Human complement deficiency states and infection

Densen, Peter

doi:10.1007/978-94-011-2214-6_6

Cited by 5 publications

(3 citation statements)

References 90 publications

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“…However, even though MACs are considered antifungal, they are not able to effectively lyse candidal cells, indicating the complement system to play a more modulatory role in C. albicans immunity [ 89 ]. Immune modulation by the complement system is facilitated through opsonization of C. albicans cells with C3 and Mannose-binding lectin (MBL) which promote phagocytosis by local phagocytes when possible [ 95 , 96 ]. Furthermore, MBL is able to stimulate ROS production by nearby neutrophils which are readily attracted to the site of infection via complement factor C5a, a cleavage product of C5 [ 97 , 98 ].…”

Section: Extra-epithelial Oral Immunitymentioning

confidence: 99%

The Role of the Oral Immune System in Oropharyngeal Candidiasis-Facilitated Invasion and Dissemination of Staphylococcus aureus

Pasman

Krom

Zaat

et al. 2022

Front. Oral. Health

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Candida albicans and Staphylococcus aureus account for most invasive fungal and bacterial bloodstream infections (BSIs), respectively. However, the initial point of invasion responsible for S. aureus BSIs is often unclear. Recently, C. albicans has been proposed to mediate S. aureus invasion of immunocompromised hosts during co-colonization of oral mucosal surfaces. The status of the oral immune system crucially contributes to this process in two distinct ways: firstly, by allowing invasive C. albicans growth during dysfunction of extra-epithelial immunity, and secondly following invasion by some remaining function of intra-epithelial immunity. Immunocompromised individuals at risk of developing invasive oral C. albicans infections could, therefore, also be at risk of contracting concordant S. aureus BSIs. Considering the crucial contribution of both oral immune function and dysfunction, the aim of this review is to provide an overview of relevant aspects of intra and extra-epithelial oral immunity and discuss predominant immune deficiencies expected to facilitate C. albicans induced S. aureus BSIs.

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Section: Extra-epithelial Oral Immunitymentioning

confidence: 99%

The Role of the Oral Immune System in Oropharyngeal Candidiasis-Facilitated Invasion and Dissemination of Staphylococcus aureus

Pasman

Krom

Zaat

et al. 2022

Front. Oral. Health

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“…One predominant role of complement factor C3 is the opsonization of foreign structures to facilitate their uptake by complement receptor-bearing phagocytes ( 71 ). Opsonization of the Candida surface with C3 fragments is a very fast and efficient process, underlining the relevance of this mechanism particularly in early stages of infection ( 28 ).…”

Section: Complement-mediated Anti- Candida Effectsmentioning

confidence: 99%

Candida and Complement: New Aspects in an Old Battle

et al. 2020

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Candida is a dominant fungal pathogen in immunocompromised hosts, leading to opportunistic infections. Complement with its multifaceted functions is involved in the immune defense against this yeast, and recently several novel aspects have emerged in this old battle. It is clear that Candida can adopt both roles as a colonizer or as a pathogen. In our article, we focus on the molecular mechanisms of the Candida-complement interplay, which occur in disseminated disease as well as locally on skin or on mucous membranes in mouth and vagina; the mechanisms can be supposed to be the same. Activation of the complement system by Candida is facilitated by directly triggering the three dominant pathways, but also indirectly via the coagulation and fibrinolysis systems. The complement-mediated anti-Candida effects induced thereby clearly extend chemotaxis, opsonization, and phagocytosis, and even the membrane attack complex formed on the fungal surface plays a modulatory role, although lysis of the yeast per se cannot be induced due to the thick fungal cell wall. In order to avoid the hostile action of complement, several evasion mechanisms have evolved during co-evolution, comprising the avoidance of recognition, and destruction. The latter comes in many flavors, in particular the cleavage of complement proteins by yeast enzymes and the exploitation of regulatory proteins by recruiting them on the cell wall, such as factor H. The rationale behind that is that the fluid phase regulators on the fungal cell surface down-regulate complement locally. Interestingly, however, evasion protein knockout strains do not necessarily lead to an attenuated disease, so it is likely more complex in vivo than initially thought. The interactions between complement and non-albicans species also deserve attention, especially Candida auris, a recently identified drug-resistant species of medical importance. This is in particular worth investigating, as deciphering of these interactions may lead to alternative anti-fungal therapies directly targeting the molecular mechanisms.

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“…A plethora of excellent reviews on complement deficiencies have appeared over the last 2 years, reflecting the increased recognition of, and interest in, these conditions [I I , 12,85,86,87]. Increased awareness and the widespread availabilty of functional screening assays have both contributed to a huge apparent increase in the incidence of some deficiencies.…”

Section: Complement Deficiencies and Diseusementioning

confidence: 99%

Clinical complementology: recent progress and future trends

Morgan

1994

Eur J Clin Investigation

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Human complement deficiency states and infection

Cited by 5 publications

References 90 publications

The Role of the Oral Immune System in Oropharyngeal Candidiasis-Facilitated Invasion and Dissemination of Staphylococcus aureus

The Role of the Oral Immune System in Oropharyngeal Candidiasis-Facilitated Invasion and Dissemination of Staphylococcus aureus

Candida and Complement: New Aspects in an Old Battle

Clinical complementology: recent progress and future trends

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