.66.8.3485-3491.1998.

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ABSTRACT Current evidence suggests that host defense in respiratory mycoplasmosis is dependent on both innate and humoral immunity. To further delineate the roles of innate and adaptive immunity in antimycoplasmal defenses, we intranasally infected C3H/HeSnJ-scid/scid (C3H-SCID), C3H/HeSnJ (C3H), C57BL/6J-scid/scid (C57-SCID), and C57BL/6N (C57BL) mice with Mycoplasma pulmonis and at 14 and 21 days postinfection performed quantitative cultures of lungs and spleens, quantification of lung lesions, and histopathologic assessments of all other major organs. We found that numbers of mycoplasmas in lungs were associated with genetic background (C3H susceptible, C57BL resistant) rather than functional state of adaptive immunity, indicating that innate immunity is the main contributor to antimycoplasmal defense of the lungs. Extrapulmonary dissemination of mycoplasmas with colonization of spleens and histologic lesions in multiple organs was a common occurrence in all mice. The absence of adaptive immune responses in severe combined immunodeficient (SCID) mice resulted in increased mycoplasmal colonization of spleens and lesions in extrapulmonary sites, particularly spleens, hearts, and joints, and also reduced lung lesion severity. The transfer of anti-M. pulmonis serum to infected C3H-SCID mice prevented extrapulmonary infection and disease, while the severity of lung lesions was restored by transfer of naive spleen cells to infected C3H-SCID mice. Collectively, our results strongly support the conclusions that innate immunity provides antimycoplasmal defense of the lungs and humoral immunity has the major role in defense against systemic dissemination of mycoplasmal infection, but cellular immune responses may be important in exacerbation of mycoplasmal lung disease.

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19

Černý, Jan, and Ilja Stříž. "Adaptive innate immunity or innate adaptive immunity?" Clinical Science 133, no. 14 (July 2019): 1549–65. http://dx.doi.org/10.1042/cs20180548.

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Abstract The innate immunity is frequently accepted as a first line of relatively primitive defense interfering with the pathogen invasion until the mechanisms of ‘privileged’ adaptive immunity with the production of antibodies and activation of cytotoxic lymphocytes ‘steal the show’. Recent advancements on the molecular and cellular levels have shaken the traditional view of adaptive and innate immunity. The innate immune memory or ‘trained immunity’ based on metabolic changes and epigenetic reprogramming is a complementary process insuring adaptation of host defense to previous infections. Innate immune cells are able to recognize large number of pathogen- or danger- associated molecular patterns (PAMPs and DAMPs) to behave in a highly specific manner and regulate adaptive immune responses. Innate lymphoid cells (ILC1, ILC2, ILC3) and NK cells express transcription factors and cytokines related to subsets of T helper cells (Th1, Th2, Th17). On the other hand, T and B lymphocytes exhibit functional properties traditionally attributed to innate immunity such as phagocytosis or production of tissue remodeling growth factors. They are also able to benefit from the information provided by pattern recognition receptors (PRRs), e.g. γδT lymphocytes use T-cell receptor (TCR) in a manner close to PRR recognition. Innate B cells represent another example of limited combinational diversity usage participating in various innate responses. In the view of current knowledge, the traditional black and white classification of immune mechanisms as either innate or an adaptive needs to be adjusted and many shades of gray need to be included.

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20

Wang, Zhen, and Ying Zheng. "lncRNAs Regulate Innate Immune Responses and Their Roles in Macrophage Polarization." Mediators of Inflammation 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/8050956.

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The innate immune system is the first line of defense against microbial pathogens. The activated innate immune system plays important roles in eliciting antimicrobial defenses. Despite the benefits of innate immune responses, excessive inflammation will cause host damage. Thus, tight regulation of these processes is required for the maintenance of immune homeostasis. Recently, a new class of long noncoding RNAs (lncRNAs) has emerged as important regulators in many physiological and pathological processes. Dysregulated lncRNAs have been found to be associated with excessive or uncontrolled inflammation. In this brief review, we summarize the roles of functional lncRNAs in regulating innate immune responses. We also discuss the roles of lncRNAs in macrophage polarization, an important molecular event in the innate immune responses.

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21

Christophers, Enno, and Jens‐Michael Schröder. "Evolution of innate defense in human skin." Experimental Dermatology 31, no. 3 (November 3, 2021): 304–11. http://dx.doi.org/10.1111/exd.14482.

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22

Afshar, Maryam, and Richard L. Gallo. "Innate immune defense system of the skin." Veterinary Dermatology 24, no. 1 (January 19, 2013): 32—e9. http://dx.doi.org/10.1111/j.1365-3164.2012.01082.x.

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23

Drenth, Joost P. H., and Jos W. M. van der Meer. "The Inflammasome — A Linebacker of Innate Defense." New England Journal of Medicine 355, no. 7 (August 17, 2006): 730–32. http://dx.doi.org/10.1056/nejmcibr063500.

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24

Kumar, Ajit. "RNA interference: a multifaceted innate antiviral defense." Retrovirology 5, no. 1 (2008): 17. http://dx.doi.org/10.1186/1742-4690-5-17.

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25

Jo, Eun-Kyeong. "Autophagy as an innate defense against mycobacteria." Pathogens and Disease 67, no. 2 (February 21, 2013): 108–18. http://dx.doi.org/10.1111/2049-632x.12023.

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26

Gao, Nan, Ashok Kumar, Hui Guo, Xinyi Wu, Michelle Wheater, and Fu-Shin X. Yu. "Topical Flagellin-Mediated Innate Defense againstCandida albicansKeratitis." Investigative Opthalmology & Visual Science 52, no. 6 (May 10, 2011): 3074. http://dx.doi.org/10.1167/iovs.10-5928.

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27

Wang, Guoshun, and William M. Nauseef. "Salt, chloride, bleach, and innate host defense." Journal of Leukocyte Biology 98, no. 2 (June 5, 2015): 163–72. http://dx.doi.org/10.1189/jlb.4ru0315-109r.

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28

Nelson, Steve, and Warren R. Summer. "INNATE IMMUNITY, CYTOKINES, AND PULMONARY HOST DEFENSE." Infectious Disease Clinics of North America 12, no. 3 (September 1998): 555–67. http://dx.doi.org/10.1016/s0891-5520(05)70198-7.

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29

Luhachack, Lyly, and Evgeny Nudler. "Bacterial gasotransmitters: an innate defense against antibiotics." Current Opinion in Microbiology 21 (October 2014): 13–17. http://dx.doi.org/10.1016/j.mib.2014.06.017.

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30

dos Santos, C., and J. C. Marshall. "Bridging Lipid Metabolism and Innate Host Defense." Science Translational Medicine 6, no. 258 (October 15, 2014): 258fs41. http://dx.doi.org/10.1126/scitranslmed.3010501.

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31

Linde, A., B. Wachter, O. P. Höner, L. Dib, C. Ross, A. R. Tamayo, F. Blecha, and T. Melgarejo. "Natural History of Innate Host Defense Peptides." Probiotics and Antimicrobial Proteins 1, no. 2 (December 2009): 97–112. http://dx.doi.org/10.1007/s12602-009-9031-x.

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32

de Jong, Marein A. W. P., and Teunis B. H. Geijtenbeek. "Langerhans cells in innate defense against pathogens." Trends in Immunology 31, no. 12 (December 2010): 452–59. http://dx.doi.org/10.1016/j.it.2010.08.002.

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33

Ip, W. K. Eddie, Kazue Takahashi, Kathryn J. Moore, Lynda M. Stuart, and R. Alan B. Ezekowitz. "Mannose-binding lectin enhances Toll-like receptors 2 and 6 signaling from the phagosome." Journal of Experimental Medicine 205, no. 1 (January 7, 2008): 169–81. http://dx.doi.org/10.1084/jem.20071164.

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Innate immunity is the first-line defense against pathogens and relies on phagocytes, soluble components, and cell-surface and cytosolic pattern recognition receptors. Despite using hard-wired receptors and signaling pathways, the innate immune response demonstrates surprising specificity to different pathogens. We determined how combinatorial use of innate immune defense mechanisms defines the response. We describe a novel cooperation between a soluble component of the innate immune system, the mannose-binding lectin, and Toll-like receptor 2 that both specifies and amplifies the host response to Staphylococcus aureus. Furthermore, we demonstrate that this cooperation occurs within the phagosome, emphasizing the importance of engulfment in providing the appropriate cellular environment to facilitate the synergy between these defense pathways.

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34

van Crevel, Reinout, Tom H. M. Ottenhoff, and Jos W. M. van der Meer. "Innate Immunity to Mycobacterium tuberculosis." Clinical Microbiology Reviews 15, no. 2 (April 2002): 294–309. http://dx.doi.org/10.1128/cmr.15.2.294-309.2002.

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SUMMARY The different manifestations of infection with Mycobacterium tuberculosis reflect the balance between the bacillus and host defense mechanisms. Traditionally, protective immunity to tuberculosis has been ascribed to T-cell-mediated immunity, with CD4+ T cells playing a crucial role. Recent immunological and genetic studies support the long-standing notion that innate immunity is also relevant in tuberculosis. In this review, emphasis is on these natural, innate host defense mechanisms, referring to experimental data (e.g., studies in gene knockout mice) and epidemiological, immunological, and genetic studies in human tuberculosis. The first step in the innate host defense is cellular uptake of M. tuberculosis, which involves different cellular receptors and humoral factors. Toll-like receptors seem to play a crucial role in immune recognition of M. tuberculosis, which is the next step. The subsequent inflammatory response is regulated by production of pro- and anti-inflammatory cytokines and chemokines. Different natural effector mechanisms for killing of M. tuberculosis have now been identified. Finally, the innate host response is necessary for induction of adaptive immunity to M. tuberculosis. These basic mechanisms augment our understanding of disease pathogenesis and clinical course and will be of help in designing adjunctive treatment strategies.

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35

Wu, Xiaoyun, Adrian Valli, Juan García, Xueping Zhou, and Xiaofei Cheng. "The Tug-of-War between Plants and Viruses: Great Progress and Many Remaining Questions." Viruses 11, no. 3 (February 28, 2019): 203. http://dx.doi.org/10.3390/v11030203.

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Plants are persistently challenged by various phytopathogens. To protect themselves, plants have evolved multilayered surveillance against all pathogens. For intracellular parasitic viruses, plants have developed innate immunity, RNA silencing, translation repression, ubiquitination-mediated and autophagy-mediated protein degradation, and other dominant resistance gene-mediated defenses. Plant viruses have also acquired diverse strategies to suppress and even exploit host defense machinery to ensure their survival. A better understanding of the defense and counter-defense between plants and viruses will obviously benefit from the development of efficient and broad-spectrum virus resistance for sustainable agriculture. In this review, we summarize the cutting edge of knowledge concerning the defense and counter-defense between plants and viruses, and highlight the unexploited areas that are especially worth investigating in the near future.

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36

Ng, Wy Ching, Michelle D. Tate, Andrew G. Brooks, and Patrick C. Reading. "Soluble Host Defense Lectins in Innate Immunity to Influenza Virus." Journal of Biomedicine and Biotechnology 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/732191.

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Host defenses against viral infections depend on a complex interplay of innate (nonspecific) and adaptive (specific) components. In the early stages of infection, innate mechanisms represent the main line of host defense, acting to limit the spread of virus in host tissues prior to the induction of the adaptive immune response. Serum and lung fluids contain a range of lectins capable of recognizing and destroying influenza A viruses (IAV). Herein, we review the mechanisms by which soluble endogenous lectins mediate anti-IAV activity, including their role in modulating IAV-induced inflammation and disease and their potential as prophylactic and/or therapeutic treatments during severe IAV-induced disease.

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37

Sellegounder, Durai, Yiyong Liu, Phillip Wibisono, Chia-Hui Chen, David Leap, and Jingru Sun. "Neuronal GPCR NPR-8 regulates C. elegans defense against pathogen infection." Science Advances 5, no. 11 (November 2019): eaaw4717. http://dx.doi.org/10.1126/sciadv.aaw4717.

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Increasing evidence indicates that infection-triggered host defenses are regulated by the nervous system. However, the precise mechanisms of this regulation are not well understood. Here, we demonstrate that neuronal G protein-coupled receptor NPR-8 negatively regulates Caenorhabditis elegans defense against pathogen infection by suppressing cuticular collagen expression. NPR-8 controls the dynamics of cuticle structure in response to infection, likely through its regulation of cuticular collagen genes which, in turn, affects the nematode’s defense. We further show that the defense activity of NPR-8 is confined to amphid sensory neurons AWB, ASJ, and AWC. It is generally believed that physical barrier defenses are not a response to infections but are part of the body’s basic innate defense against pathogens. Our results challenge this view by showing not only that C. elegans cuticle structure dynamically changes in response to infection but also that the cuticle barrier defense is regulated by the nervous system.

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38

Lotfalizadeh, Narges, Soheil Sadr, Safa Moghaddam, Mahdis Saberi Najjar, Amin Khakshoor, and Pouria Ahmadi Simab. "The Innate Immunity Defense against Gastrointestinal Nematodes: Vaccine Development." Farm Animal Health and Nutrition 1, no. 2 (December 25, 2022): 31–38. http://dx.doi.org/10.58803/fahn.v1i2.10.

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The nematode parasite infects both humans and animals, causing severe infections. Their unusual surface structures, in particular, pose significant challenges to the immune system. Vaccine-induced immunity, mediated by the innate immune system, could be crucial in the development of an adaptive effector response. The purpose of this paper was to provide an overview of recent research on the host's innate immune system, barriers, and cells that respond to parasitic nematodes. This study investigated the nematode-associated molecular patterns that may recognize by host. Given the innate defense is more than just a static barrier against pathogen infections. It can actively contribute as a director of the adaptive immune response, which is ultimately responsible for the rejection of invasions. The role of innate defense against pathogen infections is located in zone of researcher concentration. Some nematode parasites can actively move through tissues, they pose a challenge to the innate immune system. Furthermore, their cuticular surface, which varies with each molting, cannot be phagocytosed. The nematode's thin, carbohydrate-rich surface layer, as well as the chemicals produced by this layer, cause the first contact with the host's innate immune system. Notably, all components of the innate immune response can be activated and play an important role in the adaptive immune effector response.

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Chin, Chue Vin, and Mohsan Saeed. "Surgical Strikes on Host Defenses: Role of the Viral Protease Activity in Innate Immune Antagonism." Pathogens 11, no. 5 (April 28, 2022): 522. http://dx.doi.org/10.3390/pathogens11050522.

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As a frontline defense mechanism against viral infections, the innate immune system is the primary target of viral antagonism. A number of virulence factors encoded by viruses play roles in circumventing host defenses and augmenting viral replication. Among these factors are viral proteases, which are primarily responsible for maturation of viral proteins, but in addition cause proteolytic cleavage of cellular proteins involved in innate immune signaling. The study of these viral protease-mediated host cleavages has illuminated the intricacies of innate immune networks and yielded valuable insights into viral pathogenesis. In this review, we will provide a brief summary of how proteases of positive-strand RNA viruses, mainly from the Picornaviridae, Flaviviridae and Coronaviridae families, proteolytically process innate immune components and blunt their functions.

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Kirkland, Theo N., and Joshua Fierer. "Innate Immune Receptors and Defense Against Primary Pathogenic Fungi." Vaccines 8, no. 2 (June 13, 2020): 303. http://dx.doi.org/10.3390/vaccines8020303.

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The innate immune system is critical for natural resistance to all pathogenic microorganisms, including fungi. The innate response plays a vital role in resistance to infections before the antigen-specific immune response and also influences antigen-specific adaptive immunity. There are many different receptors for the innate immune response to fungi, and some receptors have been found to play a significant role in the response to human infections with opportunistic fungi. Most human infections are caused by opportunistic fungi, but a small number of organisms are capable of causing infections in normal hosts. The primary pathogenic fungi that cause invasive infections include Blastomyces spp., Cryptococcus gattii, Coccidioides spp., Histoplasma spp., and Paracoccidioides spp. In this review of innate immune receptors that play a role in infections caused by these organisms, we find that innate immunity differs between organisms.

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41

Mailliard, Robbie B. "Dendritic Cells and Antiviral Defense." Viruses 12, no. 10 (October 12, 2020): 1152. http://dx.doi.org/10.3390/v12101152.

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42

Dai, Lingli, Zaixia Liu, Lili Guo, Yuan Chai, Yanda Yang, Yu Wang, Yanfen Ma, Caixia Shi, and Wenguang Zhang. "Multi-Tissue Transcriptome Study of Innate Immune Gene Expression Profiling Reveals Negative Energy Balance Altered the Defense and Promoted System Inflammation of Dairy Cows." Veterinary Sciences 10, no. 2 (February 1, 2023): 107. http://dx.doi.org/10.3390/vetsci10020107.

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Negative energy balance (NEB) during the perinatal period leads to metabolic and immunological disorders in dairy cows, resulting in systemic responses and inflammation. The innate immune system is crucial for the host’s protection and inflammatory response. However, systematic research is still lacking on how NEB affects the innate immune system to alter the ’host defense capability and inflammatory response. In this investigation, raw transcriptome data of adipose, blood, endometrial, hypothalamus, and liver tissues were downloaded from a public database, cleaned, aligned, quantified, and batch-corrected. The innate immune gene list was retrieved from innateDB, followed by the expression matrix of innate immune genes in various tissues for differential expression analysis, principle component analysis (PCA), and gene set enrichment analysis (GSEA). Under the effect of NEB, adipose tissue had the most differentially expressed genes, which were predominantly up-regulated, whereas blood GSEA had the most enriched biological processes, which were predominantly down-regulated. The gene sets shared by different tissues, which are predominantly involved in biological processes associated with defense responses and inflammation, were dramatically down-regulated in endometrial tissues and highly up-regulated in other tissues. Under the impact of NEB, LBP, PTX3, S100A12, and LCN2 play essential roles in metabolism and immunological control. In conclusion, NEB can downregulate the defensive response of innate immune genes in endometrial, upregulate the immune and inflammatory response of other tissues, activate the host defense response, and increase the systemic inflammatory response. The analysis of the effects of NEB on innate immune genes from the multiple tissues analysis provides new insights into the crosstalk between metabolism and immunity and also provides potential molecular targets for disease diagnosis and disease resistance breeding in dairy cows.

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43

Li, Lupeng, Stephen B. Kovacs, Ine Jørgensen, Heather N. Larson, Helen M. Lazear, and Edward A. Miao. "Role of Caspases and Gasdermin A during HSV-1 Infection in Mice." Viruses 14, no. 9 (September 13, 2022): 2034. http://dx.doi.org/10.3390/v14092034.

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Herpes simplex virus type 1 (HSV-1) infection can manifest locally as mucocutaneous lesions or keratitis and can also spread to the central nervous system to cause encephalitis. HSV-1 establishes a lifelong latent infection and neither cure nor vaccine is currently available. The innate immune response is the first line of defense against infection. Caspases and gasdermins are important components of innate immunity. Caspases are a family of cysteine proteases, most of which mediate regulated cell death. Gasdermins are a family of pore-forming proteins that trigger lytic cell death. To determine whether caspases or gasdermins contribute to innate immune defenses against HSV-1, we screened mice deficient in specific cell death genes. Our results indicate a modest role for caspase-6 in defense against HSV-1. Further, Asc–/–Casp1/11–/– mice also had a modest increased susceptibility to HSV-1 infection. Caspase-7, -8, and -14 did not have a notable role in controlling HSV-1 infection. We generated Gsdma1-Gsdma2-Gsdma3 triple knockout mice, which also had normal susceptibility to HSV-1. We confirmed that the previously published importance of RIPK3 during systemic HSV-1 infection also holds true during skin infection. Overall, our data highlight that as a successful pathogen, HSV-1 has multiple ways to evade host innate immune responses.

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Garth, Jaleesa M., and Chad Steele. "Innate Lung Defense during Invasive Aspergillosis: New Mechanisms." Journal of Innate Immunity 9, no. 3 (2017): 271–80. http://dx.doi.org/10.1159/000455125.

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Invasive aspergillosis (IA) is one of the most difficult to treat and, consequently, one of the most lethal fungal infections known to man. Continued use of immunosuppressive agents during chemotherapy and organ transplantation often leads to the development of neutropenia, the primary risk factor for IA. However, IA is also becoming more appreciated in chronic diseases associated with corticosteroid therapy. The innate immune response to Aspergillus fumigatus, the primary agent in IA, plays a pivotal role in the recognition and elimination of organisms from the pulmonary system. This review highlights recent findings about innate host defense mechanisms, including novel aspects of innate cellular immunity and pathogen recognition, and the inflammatory mediators that control infection with A. fumigatus.

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Power Coombs, Melanie R., Kenny Kronforst, and Ofer Levy. "Neonatal Host Defense against Staphylococcal Infections." Clinical and Developmental Immunology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/826303.

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Preterm infants are especially susceptible to late-onset sepsis that is often due to Gram-positive bacterial infections resulting in substantial morbidity and mortality. Herein, we will describe neonatal innate immunity toStaphylococcusspp. comparing differences between preterm and full-term newborns with adults. Newborn innate immunity is distinct demonstrating diminished skin integrity, impaired Th1-polarizing responses, low complement levels, and diminished expression of plasma antimicrobial proteins and peptides, especially in preterm newborns. Characterization of distinct aspects of the neonatal immune response is defining novel approaches to enhance host defense to prevent and/or treat staphylococcal infection in this vulnerable population.

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Gonzalez-Cao, Maria, Niki Karachaliou, Mariacarmela Santarpia, Santiago Viteri, Andreas Meyerhans, and Rafael Rosell. "Activation of viral defense signaling in cancer." Therapeutic Advances in Medical Oncology 10 (January 2018): 175883591879310. http://dx.doi.org/10.1177/1758835918793105.

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A coordinated action of innate and adaptive immune responses is required to efficiently combat a microbial infection. It has now become clear that cancer therapies also largely benefit when both arms of the immune response are engaged. In this review, we will briefly describe the current knowledge of innate immunity and how this can be utilized to prime tumors for a better response to immune checkpoint inhibitors. Comments on compounds in development and ongoing clinical trials will be provided.

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Sander, Leif, Michael Davis, Mark Boekschoten, Christopher Dascher, Bernard Ryffel, Derk Amsen, Joel Swanson, Michael Mueller, and Julie Blander. "Sensing bacterial viability for host defense (116.23)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 116.23. http://dx.doi.org/10.4049/jimmunol.186.supp.116.23.

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Abstract The innate immune system safeguards the host from invading microorganisms by eliciting carefully measured responses. For example, weaker responses are mounted to dead than to viable microorganisms, a property with important implications for vaccination and host defense. Pathogen associated molecular patterns (PAMPs), which serve to alert the immune system, are present in dead and viable bacteria, raising the question as to how the immune system discriminates between the two. Here we show that the innate immune system can directly sense bacterial viability through detection of a special class of viability-associated PAMPs (vita-PAMPs). We identify prokaryotic messenger RNA (mRNA) as a vita-PAMP present only in viable bacteria, recognition of which elicits a unique innate immune response. Detection of vita-PAMPs in phagocytosed bacteria induces robust production of IFN-β and activation of the NLRP3 inflammasome in various innate immune cells. All responses require the Toll-like receptor adaptor protein TRIF. Importantly, recognition of vita-PAMPs in vivo induces host protective antibody mediated immunity. Thus, the immune system actively gauges the infectious risk by scouring PAMPs for signatures of microbial life and thus infectivity. Detection of vita-PAMPs triggers an alert mode not warranted for dead bacteria. Vaccine formulations that incorporate vita-PAMPs could combine the superior protection of live vaccines with the safety of dead vaccines.

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Suresh, Rahul, and David M. Mosser. "Pattern recognition receptors in innate immunity, host defense, and immunopathology." Advances in Physiology Education 37, no. 4 (December 2013): 284–91. http://dx.doi.org/10.1152/advan.00058.2013.

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Infection by pathogenic microbes initiates a set of complex interactions between the pathogen and the host mediated by pattern recognition receptors. Innate immune responses play direct roles in host defense during the early stages of infection, and they also exert a profound influence on the generation of the adaptive immune responses that ensue. An improved understanding of the pattern recognition receptors that mediate innate responses and their downstream effects after receptor ligation has the potential to lead to new ways to improve vaccines and prevent autoimmunity. This review focuses on the control of innate immune activation and the role that innate immune receptors play in helping to maintain tissue homeostasis.

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Werner, Jessica L., and Chad Steele. "Innate Receptors and Cellular Defense against Pulmonary Infections." Journal of Immunology 193, no. 8 (October 3, 2014): 3842–50. http://dx.doi.org/10.4049/jimmunol.1400978.

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Weinberger, Florian. "Pathogen-Induced Defense and Innate Immunity in Macroalgae." Biological Bulletin 213, no. 3 (December 2007): 290–302. http://dx.doi.org/10.2307/25066646.

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