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Journal articles on the topic 'Mechanism of infection'

Author: Grafiati

Published: 4 June 2025

Last updated: 1 August 2025

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1

Palca, Joseph. "Infection mechanism?" Nature 319, no. 6050 (1986): 170. http://dx.doi.org/10.1038/319170b0.

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2

Jones, L., B. D. Braithwaite, B. Davies, B. P. Heather, and J. J. Earnshaw. "Mechanism of Late Prosthetic Vascular Graft Infection." Cardiovascular Surgery 5, no. 5 (1997): 486–89. http://dx.doi.org/10.1177/096721099700500511.

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This study was a retrospective analysis of 41 patients with late prosthetic graft infections (> 30 days after operation) from six hospitals in the south-west of England. The 41 patients had a median age of 66 years and generally accepted risk factors for infection were documented in 19 patients preoperatively. Thirteen patients had postoperative wound complications and three had early reoperation at the site of subsequent infection. The median time between index operation and symptoms of infection was 10 (range 1–224) months. Abscess (46%) was the most common presentation followed by false

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Dahiya, Sunita, Suman Kumari, Payal Rani, Suneel Kumar Onteru, and Dheer Singh. "Postpartum uterine infection & ovarian dysfunction." Indian Journal of Medical Research 148, Suppl 1 (2018): S64—S70. https://doi.org/10.4103/ijmr.ijmr_961_18.

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Postpartum uterine infections such as metritis, endometritis and mastitis have been considered as underlying causes for ovarian dysfunction in mammals. Almost all mammals, particularly dairy animals are susceptible to postpartum uterine infections, resulting in impaired fertility and economic loss. One of the factors for low fertility in females is ovarian dysfunction, which is exhibited as impaired growth and function of ovarian follicles by the postpartum infection. Immune system of mammals provides a host defence mechanism against pathogenic microbes through the recognition of pathogen-asso

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Yasukawa, Masaki. "3. Etiological Mechanism (Infection)." Nihon Naika Gakkai Zasshi 97, no. 7 (2008): 1531–36. http://dx.doi.org/10.2169/naika.97.1531.

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5

Tudor, Cristina Anca, Cristian Boros, Raluca Petre, Adriana Elena Nica, and Christina Chatzifilippidou. "The immune response in Acinetobacter baumannii pneumonia." Romanian Journal of Infectious Diseases 19, no. 1 (2016): 16–21. http://dx.doi.org/10.37897/rjid.2016.1.3.

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Acinetobacter baumannii is a bacterium that is commonly causes of nosocomial infections, the most common site of infection and colonization is the lower respiratory tract. Although it is present more often in immunocompromised patients, the defense mechanism against infection with Acinetobacter baumanii remains incomplete elucidated. Among the virulence factors involved in infection with Acinetobacter baumanii are production and release of exopolysaccharide, and ability to biofilm formation in tissues. Understanding of virulence mechanisms is important for early initiation of treatment.

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NOMOTO, KIKUO. "Host defense mechanism against infection." Nishi Nihon Hifuka 47, no. 3 (1985): 415–28. http://dx.doi.org/10.2336/nishinihonhifu.47.415.

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SUZUKI, Yasuo, and Takashi SUZUKI. "Mechanism of Influenza Virus Infection." Kagaku To Seibutsu 35, no. 5 (1997): 339–45. http://dx.doi.org/10.1271/kagakutoseibutsu1962.35.339.

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8

Yamada, Douglas, Heidi Elsaesser, and David Brooks. "Impaired antibody effector function during persistent viral infection (VIR7P.1049)." Journal of Immunology 192, no. 1_Supplement (2014): 208.1. http://dx.doi.org/10.4049/jimmunol.192.supp.208.1.

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Abstract Persistent viral infections are associated with dysfunctional B cell responses including polyclonal B cell activation, non-virus-specific hypergammaglobulinemia, and ultimately the inability to control infection. Using the lymphocytic choriomeningitis virus (LCMV) system of murine infection, we addressed whether similar to other antiviral mechanisms, the suppressive immune environment generated during persistent infection impacted antibody effector function. We demonstrate that high levels of circulating antibodies generated during persistent infection (termed hypergammaglobulinemia)

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9

Luo, Geyang, Bo Yan, and Yinzhong Shen. "The impact and mechanism of HIV infection on tuberculous granuloma formation." AIDS 39, no. 9 (2025): 1095–105. https://doi.org/10.1097/qad.0000000000004216.

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The co-infection of Mycobacterium tuberculosis (MTB) and HIV continues to pose a major challenge to healthcare systems. Currently, the effects of HIV infection on tuberculous granulomas are not fully understood. This review discusses the impact of HIV infection on the formation and function of tuberculous granulomas, highlighting key immunological mechanisms and the interactions between HIV and MTB infections. The co-infection results in atypical granulomas with weakened immune defenses, which facilitate the dissemination of MTB and accelerate the progression of tuberculosis. Additionally, thi

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Wu, Jian, Huiqing Wang, Ze Xiang, et al. "Role of viral hepatitis in pregnancy and its triggering mechanism." Journal of Translational Internal Medicine 12, no. 4 (2024): 344–54. http://dx.doi.org/10.2478/jtim-2024-0015.

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Abstract Hepatitis viral infection can cause severe complications, even mortality in pregnant women and their offspring. Multiple studies have shown that vertical transmission can cause viral hepatitis infections in newborns, especially in hepatitis B, C, and E. Screening for hepatitis viral infection in pregnant women is essential. Once infected, pregnant women should be given timely antiviral treatments, which could effectively alleviate the disease progression and reduce adverse outcomes. Besides, the mechanism of viral hepatitis mediating adverse pregnancy outcomes has been a hot topic. He

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11

Yang, Chao-Tsung, Laura E. Swaim, and Lalita Ramakrishnan. "Mechanism of M-CSF pathway-mediated innate resistance to tuberculosis (134.76)." Journal of Immunology 182, no. 1_Supplement (2009): 134.76. http://dx.doi.org/10.4049/jimmunol.182.supp.134.76.

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Abstract The outcome of mycobacterial infections is determined by interactions between host and bacterial factors yet only very few host factors that affect the susceptibility to the infections are known. In particular, there has been an increasing appreciation that both innate immunity and hematopoietic growth factors such as M-CSF play important roles in modulating tuberculosis. The Ramakrishnan laboratory has established a model for mycobacterial pathogenesis using Mycobacterium marinum (Mm) in the optically transparent and genetically tractable zebrafish. This model allows us to dissect th

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12

Kuang, Jihui, Mingzhu Liu, Qing Yu, et al. "Antiviral Effect and Mechanism of Edaravone against Grouper Iridovirus Infection." Viruses 15, no. 11 (2023): 2237. http://dx.doi.org/10.3390/v15112237.

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Singapore grouper iridovirus (SGIV) is a virus with high fatality rate in the grouper culture industry. The outbreak of SGIV is often accompanied by a large number of grouper deaths, which has a great impact on the economy. Therefore, it is of great significance to find effective drugs against SGIV. It has been reported that edaravone is a broad-spectrum antiviral drug, most widely used clinically in recent years, but no report has been found exploring the effect of edaravone on SGIV infections. In this study, we evaluated the antiviral effect of edaravone against SGIV, and the anti-SGIV mecha

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Xu, Yaxin, Wentao Xue, Hongwei Gao, Jiabo Cui, Lingzhi Zhao, and Chongge You. "Association of toll-like receptors single nucleotide polymorphisms with HBV and HCV infection: research status." PeerJ 10 (April 19, 2022): e13335. http://dx.doi.org/10.7717/peerj.13335.

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Background Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections have become increasingly severe worldwide and are a threat to public health. There have been a number of studies conducted recently on the relationship of single nucleotide polymorphisms (SNPs) to innate immune receptor genes such as toll-like receptors (TLRs). Some literature suggests that SNPs of TLRs are associated with HBV and HCV infection. We summarized the role of TLRs gene polymorphisms associated with HBV and HCV infections and explored their possible mechanisms of action. Methodology PubMed and Web of Science w

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Arezes, João, Grace Jung, Victoria Gabayan, et al. "Hepcidin-Induced Hypoferremia Is a Host-Defense Mechanism Against Siderophilic Bacteria." Blood 122, no. 21 (2013): 176. http://dx.doi.org/10.1182/blood.v122.21.176.176.

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Abstract Introduction The iron-regulatory hormone hepcidin, a 25 amino acid peptide secreted by hepatocytes, is greatly increased during infection or inflammation, causing hypoferremia. Hypoferremia during infections has been proposed as a host defense mechanism that evolved to restrict iron availability for pathogen growth but specific support for this hypothesis has been lacking. Hereditary hemochromatosis, an iron overload disease caused by hepcidin deficiency, is associated with greatly increased risk of infections with siderophilic pathogens such as Vibrio vulnificus and Yersinia enteroco

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Martinez-Espinoza, Ivan, and Antonieta Guerrero Plata. "The role of macrophage phagocytosis on respiratory pneumovirus infection and host defense." Journal of Immunology 212, no. 1_Supplement (2024): 0154_5996. http://dx.doi.org/10.4049/jimmunol.212.supp.0154.5996.

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Abstract Lung macrophages play a pivotal role in the defense against viral and bacterial infections. These specialized cells are equipped with multiple mechanisms, such as phagocytosis, to detect the presence of pathogens and clear the infections. Human Metapneumovirus (HMPV) is a leading cause of acute lung infection, affecting particularly young children and the elderly. During and after the HMPV infection, individuals are at an increased risk of secondary bacterial infections due to a decreased immune response capacity, which increases the severity of the disease. However, the cellular cont

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Nagornyuk, V. T. "The influence of transmitted parasitic infections during pregnancy on fetal immunity system (literature review)." UKRAINIAN JOURNAL HEALTH OF WOMAN, no. 5(168) (November 20, 2023): 42–46. http://dx.doi.org/10.15574/hw.2023.168.42.

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Transmission of infections during pregnancy is known to alter the development and functioning of the fetus immune system, resulting in an inadequate immune response to common childhood infections and immunizations. Although it is a developing and actively researched topic, maternal parasitic infections remain poorly understood. Millions of women of reproductive age are currently at risk of parasite infection, while many pregnant, chronically infected women are excluded from mass drug administration due in part to a lack of resources, as well as fear of unknown adverse fetal outcomes. infection

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Han, Jiangeng, Xin Wang, Zheng Chen, Ning Gao, and Chen Wang. "Progress in clinical research complicated infection with diabetes mellitus." Infection International 7, no. 3 (2018): 101–8. http://dx.doi.org/10.2478/ii-2018-0028.

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Abstract Patients with diabetes are prone to concurrent infection. The mechanism of concurrent infection is related to factors such as hyperglycemia and weakened defense function. The infections of patients with diabetes include general and special infections. General infection includes infections in the respiratory system, urinary system, hepatobiliary system, and skin mucosa. Meanwhile, special infection includes invasive otitis externa, nasal mucormycosis, necrotizing fasciitis, and emphysema infection. Patients with special infections also have a higher mortality rate than those with gener

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18

Al-Huthaifi, Ammar Mutahar, Bakeel A. Radman, Abdullah Ali Al-Alawi, Fawad Mahmood, and Tong-Bao Liu. "Mechanisms and Virulence Factors of Cryptococcus neoformans Dissemination to the Central Nervous System." Journal of Fungi 10, no. 8 (2024): 586. http://dx.doi.org/10.3390/jof10080586.

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Cryptococcosis is a prevalent fungal infection of the central nervous system (CNS) caused by Cryptococcus neoformans, a yeast with a polysaccharide capsule in the basidiomycete group. Normally, C. neoformans infects the respiratory tract and then breaches the blood–brain barrier (BBB), leading to meningitis or meningoencephalitis, which leads to hundreds of thousands of deaths each year. Although the mechanism by which C. neoformans infiltrates the BBB to invade the brain has yet to be fully understood, research has revealed that C. neoformans can cross the BBB using transcellular penetration,

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19

Prata, Rhana Berto da Silva, and Roberta Olmo Pinheiro. "Cell Death Mechanisms in Mycobacterium abscessus Infection: A Double-Edged Sword." Pathogens 14, no. 4 (2025): 391. https://doi.org/10.3390/pathogens14040391.

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Infections caused by non-tuberculous mycobacteria (NTM), such as Mycobacterium abscessus, elicit diverse cell death mechanisms including apoptosis, necrosis, and pyroptosis, which play key roles in immunopathogenesis. NTM can manipulate these cell death pathways to evade host immune responses, ensuring their intracellular survival and persistence. Apoptosis may aid in antigen presentation and immune activation, while necrosis and pyroptosis trigger excessive inflammation, leading to tissue damage. Autophagy, a crucial cellular defense mechanism, is often induced in response to NTM infection; h

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20

KOHARA, MICHINORI, and KAZUAKI INOUE. "Mechanism of persistence in HCV infection." Uirusu 54, no. 2 (2004): 197–204. http://dx.doi.org/10.2222/jsv.54.197.

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21

NISHIMURA, Yorihiro. "The infection mechanism of enterovirus 71." Uirusu 62, no. 1 (2012): 121–28. http://dx.doi.org/10.2222/jsv.62.121.

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22

Mørch, Erna. "MECHANISM OF PNEUMOCOCCUS INFECTION IN MICE." Acta Pathologica Microbiologica Scandinavica 24, no. 2 (2009): 169–80. http://dx.doi.org/10.1111/j.1699-0463.1947.tb00586.x.

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23

Yang, Wen-Xiang, Wei Xiong, Jie Yang, and Bo-Lin Fan. "Mechanism of hepatitis C virus infection." World Chinese Journal of Digestology 19, no. 20 (2011): 2133. http://dx.doi.org/10.11569/wcjd.v19.i20.2133.

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24

Willett, Brian J., Margaret J. Hosie, James C. Neil, Julie D. Turner, and James A. Hoxie. "Common mechanism of infection by lentiviruses." Nature 385, no. 6617 (1997): 587. http://dx.doi.org/10.1038/385587a0.

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25

韩, 郝涛. "Research Progress of Rotavirus Infection Mechanism." Advances in Clinical Medicine 14, no. 02 (2024): 3825–33. http://dx.doi.org/10.12677/acm.2024.142533.

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26

Kidane, Dawit. "Molecular Mechanisms of H. pylori-Induced DNA Double-Strand Breaks." International Journal of Molecular Sciences 19, no. 10 (2018): 2891. http://dx.doi.org/10.3390/ijms19102891.

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Infections contribute to carcinogenesis through inflammation-related mechanisms. H. pylori infection is a significant risk factor for gastric carcinogenesis. However, the molecular mechanism by which H. pylori infection contributes to carcinogenesis has not been fully elucidated. H. pylori-associated chronic inflammation is linked to genomic instability via reactive oxygen and nitrogen species (RONS). In this article, we summarize the current knowledge of H. pylori-induced double strand breaks (DSBs). Furthermore, we provide mechanistic insight into how processing of oxidative DNA damage via b

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27

Valkonen, J. P. T. "Mechanisms of resistance to viruses." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (2002): S132—S135. http://dx.doi.org/10.17221/10337-pps.

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Resistance associated with a hypersensitive response (HR) and subsequent development of necrotic lesions (cell death) at the sites of virus infection can restrict virus movement in plants. Genes for HR are dominant and act on a gene-for-gene basis. Many viral proteins triggering HR have been identified. Also, several genes for HR-based virus resistance, or virus-induced cell death without resistance, have been isolated and characterized in plants, which provides novel insights to the mechanisms of virus resistance. Another international, major research frontier has formed more recently around

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Mavrov, G. I., Y. V. Scherbakova, K. Ye Ishcheikin, V. I. Kameniev, and Ya A. Yemchenko. "MECHANISM OF HIV PENETRATION." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 19, no. 2 (2019): 235–40. http://dx.doi.org/10.31718/2077-1096.19.2.235.

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Prevention of human immunodeficiency virus transmission through intercourse consists in combining highly effective biomedical, behavioural, and structural interventions. The purpose of this review was to summarize our own and global studies on the sexual transmission of human immunodeficiency virus through the mucous membranes of the genital organs. Global reports of the United Nations agency on the fight against acquired immunodeficiency syndrome, statistical reports of individual countries (in particular, Ukraine), materials of the World Health Organization for the period from 2000 to 2018 w

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Hara, Hideyuki, and Suehiro Sakaguchi. "Virus Infection, Genetic Mutations, and Prion Infection in Prion Protein Conversion." International Journal of Molecular Sciences 22, no. 22 (2021): 12439. http://dx.doi.org/10.3390/ijms222212439.

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Conformational conversion of the cellular isoform of prion protein, PrPC, into the abnormally folded, amyloidogenic isoform, PrPSc, is an underlying pathogenic mechanism in prion diseases. The diseases manifest as sporadic, hereditary, and acquired disorders. Etiological mechanisms driving the conversion of PrPC into PrPSc are unknown in sporadic prion diseases, while prion infection and specific mutations in the PrP gene are known to cause the conversion of PrPC into PrPSc in acquired and hereditary prion diseases, respectively. We recently reported that a neurotropic strain of influenza A vi

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Zarek, Christina M., Chaitanya Dende, Jaime Coronado, et al. "Preexisting helminth challenge exacerbates infection and reactivation of gammaherpesvirus in tissue resident macrophages." PLOS Pathogens 19, no. 10 (2023): e1011691. http://dx.doi.org/10.1371/journal.ppat.1011691.

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Even though gammaherpesvirus and parasitic infections are endemic in parts of the world, there is a lack of understanding about the outcome of coinfection. In humans, coinfections usually occur sequentially, with fluctuating order and timing in different hosts. However, experimental studies in mice generally do not address the variables of order and timing of coinfections. We sought to examine the variable of coinfection order in a system of gammaherpesvirus-helminth coinfection. Our previous work demonstrated that infection with the intestinal parasite, Heligmosomoides polygyrus, induced tran

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Shin, YeJu, and Kwan-Soo PARK. "Brain abscess originating from odontogenic maxillofacial fascial space abscess : report of two cases." Journal of The Korean Dental Association 62, no. 2 (2024): 94–101. http://dx.doi.org/10.22974/jkda.2024.62.2.002.

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Brain abscesses caused by dental infections are rare but potentially fatal infections with a high mortality rate. Early diagnosis and treatment are crucial, but diagnosing them is not straightforward. Various mechanisms exist through which oral bacteria can spread to the central nervous system, with hematogenous dissemination being considered the most important pathophysiological mechanism. In this report, two cases of brain abscess originating from maxillofacial fascial space infec-tion will be presented. In the first case, the infection originating from the right side secondary to the left b

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Mull, Aaron B., Ketan Sharma, Jenny L. Yu, Kevin Hsueh, Amy M. Moore, and Ida K. Fox. "Surgical Upper Extremity Infections in Immunosuppressed Patients: A Comparative Analysis With Diagnosis and Treatment Recommendations for Hand Surgeons." HAND 15, no. 1 (2018): 45–53. http://dx.doi.org/10.1177/1558944718789410.

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Background: Immunosuppression is encountered in patients with oncologic, transplant, and autoimmune disorders. The purpose of this study is to provide guidance for physicians treating surgical hand and upper extremity (UE) infections in immunosuppressed (IS) patients. Methods: We retrospectively reviewed our database of patients presenting with UE infections over 3 years. IS patients were matched randomly to non-IS patients. Patient background, infection presentation, surgical evaluation, and microbiology variables were recorded. Infection variables included mechanism, location, and type. Outc

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Shtyrkova, S. V., Y. A. Сhabaeva, S. M. Kulikov, K. I. Danishian, and E. N. Parovichnikova. "Etiology, clinical manifestations and prevention of perianal infection in patients with hematological malignancies." Russian journal of hematology and transfusiology 69, no. 4 (2024): 410–22. https://doi.org/10.35754/0234-5730-2024-69-4-410-422.

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Introduction. Perianal infection (PI) in patients with hematological malignancies is characterized by a wide spectrum of pathogens and a variety of clinical manifestations and mechanisms of development of the infectious process.Aim: to study the pathogenetic mechanisms of PI development in patients with hematological malignancies and to develop prevention tactics.Materials and methods. The prospective study included 132 patients with hematological malignancies who had episodes of PI. The infectious process in the pararectal fi ber was registered based on the data of clinical examination or mag

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Niu, Chong, Qin, Li, Wei, and Zhao. "Mechanism of Fibrosis Induced by Echinococcus spp." Diseases 7, no. 3 (2019): 51. http://dx.doi.org/10.3390/diseases7030051.

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Infection with Echinococcus spp. causes fibrosis in various vital organs, including the liver and lungs. Hepatic fibrosis is a pathological feature of Echinococcus infection that destroys normal liver tissue, leading to jaundice, cholecystitis, portal hypertension, etc. Severe Echinococcus multilocularis infections lead to liver failure and hepatic encephalopathy. The formation of peripheral fiberboards around the metacestode is a major reason as to why antiparasitic drugs fail to be effectively transported to the lesion site. Studies on the mechanism of hepatic fibrosis caused by Echinococcus

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Schneider, David S., and Janelle S. Ayres. "Us About Treating Infectious Diseases." Nature Reviews Immunology 8, vemBeR (2008): 889–95. https://doi.org/10.5281/zenodo.13532084.

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(Uploaded by Plazi for the Bat Literature Project) A host can evolve two types of defence mechanism to increase its fitness when challenged with a pathogen: resistance and tolerance. Immunology is a well-defined field in which the mechanisms behind resistance to infection are dissected. By contrast, the mechanisms behind the ability to tolerate infections are studied in a less methodical manner. In this Opinion, we provide evidence that animals have specific tolerance mechanisms and discuss their potential clinical impact. It is important to distinguish between these two defence mechanisms bec

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Schneider, David S., and Janelle S. Ayres. "Us About Treating Infectious Diseases." Nature Reviews Immunology 8, vemBeR (2008): 889–95. https://doi.org/10.5281/zenodo.13532084.

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(Uploaded by Plazi for the Bat Literature Project) A host can evolve two types of defence mechanism to increase its fitness when challenged with a pathogen: resistance and tolerance. Immunology is a well-defined field in which the mechanisms behind resistance to infection are dissected. By contrast, the mechanisms behind the ability to tolerate infections are studied in a less methodical manner. In this Opinion, we provide evidence that animals have specific tolerance mechanisms and discuss their potential clinical impact. It is important to distinguish between these two defence mechanisms bec

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Chen, Jiaying, Yifan Jing, and Zizhou Yang. "Unraveling the emergence and mechanisms of carbapenema resistance in Klebsiella pneumoniae." Theoretical and Natural Science 44, no. 1 (2024): 64–69. http://dx.doi.org/10.54254/2753-8818/44/20240492.

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The emergence and rapid spread of carbapene-resistant klebsiella pneumoniae has become a severe clinical concern. The acquisition of carbapenemase enzymes is a common mechanism contributing to resistance. Alterations in outer membrane permeability and upregulation of efflux pumps, have also been implicated. In addition, approaches to combat CRKP infections may involve the use of combination therapy, development of new antibiotics, scientific prevention and phase therapy which targets multiple bacterial mechanisms simultaneously. This review aims to look into the drug resistant mechanism and so

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Chen, Jia, and Richard Longnecker. "Epithelial cell infection by Epstein–Barr virus." FEMS Microbiology Reviews 43, no. 6 (2019): 674–83. http://dx.doi.org/10.1093/femsre/fuz023.

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ABSTRACT Epstein-Barr Virus (EBV) is etiologically associated with multiple human malignancies including Burkitt lymphoma and Hodgkin disease as well as nasopharyngeal and gastric carcinoma. Entry of EBV into target cells is essential for virus to cause disease and is mediated by multiple viral envelope glycoproteins and cell surface associated receptors. The target cells of EBV include B cells and epithelial cells. The nature and mechanism of EBV entry into these cell types are different, requiring different glycoprotein complexes to bind to specific receptors on the target cells. Compared to

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Cannas, Giovanna. "SICKLE CELL DISEASE AND INFECTIONS IN HIGH- AND LOW-INCOME COUNTRIES." Mediterranean Journal of Hematology and Infectious Diseases 11, no. 1 (2019): 02019042. http://dx.doi.org/10.4084/mjhid.2019.042.

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Infections, especially pneumococcal septicemia, meningitis, and Salmonella osteomyelitis, are a major cause of morbidity and mortality in patients with sickle cell disease (SCD). SCD increased susceptibility to infection, while infection leads to SCD-specific pathophysiological changes. The risk of infectious complications is highest in children with a palpable spleen before 6 months of age. Functional splenectomy, the results of repeated splenic infarctions, appears to be an important host-defense defect. Infection is the leading cause of death, particularly in less developed countries. Defec

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GETTI, G. T., R. A. CHEKE, and D. P. HUMBER. "Induction of apoptosis in host cells: a survival mechanism forLeishmaniaparasites?" Parasitology 135, no. 12 (2008): 1391–99. http://dx.doi.org/10.1017/s0031182008004915.

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SUMMARYLeishmaniaparasites invade host macrophages, causing infections that are either limited to skin or spread to internal organs. In this study, 3 species causing cutaneous leishmaniasis,L. major,L. aethiopicaandL. tropica, were tested for their ability to interfere with apoptosis in host macrophages in 2 different lines of human monocyte-derived macrophages (cell lines THP-1 and U937) and the results confirmed in peripheral blood mononuclear cells (PBMC). All 3 species induced early apoptosis 48 h after infection (expression of phosphatidyl serine on the outer membrane). There were signifi

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Yamaguchi, Hiroyuki, Herman Friedman, and Yoshimasa Yamamoto. "Involvement of Nicotinic Acetylcholine Receptors in Controlling Chlamydiapneumoniae Growth in Epithelial HEp-2 Cells." Infection and Immunity 71, no. 6 (2003): 3645–47. http://dx.doi.org/10.1128/iai.71.6.3645-3647.2003.

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ABSTRACT Nicotinic acetylcholine receptors (nAChRs) play an essential role in neurotransmission. Recent studies have indicated that nAChRs may be involved in the regulation of some bacterial infections through immunological mechanisms in macrophages. However, the regulation of infection with Chlamydia pneumoniae, which is a ubiquitous pneumonia-causing bacterium, by an nAChR-mediated mechanism is still unclear. In the present study, it was found that stimulation of nAChRs with ligands such as nicotine and acetylcholine altered the growth of C. pneumoniae in epithelial HEp-2 cells. Thus, the re

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Chernykh, Oleg Yu, Aleksey V. Mishchenko, Vladimir A. Mishchenko, Valentina P. Semakina, and Anton K. Karaulov. "On senecavirus transmission pathways and mechanism." Veterinaria Kubani, no. 2 (May 8, 2020): 17–20. http://dx.doi.org/10.33861/2071-8020-2020-2-17-20.

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Senecavirus infection is manifested by vesicular lesions of the skin of the distal parts of the limbs, patch and mammary gland in adult pigs and epizootic transient neonatal disease of newborn piglets. According to clinical signs and pathological changes, vesicular senecavirus infection in fattening pigs and adult pigs is indistinguishable from foot and mouth disease, porcine vesicular disease, porcine vesicular exanthema and vesicular stomatitis. The causative agent of senecavirus infection is a small, non-enveloped virus containing RNA coated with a protein capsid. Возбудитель относится к се

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Sueyoshi, Koichiro. "Clarifying the mechanism of complement activation in sepsis patients." Impact 2021, no. 5 (2021): 28–30. http://dx.doi.org/10.21820/23987073.2021.5.28.

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Sepsis occurs when the body has an extreme reaction to infection and the patient's condition worsens. Most types of infection can lead to sepsis but, commonly, infections start in the lung, urinary tract, skin or gastrointestinal tract. Sepsis can lead to multiple organ failure, complications and death. There remains uncertainty surrounding the actual causes of multiple organ failure from sepsis and greater clarity is required in order to develop treatments and improve patient outcomes. Associate Professor Koichiro Sueyoshi, Emergency and Critical Care Center, Juntendo University Urayasu Hospi

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Yang, Shanshan, Xinfei Li, Weihe Cang, et al. "Biofilm tolerance, resistance and infections increasing threat of public health." Microbial Cell 10, no. 11 (2023): 233–47. http://dx.doi.org/10.15698/mic2023.11.807.

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Microbial biofilms can cause chronic infection. In the clinical setting, the biofilm-related infections usually persist and reoccur; the main reason is the increased antibiotic resistance of biofilms. Traditional antibiotic therapy is not effective and might increase the threat of antibiotic resistance to public health. Therefore, it is urgent to study the tolerance and resistance mechanism of biofilms to antibiotics and find effective therapies for biofilm-related infections. The tolerance mechanism and host reaction of biofilm to antibiotics are reviewed, and bacterial biofilm related diseas

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Song, Ying, Yufang Qiu, Weiyou Liu, and Xiaoliang Yuan. "Research progress in immunological mechanisms of Cryptococcus." Trends in Immunotherapy 5, no. 2.1 (2021): 72. http://dx.doi.org/10.24294/ti.v5.i2.1.1370.

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Whether infection of Cryptococcus causes disease in host or not depends on the virulence of the pathogen and the immune defense ability of the host. Cryptococcus neoformans (C. neoformans) mainly causes opportunistic infections in the immunocompromised or immunodeficient patients. In contrast, Cryptococcus gattii (C. gattii) mainly attacks the immunocompetent individuals. On the one hand, the host immune cells can eliminate the invasive Cryptococcus through a complex immune mechanism; on the other hand, Cryptococcus can evade the clearance of host immune cells by adopting various strategies (i

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Kim, Chae Won, Hye Jee Yoo, Jang Hyun Park, Ji Eun Oh, and Heung Kyu Lee. "Exogenous Interleukin-33 Contributes to Protective Immunity via Cytotoxic T-Cell Priming against Mucosal Influenza Viral Infection." Viruses 11, no. 9 (2019): 840. http://dx.doi.org/10.3390/v11090840.

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Influenza is an infectious respiratory illness caused by the influenza virus. Though vaccines against influenza exist, they have limited efficacy. To additionally develop effective treatments, there is a need to study the mechanisms of host defenses from influenza viral infections. To date, the mechanism by which interleukin (IL)-33 modulates the antiviral immune response post-influenza infection is unclear. In this study, we demonstrate that exogenous IL-33 enhanced antiviral protection against influenza virus infection. Exogenous IL-33 induced the recruitment of dendritic cells, increased th

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Chapman, Nora M. "Persistent Enterovirus Infection: Little Deletions, Long Infections." Vaccines 10, no. 5 (2022): 770. http://dx.doi.org/10.3390/vaccines10050770.

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Enteroviruses have now been shown to persist in cell cultures and in vivo by a novel mechanism involving the deletion of varying amounts of the 5′ terminal genomic region termed domain I (also known as the cloverleaf). Molecular clones of coxsackievirus B3 (CVB3) genomes with 5′ terminal deletions (TD) of varying length allow the study of these mutant populations, which are able to replicate in the complete absence of wildtype virus genomes. The study of TD enteroviruses has revealed numerous significant differences from canonical enteroviral biology. The deletions appear and become the domina

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Sala, Eleonora, Marta Mangione, Chiara Laura та ін. "IFN-γ promotes TH1 at the expense of TFH differentiation during viral infections". Journal of Immunology 208, № 1_Supplement (2022): 182.24. http://dx.doi.org/10.4049/jimmunol.208.supp.182.24.

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Abstract Although humoral and cellular immunity upon viral infections usually co-exist, sometimes one of the two responses emerges and is responsible for most of the antiviral activity. For example, vescicular stomatitis virus (VSV) infection induces early and potent neutralizing antibody (nAb) responses, whereas lymphocytic choriomeningitis virus (LCMV) infection induces strong cellular responses, but weak nAb responses. Recent work from our laboratory has shown that unbalance is observed also at the level of CD4 T cells responses, with VSV inducing strong TFH polarization that support nAb re

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Weinstein, David E., Victoria H. Freedman, and Gilla Kaplan. "Molecular mechanism of nerve infection in leprosy." Trends in Microbiology 7, no. 5 (1999): 185–86. http://dx.doi.org/10.1016/s0966-842x(99)01497-3.

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Jones, L. "Mechanism of late prosthetic vascular graft infection." Cardiovascular Surgery 5, no. 5 (1997): 486–89. http://dx.doi.org/10.1016/s0967-2109(97)00056-2.

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