Journal articles: 'Infection, Immunity and Inflammation'

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Kumar, Rajiv. "Routes of Infections, Inflammation, Immunity, Immunity Response and Inflammatory Injury: Elucidation of a Biological Fight." Immunology and Inflammation Diseases Therapy 5, no. 1 (January 13, 2022): 01–04. http://dx.doi.org/10.31579/2637-8876/028.

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Infections, inflammation, immunity, and inflammatory injury are different segments of biological events and link up altogether. Route of infection has no similarity with the cellular signaling pathway of inflammation, even though when inflammation is induced by infection. The organism responds toward infection that is initiated by the pathogen via inflammation, which is a natural way of defense initiated by innate immunity as a safeguard

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Cherneva, R., and Z. Cherneva. "Infection, Inflammation and Immunity in Covid-19 Infection." Acta Medica Bulgarica 48, no. 3 (October 1, 2021): 77–82. http://dx.doi.org/10.2478/amb-2021-0040.

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Abstract The COVID-19 pandemic caused by the SARS-CoV-2 has increased the burden on healthcare system. Despite some progress in its diagnostics has been made, effective prevention and treatment are still insufficient. Since SARS-CoV-2 infections often cause systemic inflammation and multiple organ failure, the therapeutic options aimed at modulating the host immune responses to prevent subsequent systemic complications are demanding. The review provides a summary of the SARS-CoV-2 virus infection and underlines the current perception of pulmonary host’s immune response and its contributions to disease severity and systemic inflammation. Signaling pathways which have the potential to manipulate host immunity and improve clinical outcomes are also presented.

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Chmiela, Magdalena, and Pierre Michetti. "Inflammation, Immunity, Vaccines for Helicobacter Infection." Helicobacter 11, s1 (October 2006): 21–26. http://dx.doi.org/10.1111/j.1478-405x.2006.00422.x.

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Pachner, Andrew R., and Israel Steiner. "Lyme neuroborreliosis: infection, immunity, and inflammation." Lancet Neurology 6, no. 6 (June 2007): 544–52. http://dx.doi.org/10.1016/s1474-4422(07)70128-x.

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Libby, Peter, Joseph Loscalzo, Paul M. Ridker, Michael E. Farkouh, Priscilla Y. Hsue, Valentin Fuster, Ahmed A. Hasan, and Salomon Amar. "Inflammation, Immunity, and Infection in Atherothrombosis." Journal of the American College of Cardiology 72, no. 17 (October 2018): 2071–81. http://dx.doi.org/10.1016/j.jacc.2018.08.1043.

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Deretic, Vojo, Tatsuya Saitoh, and Shizuo Akira. "Autophagy in infection, inflammation and immunity." Nature Reviews Immunology 13, no. 10 (September 25, 2013): 722–37. http://dx.doi.org/10.1038/nri3532.

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Permin, Henrik, and Leif P. Andersen. "Inflammation, Immunity, and Vaccines for Helicobacter Infection." Helicobacter 10, s1 (September 2005): 21–25. http://dx.doi.org/10.1111/j.1523-5378.2005.00337.x.

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Meiers, Joscha, Eike Siebs, Eva Zahorska, and Alexander Titz. "Lectin antagonists in infection, immunity, and inflammation." Current Opinion in Chemical Biology 53 (December 2019): 51–67. http://dx.doi.org/10.1016/j.cbpa.2019.07.005.

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Raffler, Nikolai A., Jesús Rivera-Nieves, and Klaus Ley. "L-selectin in inflammation, infection and immunity." Drug Discovery Today: Therapeutic Strategies 2, no. 3 (September 2005): 213–20. http://dx.doi.org/10.1016/j.ddstr.2005.08.012.

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Huang, Y., C. Zhao, and X. Su. "Neuroimmune regulation of lung infection and inflammation." QJM: An International Journal of Medicine 112, no. 7 (July 16, 2018): 483–87. http://dx.doi.org/10.1093/qjmed/hcy154.

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Abstract The distal airway of the lung is innervated by vagus nerve. Upon stimulation, vagus nerve endings release acetylcholine or neuropeptides via C-fiber afferents to regulate lung infection and immunity. Vagal sensory nerve endings, brain integration center, acetylcholine and α7 nicotinic acetylcholine receptor (nAChR) expressing cells are key components of pulmonary parasympathetic inflammatory reflex. Meanwhile, this local machinery synergizes with spleen (as a functional hub of cholinergic anti-inflammatory pathway) to finely tune recruitment of the splenic α7 nAChR+CD11b+ cells into the inflamed lungs during lung infection. Recent studies have showed that lung group 2 innate lymphoid cells (ILC2) express both α7 nAChR and neuropeptide receptors. Acetylcholine and neuropeptides can regulate ILC2 and reshape pulmonary infection and immunity. Among the airway epithelial cells, pulmonary neuroendocrine cells are rare cell population; however, these cells are innervated by sensory nerve endings and they could secrete neuropeptides that influence lung infection and immunity.

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Yang, Ge, Pin Wan, Yaru Zhang, Qiaoru Tan, Muhammad Suhaib Qudus, Zhaoyang Yue, Wei Luo, et al. "Innate Immunity, Inflammation, and Intervention in HBV Infection." Viruses 14, no. 10 (October 17, 2022): 2275. http://dx.doi.org/10.3390/v14102275.

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Hepatitis B virus (HBV) infection is still one of the most dangerous viral illnesses. HBV infects around 257 million individuals worldwide. Hepatitis B in many individuals ultimately develops hepatocellular carcinoma (HCC), which is the sixth most common cancer and the third leading cause of cancer-related deaths worldwide. The innate immunity acts as the first line of defense against HBV infection through activating antiviral genes. Along with the immune responses, pro-inflammatory cytokines are triggered to enhance the antiviral responses, but this may result in acute or chronic liver inflammation, especially when the clearance of virus is unsuccessful. To a degree, the host innate immune and inflammatory responses dominate the HBV infection and liver pathogenesis. Thus, it is crucial to figure out the signaling pathways involved in the activation of antiviral factors and inflammatory cytokines. Here, we review the interplay between HBV and the signal pathways that mediates innate immune responses and inflammation. In addition, we summarize current therapeutic strategies for HBV infection via modulating innate immunity or inflammation. Characterizing the mechanisms that underlie these HBV-host interplays might provide new approaches for the cure of chronic HBV infection.

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Farthing, M. J. G. "New horizons in gastroenterology: infection, inflammation, and immunity." Gut 50, Supplement 3 (May 1, 2002): iii1. http://dx.doi.org/10.1136/gut.50.suppl_3.iii1.

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Ihan, Alojz, Irina V. Pinchuk, and Ellen J. Beswick. "Inflammation, Immunity, and Vaccines for Helicobacter pylori Infection." Helicobacter 17 (September 2012): 16–21. http://dx.doi.org/10.1111/j.1523-5378.2012.00977.x.

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Velin, Dominique, Kathrin Straubinger, and Markus Gerhard. "Inflammation, immunity, and vaccines for Helicobacter pylori infection." Helicobacter 21 (August 16, 2016): 26–29. http://dx.doi.org/10.1111/hel.12336.

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Fonseca Brito, Luís, Wolfram Brune, and Felix R. Stahl. "Cytomegalovirus (CMV) Pneumonitis: Cell Tropism, Inflammation, and Immunity." International Journal of Molecular Sciences 20, no. 16 (August 8, 2019): 3865. http://dx.doi.org/10.3390/ijms20163865.

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Human cytomegalovirus (HCMV) is an opportunistic pathogen causing disease mainly in immunocompromised patients or after congenital infection. HCMV infection of the respiratory tract leads to pneumonitis in the immunocompromised host, which is often associated with a bad clinical course. The related mouse cytomegalovirus (MCMV) likewise exhibits a distinct tropism for the lung and thus provides an elegant model to study host-pathogen interaction. Accordingly, fundamental features of cytomegalovirus (CMV) pneumonitis have been discovered in mice that correlate with clinical data obtained from humans. Recent studies have provided insight into MCMV cell tropism and localized inflammation after infection of the respiratory tract. Accordingly, the nodular inflammatory focus (NIF) has been identified as the anatomical correlate of immune control in lungs. Several hematopoietic cells involved in antiviral immunity reside in NIFs and their key effector molecules have been deciphered. Here, we review what has been learned from the mouse model with focus on the microanatomy of infection sites and antiviral immunity in MCMV pneumonitis.

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Owyang, Alexander M., Colby Zaph, Emma H. Wilson, Katherine J. Guild, Terrill McClanahan, Hugh R. P. Miller, Daniel J. Cua, et al. "Interleukin 25 regulates type 2 cytokine-dependent immunity and limits chronic inflammation in the gastrointestinal tract." Journal of Experimental Medicine 203, no. 4 (April 10, 2006): 843–49. http://dx.doi.org/10.1084/jem.20051496.

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The cytokine interleukin (IL) 25 has been implicated in the initiation of type 2 immunity by driving the expression of type 2 cytokines such as IL-5 and IL-13, although its role in the regulation of immunity and infection-induced inflammation is unknown. Here, we identify a dual function for IL-25: first, in promoting type 2 cytokine-dependent immunity to gastrointestinal helminth infection and, second, in limiting proinflammatory cytokine production and chronic intestinal inflammation. Treatment of genetically susceptible mice with exogenous IL-25 promoted type 2 cytokine responses and immunity to Trichuris. IL-25 was constitutively expressed by CD4+ and CD8+ T cells in the gut of mouse strains that are resistant to Trichuris, and IL-25–deficient mice on a genetically resistant background failed to develop a type 2 immune response or eradicate infection. Furthermore, chronically infected IL-25−/− mice developed severe infection-induced intestinal inflammation associated with heightened expression of interferon-γ and IL-17, identifying a role for IL-25 in limiting pathologic inflammation at mucosal sites. Therefore, IL-25 is not only a critical mediator of type 2 immunity, but is also required for the regulation of inflammation in the gastrointestinal tract.

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Casanova, Jean-Laurent, and Laurent Abel. "Mechanisms of viral inflammation and disease in humans." Science 374, no. 6571 (November 26, 2021): 1080–86. http://dx.doi.org/10.1126/science.abj7965.

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Disease and accompanying inflammation are uncommon outcomes of viral infection in humans. Clinical inflammation occurs if steady-state cell-intrinsic and leukocytic immunity to viruses fails. Inflammation attests to the attempts of newly recruited and activated leukocytes to resolve infection in the blood or tissues. In the confusing battle between a myriad of viruses and cells, studies of human genetics can separate the root cause of inflammation and disease from its consequences. Single-gene inborn errors of cell-intrinsic or leukocytic immunity underlying diverse infections in the skin, brain, or lungs can help to clarify the human determinants of viral disease. The genetic elucidation of immunological deficits in a single patient with a specific vulnerability profile can reveal mechanisms of inflammation and disease that may be triggered by other causes, inherited or otherwise, in other patients. This human genetic dissection of viral infections is giving rise to a new biology and a new medicine.

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Shastri, Abhishek, Domenico Marco Bonifati, and Uday Kishore. "Innate Immunity and Neuroinflammation." Mediators of Inflammation 2013 (2013): 1–19. http://dx.doi.org/10.1155/2013/342931.

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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.

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Di Cara, Francesca, Pierre Andreoletti, Doriane Trompier, Anne Vejux, Margret H. Bülow, Julia Sellin, Gérard Lizard, Mustapha Cherkaoui-Malki, and Stéphane Savary. "Peroxisomes in Immune Response and Inflammation." International Journal of Molecular Sciences 20, no. 16 (August 8, 2019): 3877. http://dx.doi.org/10.3390/ijms20163877.

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The immune response is essential to protect organisms from infection and an altered self. An organism’s overall metabolic status is now recognized as an important and long-overlooked mediator of immunity and has spurred new explorations of immune-related metabolic abnormalities. Peroxisomes are essential metabolic organelles with a central role in the synthesis and turnover of complex lipids and reactive species. Peroxisomes have recently been identified as pivotal regulators of immune functions and inflammation in the development and during infection, defining a new branch of immunometabolism. This review summarizes the current evidence that has helped to identify peroxisomes as central regulators of immunity and highlights the peroxisomal proteins and metabolites that have acquired relevance in human pathologies for their link to the development of inflammation, neuropathies, aging and cancer. This review then describes how peroxisomes govern immune signaling strategies such as phagocytosis and cytokine production and their relevance in fighting bacterial and viral infections. The mechanisms by which peroxisomes either control the activation of the immune response or trigger cellular metabolic changes that activate and resolve immune responses are also described.

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Zhang, Qian, and Xuetao Cao. "Epigenetic Remodeling in Innate Immunity and Inflammation." Annual Review of Immunology 39, no. 1 (April 26, 2021): 279–311. http://dx.doi.org/10.1146/annurev-immunol-093019-123619.

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The innate immune response is a rapid response to pathogens or danger signals. It is precisely activated not only to efficiently eliminate pathogens but also to avoid excessive inflammation and tissue damage. cis-Regulatory element–associated chromatin architecture shaped by epigenetic factors, which we define as the epiregulome, endows innate immune cells with specialized phenotypes and unique functions by establishing cell-specific gene expression patterns, and it also contributes to resolution of the inflammatory response. In this review, we focus on two aspects: ( a) how niche signals during lineage commitment or following infection and pathogenic stress program epiregulomes by regulating gene expression levels, enzymatic activities, or gene-specific targeting of chromatin modifiers and ( b) how the programed epiregulomes in turn mediate regulation of gene-specific expression, which contributes to controlling the development of innate cells, or the response to infection and inflammation, in a timely manner. We also discuss the effects of innate immunometabolic rewiring on epiregulomes and speculate on several future challenges to be encountered during the exploration of the master regulators of epiregulomes in innate immunity and inflammation.

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Andersson, Ulf, and Kevin J. Tracey. "Neural reflexes in inflammation and immunity." Journal of Experimental Medicine 209, no. 6 (June 4, 2012): 1057–68. http://dx.doi.org/10.1084/jem.20120571.

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The mammalian immune system and the nervous system coevolved under the influence of infection and sterile injury. Knowledge of homeostatic mechanisms by which the nervous system controls organ function was originally applied to the cardiovascular, gastrointestinal, musculoskeletal, and other body systems. Development of advanced neurophysiological and immunological techniques recently enabled the study of reflex neural circuits that maintain immunological homeostasis, and are essential for health in mammals. Such reflexes are evolutionarily ancient, dating back to invertebrate nematode worms that possess primitive immune and nervous systems. Failure of these reflex mechanisms in mammals contributes to nonresolving inflammation and disease. It is also possible to target these neural pathways using electrical nerve stimulators and pharmacological agents to hasten the resolution of inflammation and provide therapeutic benefit.

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Ashraf T Soliman, Nada M Alaaraj, and Alan D Rogol. "The link between malnutrition, immunity, infection, inflammation and growth: New pathological mechanisms." World Journal of Advanced Research and Reviews 15, no. 1 (July 30, 2022): 157–67. http://dx.doi.org/10.30574/wjarr.2022.15.1.0673.

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Primary (acute and chronic) malnutrition is still prevalent in developing countries because of inadequate nutrition and poor sanitation caused by social, economic, and environmental factors. In addition, acute malnutrition can occur secondary to an underlying disease that interferes with the intake, digestion, absorption, or assimilation of different nutrients increases nutrient loss, and/or increases energy expenditure. Immune dysfunction and infection are tightly linked to and actively contribute to the metabolic and hormonal dysregulation as well as to the progression of malnutrition. An inadequate dietary intake of macro-and micronutrients is proposed to adversely affect local intestinal and systemic immunity, intestinal mucosal integrity, and the interaction between host defense and pathogens. Lowered immunity, mucosal damage, recurrent and prolonged infections, and gut inflammation negatively affect the malnourished child growth in weight and height as well as psycho-mental development in endemic areas. Both infection and inflammation aggressively contribute to malnutrition triggering a vicious cycle. Almost all infantile and childhood malnutrition in endemic settings (unlike anorexia nervosa) results from deficient diet, infection, inflammation, and intestinal dysfunction (most children in endemic areas have environmental enteric dysfunction (EED), often with high fecal inflammatory markers. We highlight gaps in our understanding of the current interaction among immune dysfunction, infection, and inflammation in malnourished children, and evaluate the possible responsibility of pro-inflammatory cytokines in the initiation and progression of severe malnutrition. Breach of the malicious cycle between malnutrition and infection/inflammation requires innovative interferences to recover the immune defense and enforce host defense against pathogens and reduce morbidity and mortality.

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Ablasser, Andrea, and Zhijian J. Chen. "cGAS in action: Expanding roles in immunity and inflammation." Science 363, no. 6431 (March 7, 2019): eaat8657. http://dx.doi.org/10.1126/science.aat8657.

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DNA is highly immunogenic. It represents a key pathogen-associated molecular pattern (PAMP) during infection. Host DNA can, however, also act as a danger-associated molecular pattern (DAMP) and elicit strong inflammatory responses. The cGAS-STING pathway has emerged as a major pathway that detects intracellular DNA. Here, we highlight recent advances on how cGAS and STING mediate inflammatory responses and how these are regulated, allowing cells to readily respond to infections and noxious agents while avoiding the inappropriate sensing of self-DNA. A particular focus is placed on the role of cGAS in the context of sterile inflammatory conditions. Manipulating cGAS or STING may open the door for new therapeutic strategies for the treatment of acute and chronic inflammation relevant to many human diseases.

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Lopes, Marcela Freitas, Ana Caroline Costa-da-Silva, and George Alexandre DosReis. "Innate Immunity toLeishmaniaInfection: Within Phagocytes." Mediators of Inflammation 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/754965.

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Infection byLeishmaniatakes place in the context of inflammation and tissue repair. Besides tissue resident macrophages, inflammatory macrophages and neutrophils are recruited to the infection site and serve both as host cells and as effectors against infection. Recent studies suggest additional important roles for monocytes and dendritic cells. This paper addresses recent experimental findings regarding the regulation ofLeishmania majorinfection by these major phagocyte populations. In addition, the role of IL-4 on dendritic cells and monocytes is discussed.

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Musicki, Korana, Helen Briscoe, Stephen Tran, Warwick J. Britton, and Bernadette M. Saunders. "DifferentialRequirements for Soluble and Transmembrane Tumor Necrosis Factor in theImmunological Control of Primary and Secondary Listeria monocytogenesInfection." Infection and Immunity 74, no. 6 (June 2006): 3180–89. http://dx.doi.org/10.1128/iai.02004-05.

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ABSTRACT The relative contributions of transmembrane tumor necrosis factor (memTNF) and soluble tumor necrosis factor (solTNF) in innate and adaptive immunity are poorly defined. We examined the capacities of wild-type (WT) mice, TNF−/− mice, and memTNF mice, which express only transmembrane TNF, to control primary and secondary Listeria monocytogenes infections. Soluble TNF was not required for induction or maintenance of protective immunity against a low-dose (200-CFU) Listeria infection. In contrast to TNF−/− mice, both WT and memTNF mice cleared the bacilli within 10 days and were fully protected against rechallenge with a lethal infective dose. Furthermore, T cells transferred from immune mice, but not from naïve, WT, and memTNF mice, protected TNF−/− recipients against an otherwise lethal infection. By contrast, infection with a higher dose of Listeria (2,000 CFU) clearly demonstrated that solTNF is required to coordinate an optimal protective inflammatory response. memTNF mice were more susceptible to a high-dose infection, and they exhibited delayed bacterial clearance, increased inflammation, and necrosis in the liver that resulted in 55% mortality. The dysregulated inflammation was accompanied by prolonged elevated expression of mRNAs for several chemokines as well as the macrophage effector molecules inducible nitric oxide synthase and LRG-47 in the livers of memTNF mice but not in the livers of WT mice. These data demonstrated that memTNF is sufficient for establishing protective immunity against a primary low-dose Listeria infection but that solTNF is required for optimal control of cellular inflammation and resistance to a primary high-dose infection. By contrast, memTNF alone is sufficient for resolution of a secondary, high-dose infection and for the transfer of protective immunity with memory T cells.

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Uauy, Ricardo. "Academic-industry partnerships in addressing nutrition – [Infection-immunity-inflammation] interactions." British Journal of Nutrition 98, S1 (October 2007): S17—S23. http://dx.doi.org/10.1017/s0007114507832892.

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The interaction between nutrition and infection is a key determinant of human health. Traditionally the interaction has centered on the role of nutrients in defining host defenses and the impact of infection in defining nutritional needs and status. Over the past decades the interaction has expanded its scope to encompass the role of specific nutrients in defining acquired immune function, in the modulation of inflammatory processes and on the virulence of the infectious agent itself. More recently the role of micronutrients and fatty acids on the response of cells and tissues to hypoxic and toxic damage has been recognized suggesting a fourth dimension to the interaction. The list of nutrients affecting infection, immunity, inflammation and cell injury has expanded from traditional protein-energy supply to several vitamins, multiple minerals and more recently specific lipid components of the diet. The promise of nutrition in the defense against infection, inflammation and tissue injury has spawned a thriving pharma-nutritional supplement industry and the development of novel foods that require appropriate evaluation of efficacy, safety and effectiveness relative to costs. Academics need to aware of the ethics and the pitfalls in the interaction with industry; conversely industry has to define its role in the process of bringing new knowledge to useful products. The process needs to be interactive, transparent and clearly place public interest above all other considerations.

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Hod, E. A., and S. L. Spitalnik. "Stored red blood cell transfusions: Iron, inflammation, immunity, and infection." Transfusion Clinique et Biologique 19, no. 3 (June 2012): 84–89. http://dx.doi.org/10.1016/j.tracli.2012.04.001.

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Younger, David S. "I-Cubed (Infection, Immunity, and Inflammation) and the Human Microbiome." Neurologic Clinics 34, no. 4 (November 2016): 863–74. http://dx.doi.org/10.1016/j.ncl.2016.05.006.

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Spitalnik, Steven L. "Stored red blood cell transfusions: iron, inflammation, immunity, and infection." Transfusion 54, no. 10 (September 4, 2014): 2365–71. http://dx.doi.org/10.1111/trf.12848.

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Cribbs, Sushma K., Kristina Crothers, and Alison Morris. "Pathogenesis of HIV-Related Lung Disease: Immunity, Infection, and Inflammation." Physiological Reviews 100, no. 2 (April 1, 2020): 603–32. http://dx.doi.org/10.1152/physrev.00039.2018.

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Despite anti-retroviral therapy (ART), human immunodeficiency virus-1 (HIV)-related pulmonary disease continues to be a major cause of morbidity and mortality for people living with HIV (PLWH). The spectrum of lung diseases has changed from acute opportunistic infections resulting in death to chronic lung diseases for those with access to ART. Chronic immune activation and suppression can result in impairment of innate immunity and progressive loss of T cell and B cell functionality with aberrant cytokine and chemokine responses systemically as well as in the lung. HIV can be detected in the lungs of PLWH and has profound effects on cellular immune functions. In addition, HIV-related lung injury and disease can occur secondary to a number of mechanisms including altered pulmonary and systemic inflammatory pathways, viral persistence in the lung, oxidative stress with additive effects of smoke exposure, microbial translocation, and alterations in the lung and gut microbiome. Although ART has had profound effects on systemic viral suppression in HIV, the impact of ART on lung immunology still needs to be fully elucidated. Understanding of the mechanisms by which HIV-related lung diseases continue to occur is critical to the development of new preventive and therapeutic strategies to improve lung health in PLWH.

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Waickman, Adam T., Joseph Q. Lu, HengSheng Fang, Mitchell J. Waldran, Chad Gebo, Liesbeth Van Wesenbeeck, Nathalie Verpoorten, et al. "Evolution of inflammation and immunity in a dengue virus 1 human infection model." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 126.21. http://dx.doi.org/10.4049/jimmunol.208.supp.126.21.

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Abstract Dengue virus (DENV) is a significant source of morbidity and mortality throughout the tropics and subtropics. Over 400 million infections are thought to occur every year, resulting in nearly 100 million symptomatic infections and over 20,000 deaths. Early immune response kinetics to DENV infection remain unclear in large part due to the highly variable incubation period exhibited by the virus after introduction into a susceptible host. To fill this knowledge gap, we performed a comprehensive virologic and immunologic analysis of individuals experimentally infected with an under-attenuated DENV-1 strain 45AZ5. This analysis captured both the kinetics and composition of the innate, humoral, and cellular immune response elicited by experimental DENV-1 challenge, as well as the virologic and clinical feature of DENV-1 infection. Revealed in this analysis was an unexpectedly robust DENV-specific IgA antibody response that manifested between the appearance of DENV-specific IgM and IgG in all challenged individuals, as well as the presence of a non-neutralizing/NS1-specific antibody response that was delayed relative to the appearance of DENV-virion specific humoral immunity. RNAseq analysis also revealed several distinct and temporally-restricted gene modules that allowed for the identification and differentiation of the innate and adaptive immune response to DENV-infection. Our analysis provides a detailed description, in time and space, of the evolving matrix of DENV-elicited human inflammation and immunity, and reveals several previously unappreciated immunological aspects of primary DENV-1 infection.

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Loebbermann, Jens, Hannah Thornton, Tim Sparwasser, Cecilia Johansson, and Peter Openshaw. "Regulation of immunity during viral lung infection (168.1)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 168.1. http://dx.doi.org/10.4049/jimmunol.186.supp.168.1.

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Abstract Regulatory T cells (Tregs) play a clear role in chronic infections and inflammatory disorders, but their role in acute infections have not been fully elucidated. Respiratory syncytial virus (RSV) is the major cause of serious lower respiratory tract infection in infants, resulting in over-exuberant immune responses. In order to examine the role of Tregs in primary RSV primary infection, we infected “Depletion of regulatory T cells” (DEREG) mice which express the diphteria toxin (DT) receptor enhanced GFP fusion protein under the control of FOXP3 gene locus. Injections of DT ablated Tregs, and depletion prior to RSV primary infection caused increased weight loss and increased influx of cells into the lung and the airways (bronchioalveolar lavage, BAL) with lung and BAL showing elevated numbers of CD4+ and CD8+ T cells on d4, d8 and d14 post RSV infection. Interestingly, Treg depletion also caused an increase in neutrophils and eosinophils in the airways. Therefore, Tregs do not only control the magnitude of the T cell response, but also the quality of the responses that follow. The effects of RSV infection in mice with defective immune regulation closely parallels the observed effects of RSV in children with bronchiolitis, suggesting that the pathogenesis of bronchiolitis may involve an inability to regulate virus-induced inflammation

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Greber, Urs F., and Justin W. Flatt. "Adenovirus Entry: From Infection to Immunity." Annual Review of Virology 6, no. 1 (September 29, 2019): 177–97. http://dx.doi.org/10.1146/annurev-virology-092818-015550.

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More than 80 different adenovirus (AdV) types infect humans through the respiratory, ocular, or gastrointestinal tracts. They cause acute clinical mani-festations or persist under humoral and cell-based immunity. Immuno-suppressed individuals are at risk of death from an AdV infection. Concepts about cell entry of AdV build on strong foundations from molecular and cellular biology—and increasingly physical virology. Here, we discuss how virions enter and deliver their genome into the nucleus of epithelial cells. This process breaks open the virion at distinct sites because the particle has nonisometric mechanical strength and reacts to specific host factors along the entry pathway. We further describe how macrophages and dendritic cells resist AdV infection yet enhance productive entry into polarized epithelial cells. A deep understanding of the viral mechanisms and cell biological and biophysical principles will continue to unravel how epithelial and antigen-presenting cells respond to AdVs and control inflammation and persistence in pathology and therapy.

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Bagchi, Debasis, Bernard W. Downs, Samudra Prosad Banik, Tandra R. Chakraborty, Sanjoy Chakraborty, and Steve Kushner. "Inflammatory responses and obesity: Nutrition as an epigenetic modulator." American Journal of Biopharmacy and Pharmaceutical Sciences 2 (October 13, 2022): 9. http://dx.doi.org/10.25259/ajbps_14_2022.

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The onset of inflammation takes place in a human body due to an injury or infection during which the tissue becomes inflamed/reddened, swollen, hot, and painful. Basically, it is a collection of host defenses that occurs during an injury and infection in which the white blood cells protect the body from infection from bacteria, fungi, parasites, or viruses. Innate immunity provides the first challenging defense against the diverse foreign harmful invaders, while adaptive immunity, also known as acquired immunity, utilizes specialized immune cells and antibodies, which provide a counterattack and destroy these diverse foreign invaders. Moreover, they can prevent infections/diseases in the future by recognizing those invaders and providing a new immune response. However, when an immune system responds too aggressively to an infection, a condition termed a cytokine storm takes place, which may lead to multi-organ failure and even death. Inflammatory response in advancing age and obesity is intricately associated. Obesity has been identified as a low-grade systemic inflammatory response. Particularly, elevated levels of serum C-reactive protein, interleukin-6, tumor necrosis factor-α, and leptin, well characterized biomarkers of inflammation, are observed predominantly in obese individuals.

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Xiao, Tsan Sam. "Innate immunity and inflammation." Cellular & Molecular Immunology 14, no. 1 (August 22, 2016): 1–3. http://dx.doi.org/10.1038/cmi.2016.45.

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Pavlovic, Mladen, Ivan Jovanovic, and Nebojsa Arsenijevic. "Interleukin-32 in Infection, Inflammation and Cancer Biology." Serbian Journal of Experimental and Clinical Research 21, no. 1 (March 1, 2020): 75–82. http://dx.doi.org/10.1515/sjecr-2016-0085.

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AbstractCytokines are small pleiotropic polypeptids secreted dominantly by the cells of the immune system. These polypeptids are main mediators of innate and acquired immunity, responsible for clonal expansion and differentiation of immune cells, initiation of immune response and enhancing of effector functions of leukocytes. Cytokine-related effects are most studied in the fields of inflammation, immunology, and cancer biology. In this review we discuss one of the most intriguing, recently discovered proinflammatory cytokine, interleukin 32.

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NAYAK, KAUSTUV, Vineet Jain, Manpreet Kaur, Naushad Khan, Ramesh Chandra Rai, Kritika Dixit, Rohit Sagar, et al. "Human immunity to chikungunya infection." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 249.3. http://dx.doi.org/10.4049/jimmunol.204.supp.249.3.

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Abstract Chikungunyna virus is expanding globally and continue to cause major public health threat to Indian populations. Vaccine efforts are underway, and it is hoped that these will eventually progress to human evaluation. However, currently we have little understanding of the phenotypes and functions of the human T cells in chikungunya patients, a knowledge that is essential for improving vaccine design/testing and evaluation efforts. Here, we provide a detailed analysis of the CD8 T cell responses in chikungunya patients from India. We found that CD38+ HLADR+ CD8 T cell subset expanded dramatically in chikungunya febrile patients with frequencies averaging about 20% of the total CD8 T cells, and reaching as high as 50% of the CD8 T cells in some patients. The frequencies of these activated CD8 T cells were substantially low and barely above background levels in afebrile patients reporting to the clinic with persistent arthralgia/arthritis that was lasting for more than 30 days. These massively expanding CD8 T cells observed in the acute febrile patients were highly proliferating (KI67 ), robustly expressing markers indicative strong Th1 differentiation (T-bet), cytotoxic functions (Perforin) and inflammatory/synovial tissue homing characteristics (CX3CR1 and CXCR4). Interestingly, antigen-stimulation mediated IFN-g producing functions of these cells was highly compromized, reminiscent of the “cytokine stunned” phenotype. Taken together, these results suggest that these highly differentiated effector CD8 T cell that were massively expanding during acute chikungunya febrile infection might be involved in protection by homing to infected tissues and eliminating infected targets rather than causing inflammation.

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Fitton, J. Helen, Ah Young Park, Samuel S. Karpiniec, and Damien N. Stringer. "Fucoidan and Lung Function: Value in Viral Infection." Marine Drugs 19, no. 1 (December 24, 2020): 4. http://dx.doi.org/10.3390/md19010004.

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Compromised lung function is a feature of both infection driven and non-infective pathologies. Viral infections—including the current pandemic strain SARS-CoV-2—that affect lung function can cause both acute and long-term chronic damage. SARS-CoV-2 infection suppresses innate immunity and promotes an inflammatory response. Targeting these aspects of SARS-CoV-2 is important as the pandemic affects greater proportions of the population. In clinical and animal studies, fucoidans have been shown to increase innate immunity and decrease inflammation. In addition, dietary fucoidan has been shown to attenuate pulmonary damage in a model of acute viral infection. Direct inhibition of SARS-CoV-2 in vitro has been described, but is not universal. This short review summarizes the current research on fucoidan with regard to viral lung infections and lung damage.

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Nair, Meera. "The macrophage-derived proteins murine RELMα and human resistin regulate host immunity to helminth infection (MPF3P.801)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 132.1. http://dx.doi.org/10.4049/jimmunol.192.supp.132.1.

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Abstract Th2 cells are essential for protective immunity to helminths but also contribute to chronic inflammation. Here we identify the REsistin-Like Molecules RELMα and Resistin as critical mediators of this balance between helminth Th2-mediated immunity and inflammation in both murine infection and human studies. Following infection with Nippostrongylus brasiliensis, we observed significant macrophage expression of RELMα in the lungs. When RELMα-/- mice were infected with N. brasiliensis, there were increased Th2-type responses, accelerated worm expulsion and exacerbated lung inflammation compared to wild-type mice, implicating a role for RELMα in dampening Th2 immune responses. Selective depletion of macrophages in RELMα-/- mice ameliorated N. brasiliensis-induced chronic lung inflammation, suggesting that RELMα modulates inflammation through effects on macrophages. In new translational studies, we investigated the function of human Resistin (hResistin) which shares sequence homology with RELMα. Employing transgenic mice that express hResistin, we observed increased macrophage expression of hResistin in N. brasiliensis-infected lungs. Moreover, hResistin inhibited Th2 immune responses and immunity to N. brasiliensis. Finally, we observed a strong correlation between parasite number and serum Resistin levels in a population of helminth-infected patients (n=46). Taken together, these studies identify a new RELM-mediated regulatory pathway in helminth immunity and inflammation.

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Hayward, Sarah L., Shiki Takamura, and Jacob E. Kohlmeier. "Unrelated respiratory infections promote the loss of pre-existing tissue resident influenza-specific memory CD8 T cells in the lung." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 153.1. http://dx.doi.org/10.4049/jimmunol.198.supp.153.1.

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Abstract Tissue resident memory CD8 T cells mediate protective immunity at common sites of infection such as the skin, gut, female reproductive tract, and lung. Lung-resident memory T cells (lung TRM) have been found to be important for protective heterosubtypic immunity to influenza, however the efficacy of cellular immunity to influenza viruses wanes over time. Our data suggests this decline in protective immunity is due to the gradual loss of flu-specific lung TRM, which, in contrast to circulating flu-specific memory T cells and TRM in other tissues, steadily decrease in number for several months following primary infection. Notably, the loss of flu-specific lung TRM occurs throughout the TRM pool regardless of expression of the tissue residency markers CD69 and CD103. Furthermore, parabiosis experiments using influenza memory mice show that flu-specific lung TRM are not exiting the tissue, and thus the gradual loss of these cells is likely due to increased cell death compared to the systemic memory T cell pool. As the lung is continually exposed to environmental and biological insults that can result in localized inflammation, we sought to determine whether lung inflammation could promote the loss of pre-existing flu-specific lung TRM. Infection of influenza-immune mice with Sendai virus resulted in a significant decrease of the number of pre-existing flu-specific lung CD8 TRM compared to PBS controls. Importantly, Sendai infection had no impact on the number of systemic flu-specific memory CD8 T cells in the spleen. Together, these data show that lung inflammation induced by unrelated respiratory infections can promote the loss of pre-existing lung TRM and may explain the gradual loss of cellular immunity in the lung.

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Campbell, Robert A., Hansjorg Schwertz, Eugenio D. Hottz, Jesse W. Rowley, Bhanu Kanth Manne, A. Valance Washington, Robert Hunter-Mellado, et al. "Human megakaryocytes possess intrinsic antiviral immunity through regulated induction of IFITM3." Blood 133, no. 19 (May 9, 2019): 2013–26. http://dx.doi.org/10.1182/blood-2018-09-873984.

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Abstract Evolving evidence indicates that platelets and megakaryocytes (MKs) have unexpected activities in inflammation and infection; whether viral infections upregulate biologically active, antiviral immune genes in platelets and MKs is unknown, however. We examined antiviral immune genes in these cells in dengue and influenza infections, viruses that are global public health threats. Using complementary biochemical, pharmacological, and genetic approaches, we examined the regulation and function of interferon-induced transmembrane protein 3 (IFITM3), an antiviral immune effector gene not previously studied in human platelets and MKs. IFITM3 was markedly upregulated in platelets isolated from patients during clinical influenza and dengue virus (DENV) infections. Lower IFITM3 expression in platelets correlated with increased illness severity and mortality in patients. Administering a live, attenuated DENV vaccine to healthy subjects significantly increased platelet IFITM3 expression. Infecting human MKs with DENV selectively increased type I interferons and IFITM3. Overexpression of IFITM3 in MKs was sufficient to prevent DENV infection. In naturally occurring, genetic loss-of-function studies, MKs from healthy subjects harboring a homozygous mutation in IFITM3 (rs12252-C, a common single-nucleotide polymorphism in areas of the world where DENV is endemic) were significantly more susceptible to DENV infection. DENV-induced MK secretion of interferons prevented infection of bystander MKs and hematopoietic stem cells. Thus, viral infections upregulate IFITM3 in human platelets and MKs, and IFITM3 expression is associated with adverse clinical outcomes. These observations establish, for the first time, that human MKs possess antiviral functions, preventing DENV infection of MKs and hematopoietic stem cells after local immune signaling.

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Hennemann, Lisa C., and Dao Nguyen. "LasR-regulated proteases in acute vs. chronic lung infection: a double-edged sword." Microbial Cell 8, no. 7 (July 5, 2021): 161–63. http://dx.doi.org/10.15698/mic2021.07.755.

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Pseudomonas aeruginosa is a gram-negative opportunistic pathogen capable of causing both acute and chronic infections, particularly in individuals with compromised host defenses. The quorum sensing transcriptional activator LasR is widely recognized for its role in regulating the expression of acute virulence factors, notably several secreted proteases which cause direct host damage and subvert host immunity in acute infections. Paradoxically, lung infections caused by LasR-deficient variants, which are found in at least a third of cystic fibrosis (CF) patients with chronic P. aeruginosa infections, are associated with accelerated lung disease and increased markers of inflammation compared to infections caused by strains with a functional LasR system. While the loss of LasR function often (although not always) results in impaired production of LasR-controlled acute virulence factors, the implication of this pathoadaptation on host-pathogen interactions and chronic disease pathology is less well recognized. We recently observed that loss of LasR function in lasR variants, which results in impaired secreted protease production, led to increased expression of the membrane-bound surface adhesion molecule mICAM-1 in the airway epithelium, and increased neutrophilic inflammation. Specifically, human airway epithelial cells stimulated with lasR variants had higher mICAM-1 expression and greater neutrophil binding in vitro compared to stimulation with wild-type P. aeruginosa. In a subacute non-lethal P. aeruginosa lung infection model, lasR variant infection also induced higher mICAM-1 expression in the murine airway epithelium and was associated with increased neutrophilic pulmonary inflammation in vivo. Here, we discuss how (loss of) LasR function and LasR-regulated proteases affect host immunity, inflammation and tissue pathology in acute vs. chronic P. aeruginosa lung infection.

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Nuriev, Rinat, and Cecilia Johansson. "Chemokine regulation of inflammation during respiratory syncytial virus infection." F1000Research 8 (October 31, 2019): 1837. http://dx.doi.org/10.12688/f1000research.20061.1.

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Respiratory syncytial virus (RSV) can cause severe lower respiratory tract infections especially in infants, immunocompromised individuals and the elderly and is the most common cause of infant hospitalisation in the developed world. The immune responses against RSV are crucial for viral control and clearance but, if dysregulated, can also result in immunopathology and impaired gas exchange. Lung immunity to RSV and other respiratory viruses begins with the recruitment of immune cells from the bloodstream into the lungs. This inflammatory process is controlled largely by chemokines, which are small proteins that are produced in response to innate immune detection of the virus or the infection process. These chemokines serve as chemoattractants for granulocytes, monocytes, lymphocytes and other leukocytes. In this review, we highlight recent advances in the field of RSV infection and disease, focusing on how chemokines regulate virus-induced inflammation.

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Brown, Rebecca L., Max L. Y. Larkinson, and Thomas B. Clarke. "Immunological design of commensal communities to treat intestinal infection and inflammation." PLOS Pathogens 17, no. 1 (January 19, 2021): e1009191. http://dx.doi.org/10.1371/journal.ppat.1009191.

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The immunological impact of individual commensal species within the microbiota is poorly understood limiting the use of commensals to treat disease. Here, we systematically profile the immunological fingerprint of commensals from the major phyla in the human intestine (Actinobacteria, Bacteroidetes, Firmicutes and Proteobacteria) to reveal taxonomic patterns in immune activation and use this information to rationally design commensal communities to enhance antibacterial defenses and combat intestinal inflammation. We reveal that Bacteroidetes and Firmicutes have distinct effects on intestinal immunity by differentially inducing primary and secondary response genes. Within these phyla, the immunostimulatory capacity of commensals from the Bacteroidia class (Bacteroidetes phyla) reflects their robustness of TLR4 activation and Bacteroidia communities rely solely on this receptor for their effects on intestinal immunity. By contrast, within the Clostridia class (Firmicutes phyla) it reflects the degree of TLR2 and TLR4 activation, and communities of Clostridia signal via both of these receptors to exert their effects on intestinal immunity. By analyzing the receptors, intracellular signaling components and transcription factors that are engaged by different commensal species, we identify canonical NF-κB signaling as a critical rheostat which grades the degree of immune stimulation commensals elicit. Guided by this immunological analysis, we constructed a cross-phylum consortium of commensals (Bacteroides uniformis, Bacteroides ovatus, Peptostreptococcus anaerobius and Clostridium histolyticum) which enhances innate TLR, IL6 and macrophages-dependent defenses against intestinal colonization by vancomycin resistant Enterococci, and fortifies mucosal barrier function during pathological intestinal inflammation through the same pathway. Critically, the setpoint of intestinal immunity established by this consortium is calibrated by canonical NF-κB signaling. Thus, by profiling the immunological impact of major human commensal species our work paves the way for rational microbiota reengineering to protect against antibiotic resistant infections and to treat intestinal inflammation.

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Sheldon, M. "Infection, inflammation and immunity in the female genital tract of cattle." Japanese Journal of Large Animal Clinics 2, no. 4 (2011): 211. http://dx.doi.org/10.4190/jjlac.2.211.

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Feske, Stefan. "CRAC channels as critical regulators of immunity to infection and inflammation." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): SY75–2. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_sy75-2.

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Jian, J., J. Konopka, and C. Liu. "Insights into the role of progranulin in immunity, infection, and inflammation." Journal of Leukocyte Biology 93, no. 2 (October 22, 2012): 199–208. http://dx.doi.org/10.1189/jlb.0812429.

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Shui, J. W., M. W. Steinberg, and M. Kronenberg. "Regulation of inflammation, autoimmunity, and infection immunity by HVEM-BTLA signaling." Journal of Leukocyte Biology 89, no. 4 (November 24, 2010): 517–23. http://dx.doi.org/10.1189/jlb.0910528.

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Groer, Maureen Wimberly, Mitzi W. Davis, Kathlene Smith, Karyn Casey, Valerie Kramer, and Eva Bukovsky. "Immunity, Inflammation and Infection in Post-partum Breast and Formula Feeders." American Journal of Reproductive Immunology 54, no. 4 (August 31, 2005): 222–31. http://dx.doi.org/10.1111/j.1600-0897.2005.00301.x.

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LUGER, T. "Mediators of immunity and inflammation." Journal of the European Academy of Dermatology and Venereology 11 (September 1998): S25—S26. http://dx.doi.org/10.1016/s0926-9959(98)94625-6.

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Journal articles on the topic 'Infection, Immunity and Inflammation'

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