Innate and adaptive immunologic functions of complement in the host response to Listeria monocytogenes infection

Calame, Daniel G.; Mueller‐Ortiz, Stacey L.; Wetsel, Rick A.

doi:10.1016/j.imbio.2016.07.004

Cited by 26 publications

(21 citation statements)

References 139 publications

(152 reference statements)

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“…Cellular activation leads to release of secondary immune mediators and subsequent induction of the adaptive immune responses ( 50 ). In parallel, the complement system, an assembly of soluble enzymatic proteins and peptides in the blood and body fluids, actively regulates these inflammatory responses ( 51 ), many of which are identified as contributing toward regulation of higher immune function ( 52 ). The multiple interconnections among immune cells, cytokines, chemokines, and complement proteins protect against development of systemic infections and support damaged tissue repair.…”

Section: Inflammation: An Immune Response To Injurymentioning

confidence: 99%

Lactoferrin in a Context of Inflammation-Induced Pathology

2017

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Much progress has been achieved to elucidate the function of lactoferrin (LTF), an iron-binding glycoprotein, in the milieu of immune functionality. This review represents a unique examination of LTF toward its importance in physiologic homeostasis as related to development of disease-associated pathology. The immunomodulatory nature of this protein derives from its unique ability to “sense” the immune activation status of an organism and act accordingly. Underlying mechanisms are proposed whereby LTF controls disease states, thereby pinpointing regions of entry for LTF in maintenance of various physiological pathways to limit the magnitude of tissue damage. LTF is examined as a first line mediator in immune defense and response to pathogenic and non-pathogenic injury, as well as a molecule critical for control of oxidative cell function. Mechanisms of interaction of LTF with its receptors are examined, with a focus on protective effects via regulation of enzyme activities and reactive oxygen species production, immune deviation, and prevention of cell apoptosis. Indeed, LTF serves as a critical control point in physiologic homeostasis, functioning as a sensor of immunological performance related to pathology. Specific mediation of tissue pathophysiology is described for maintenance of intestinal integrity during endotoxemia, elicited airway inflammation due to allergens, and pulmonary damage during tuberculosis. Finally, the role of LTF to alter differentiation of adaptive immune function is examined, with specific recognition of its utility as a vaccine adjuvant to control subsequent lymphocytic reactivity. Overall, it is clear that while the ability of LTF to both sequester iron and to direct reactive oxygen intermediates is a major factor in lessening damage due to excessive inflammatory responses, further effects are apparent through direct control over development of higher order immune functions that regulate pathology due to insult and injury. This culminates in attenuation of pathological damage during inflammatory injury.

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Section: Inflammation: An Immune Response To Injurymentioning

confidence: 99%

Lactoferrin in a Context of Inflammation-Induced Pathology

2017

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“…As an example, Listeria monocytogenes temporarily overcomes the host response by producing numerous virulence factors allowing it to evade the phagosome, replicate, hijack host actin filaments and spread between cells through protrusions of the host cell membrane (Calame, Mueller-Ortiz, et al, 2016). Among viruses, adenovirus and rhinovirus can lyse the endosome, while poliovirus and coxsackievirus form pores in the endosomal membrane (Tam, Bidgood, et al, 2014) to evade the host response.…”

Section: 0 New Insights On the Roles Of Intracellular C3mentioning

confidence: 99%

Complement’s hidden arsenal: New insights and novel functions inside the cell

Liszewski

Elvington

Kulkarni

et al. 2017

Molecular Immunology

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A key component of both innate and adaptive immunity, new understandings of the complement system are expanding its roles beyond that traditionally appreciated. Evidence is accumulating that complement has an intracellular arsenal of components that provide not only immune defense, but also assist in key interactions for host cell functions. Although early work has primarily centered on T cells, the intracellular complement system likely functions in many if not most cells of the body. Some of these functions may trace their origins to the primitive complement system that began as a primeval form of C3 likely tasked for protection from intracellular pathogen invasion. This later expanded to include extracellular defense as C3 became a secreted protein to patrol the vasculature. Other components were added to the growing system including regulators to protect host cells from the indiscriminate effects of this potent system. Contemporary cells may retain some of these vestigial remnants. We now know that a) C3 serves as a damage-associated molecular pattern (in particular by coating pathogens that translocate into cells), b) most cells store C3 and recycle C3(H2O) for immediate use, and c) C3 assists in cellular survival and metabolic reprogramming. Other components also are part of this hidden arsenal including C5, properdin, factors H and B, and complement receptors. Importantly, better definition of the intracellular complement system may translate into new target discovery to assist in creating the next generation of complement therapeutics.

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“…Notably, alemtuzumab almost immediately and transiently impairs the release of cytokines from remaining lymphocytes as well as innate immune cells [10]. Such acute and transient effects on both innate and adaptive immunity could explain the peculiar timing of listeria infection to the period immediately after treatment [11]. …”

Section: Discussionmentioning

confidence: 99%

Listeria monocytogenes infection associated with alemtuzumab – - a case for better preventive strategies

2017

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BackgroundThe mortality of septicaemia, meningitis and encephalitis caused by Listeria monocytogenes is 20–40%. Twenty-one cases of invasive listeriosis associated with alemtuzumab, including at least 16 in patients with multiple sclerosis, have been published or reported to the World Health Organization Case Safety Reports Database. Three cases were fatal, including at least one patient treated for multiple sclerosis in 2016.Case presentationWe report a patient with multiple sclerosis who developed pyrexia, nausea and abdominal discomfort few hours after the third and last infusion of her second alemtuzumab cycle. An infusion related reaction was suspected. The patient had however eaten soft cheese and raw sausage 3 days prior to treatment, and L. monocytogenes septicaemia was diagnosed based on positive blood cultures.ConclusionListeriosis associated with alemtuzumab is a potentially fatal condition that can mimic an infusion related reaction. As in most other previously reported cases symptoms started rapidly after the last infusion, suggesting that the patient already carried the bacteria prior to the alemtuzumab infusions. The summary of product characteristics recommends patients to avoid foods associated with listeria at least 1 month after treatment. This recommendation should include also the last weeks prior to treatment.

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Innate and adaptive immunologic functions of complement in the host response to Listeria monocytogenes infection

Cited by 26 publications

References 139 publications

Lactoferrin in a Context of Inflammation-Induced Pathology

Lactoferrin in a Context of Inflammation-Induced Pathology

Complement’s hidden arsenal: New insights and novel functions inside the cell

Listeria monocytogenes infection associated with alemtuzumab – - a case for better preventive strategies

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