Bacterial Superantigen Staphylococcal Enterotoxin B Induces Interstitial Pneumonia in SCID Mice Reconstituted with Peripheral Blood Mononuclear Cells from Collagen Vascular Disease Patients

Fujiki, Misae; Shinbori, Toshifumi; Suga, Moritaka; Miyakawa, Hisako; Mizobe, Takanori; Ando, Masayuki

doi:10.1006/clim.2000.4872

Cited by 5 publications

(2 citation statements)

References 22 publications

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“…As superantigens specifically activate V -bearing T cells, some that are normally quiescent and autoreactive, the danger of host autoimmunity is real. Arthritis, psoriasis, atopic dermatitis, collagen vascular disease, as well as inflammatory bowel disease have all been linked (to varying degrees) with microbial superantigens like the SEs and TSST-1 [127][128][129][174][175][176][177][178][179]. Although many proinflammatory cytokines in high concentrations can be deleterious for the host, IL-10 actually plays a protective role by preserving a self-tolerant state within the host via downregulating macrophage and monocyte functions [180].…”

Section: Superantigen Trickery: a Subversive Push Towards Autoimmunitymentioning

confidence: 99%

Staphylococcus aureus: The Toxic Presence of a Pathogen Extraordinaire

Larkin¹,

Carman²,

Krakauer³

et al. 2009

CMC

123

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Staphylococcus aureus is a facultative, Gram-positive coccus well known for its disease-causing capabilities. In particular, methicillin and vancomycin resistant strains of S. aureus (MRSA and VRSA, respectively) isolated globally represent daunting medical challenges for the 21(st) Century. This bacterium causes numerous illnesses in humans such as food poisoning, skin infections, osteomyelitis, endocarditis, pneumonia, enterocolitis, toxic shock, and autoimmune disorders. A few of the many virulence factors attributed to S. aureus include antibiotic resistance, capsule, coagulase, lipase, hyaluronidase, protein A, fibronectin-binding protein, and multiple toxins with diverse activities. One family of protein toxins is the staphylococcal enterotoxins (SEs) and related toxic shock syndrome toxin-1 (TSST-1) that act as superantigens. There are more than twenty different SEs described to date with varying amino acid sequences, common conformations, and similar biological effects. By definition, very low (picomolar) concentrations of these superantigenic toxins activate specific T-cell subsets after binding to major histocompatibility complex class II. Activated T-cells vigorously proliferate and release proinflammatory cytokines plus chemokines that can elicit fever, hypotension, and other ailments which include a potentially lethal shock. In vitro and in vivo models are available for studying the SEs and TSST-1, thus providing important tools for understanding modes of action and subsequently countering these toxins via experimental vaccines or therapeutics. This review succinctly presents the pathogenic ways of S. aureus, with a toxic twist. There will be a particular focus upon the biological and biochemical properties of, plus current neutralization strategies targeting, staphylcoccocal superantigens like the SEs and TSST-1.

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Section: Superantigen Trickery: a Subversive Push Towards Autoimmunitymentioning

confidence: 99%

Staphylococcus aureus: The Toxic Presence of a Pathogen Extraordinaire

Larkin¹,

Carman²,

Krakauer³

et al. 2009

CMC

123

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“…This causes widespread T cell proliferation, cytokine production, and apoptosis (338). Several additional superantigens have been well characterized such as SEA and SEB (16,107,130,257,291) and have been associated with pathological inflammatory responses in the lung. The USA300 strain of S. aureus encodes three characterized superantigens: SelX, SEK, and SEQ (104,465).…”

Section: F T Cell Activation By S Aureusmentioning

confidence: 99%

Innate Immune Signaling Activated by MDR Bacteria in the Airway

Parker

Ahn

Cohen

et al. 2016

Physiological Reviews

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Health care-associated bacterial pneumonias due to multiple-drug resistant (MDR) pathogens are an important public health problem and are major causes of morbidity and mortality worldwide. In addition to antimicrobial resistance, these organisms have adapted to the milieu of the human airway and have acquired resistance to the innate immune clearance mechanisms that normally prevent pneumonia. Given the limited efficacy of antibiotics, bacterial clearance from the airway requires an effective immune response. Understanding how specific airway pathogens initiate and regulate innate immune signaling, and whether this response is excessive, leading to host-induced pathology may guide future immunomodulatory therapy. We will focus on three of the most important causes of health care-associated pneumonia, Staphylococcus aureus, Pseudomonas aeruginosa, and Klebsiella pneumoniae, and review the mechanisms through which an inappropriate or damaging innate immune response is stimulated, as well as describe how airway pathogens cause persistent infection by evading immune activation.

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