Host response to<i>Candida albicans</i>bloodstream infection and sepsis

Duggan, Seána; Leonhardt, Ines; Hünniger, Kerstin; Kurzai, Oliver

doi:10.4161/21505594.2014.988096

Cited by 77 publications

(88 citation statements)

References 160 publications

(170 reference statements)

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“…Neutrophils are the only immunocyte that prevent the transition of Candida spp. from yeast to filamentous form [14]. This type of leucocyte also controls the elimination of Candida spp.…”

Section: Innate Immunitymentioning

confidence: 99%

“…penetrate the GI mucosa and get access to the host tissue, a variety of serum factors are activated. The surface proteins of Candida strongly stimulate all 3 (classical, alternative and mannose binding lectin (MBL)) complement cascade activation [14]. Complement activation leads to opsonization and intracellular killing of Candida spp.…”

Section: Innate Immunitymentioning

confidence: 99%

“…C5 also play an important role in immunity against Candida infections. Activation of C5 triggers the formation of C5b, which facilitates the phagocytosis and release of terminal complement components [14]. Binding of Candida surface proteins like Gpm1, Pra 1 and Gpd2 prevents recognition and phagocytosis [15].…”

Section: Innate Immunitymentioning

confidence: 99%

“…Among various mechanisms responsible for PMN mediated killing of Candida spp., the 'oxidative burst' appears to be the most prominent. Oxidative burst is the process of rapid formation of reactive oxygen intermediates [14,15]. This process requires assembly of the NADPH oxidase enzyme complex in the cytoplasmic or phagosomal membrane to release superoxide [14,15].…”

Section: Innate Immunitymentioning

confidence: 99%

“…Deficiency of complement leads to poor host resistance against candidiasis. Activation of complement also regulates series of signaling events during disseminated infections [14].…”

Section: Innate Immunitymentioning

confidence: 99%

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Immunity to Candida Infection: An Overview

Deorukhkar¹

2017

MOJI

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Candida is found as a commensal of gastrointestinal and genital tract. However in contrast to many other commensals, Candida possesses a prominent ability to invade any tissue of a host presenting with innate or acquired immune deficiency. Candida spp. is an opportunistic pathogen that has acquainted various virulence traits facilitating host tissue colonization and invasion, and impairment of host defenses. The immune system is a remarkably versatile defense system that protects an individual from invasion of pathogens including Candida. Host defense mechanisms against candidiasis involve activation of an acute inflammatory response by innate immunity, followed by specific T cell (cell mediated immunity) or B cell (humoral immunity) mediated immune responses.

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“…Neutrophils are the only immunocyte that prevent the transition of Candida spp. from yeast to filamentous form [14]. This type of leucocyte also controls the elimination of Candida spp.…”

Section: Innate Immunitymentioning

confidence: 99%

Section: Innate Immunitymentioning

confidence: 99%

Section: Innate Immunitymentioning

confidence: 99%

Section: Innate Immunitymentioning

confidence: 99%

“…Deficiency of complement leads to poor host resistance against candidiasis. Activation of complement also regulates series of signaling events during disseminated infections [14].…”

Section: Innate Immunitymentioning

confidence: 99%

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Immunity to Candida Infection: An Overview

Deorukhkar¹

2017

MOJI

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Sequence Variation of Candida albicans Sap2 Enhances Fungal Pathogenicity via Complement Evasion and Macrophage M2‐Like Phenotype Induction

et al. 2023

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Candida albicans (C. albicans) is an opportunistic pathogen increasingly causing candidiasis worldwide. This study aims to investigate the pattern of systemic immune responses triggered by C. albicans with disease associated variation of Sap2, identifying the novel evasion strategies utilized by clinical isolates. Specifically, a variation in clinical isolates is identified at nucleotide position 817 (G to T). This homozygous variation causes the 273rd amino acid exchange from valine to leucine, close to the proteolytic activation center of Sap2. The mutant (Sap2‐273L) generated from SC5314 (Sap2‐273V) background carrying the V273L variation within Sap2 displays higher pathogenicity. In comparison to mice infected with Sap2‐273V strain, mice infected with Sap2‐273L exhibit less complement activation indicated by less serum C3a generation and weaker C3b deposition in the kidney. This inhibitory effect is mainly achieved by Sap2273L‐mediated stronger degradation of C3 and C3b. Furthermore, mice infected with Sap2‐273L strain exhibit more macrophage phenotype switching from M0 to M2‐like and more TGF‐β release which further influences T cell responses, generating an immunosuppressed cellular microenvironment characterized by more Tregs and exhausted T cell formation. In summary, the disease‐associated sequence variation of Sap2 enhances pathogenicity by complement evasion and M2‐like phenotype switching, promoting a more efficient immunosuppressed microenvironment.

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Inflammatory mechanisms and intervention strategies for sepsis‐induced myocardial dysfunction

Nong

Wei

2023

Immunity Inflam & Disease

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Sepsis‐induced myocardial dysfunction (SIMD) is the leading cause of death in patients with sepsis in the intensive care units. The main manifestations of SIMD are systolic and diastolic dysfunctions of the myocardium. Despite our initial understanding of the SIMD over the past three decades, the incidence and mortality of SIMD remain high. This may be attributed to the large degree of heterogeneity among the initiating factors, disease processes, and host states involved in SIMD. Previously, organ dysfunction caused by sepsis was thought to be an impairment brought about by an excessive inflammatory response. However, many recent studies have shown that SIMD is a consequence of a combination of factors shaped by the inflammatory responses between the pathogen and the host. In this article, we review the mechanisms of the inflammatory responses and potential novel therapeutic strategies in SIMD.

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Host response toCandida albicansbloodstream infection and sepsis

Cited by 77 publications

References 160 publications

Immunity to Candida Infection: An Overview

Immunity to Candida Infection: An Overview

Sequence Variation of Candida albicans Sap2 Enhances Fungal Pathogenicity via Complement Evasion and Macrophage M2‐Like Phenotype Induction

Inflammatory mechanisms and intervention strategies for sepsis‐induced myocardial dysfunction

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