Evaluation of cytokines produced by β-hemolytic streptococcus in acute pharyngotonsillitis

Leão, Sydney Correia; Leal, Ivanna Oliveira; Rocha, Hertaline Menezes do Nascimento; Rodrigues, Tania Maria de Andrade

doi:10.1016/j.bjorl.2015.05.003

Cited by 5 publications

(5 citation statements)

References 18 publications

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“…BMDMs are reported to secrete IL‐6, TNF‐α, and IFN‐β in response to GAS, and PBMCs secrete IL‐1β, IL‐6, TNF‐α, and IFN‐α . Blood samples from patients with acute GAS pharyngitis showed high levels of the proinflammatory cytokines TNF‐α and IL‐6 and reduced levels of the Th2 signature cytokines IL‐4 and IL‐10, suggesting that immune responses are skewed away from a Th2 phenotype . In a murine nasopharyngeal GAS infection model, analysis of nasal turbinates revealed an early Th17‐skewed response, with enhanced secretion of TNF‐α, IL‐6, and IL‐17A .…”

Section: Innate Immune Response To Gas Pharyngitismentioning

confidence: 99%

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Soderholm

Barnett

Sweet

et al. 2017

Journal of Leukocyte Biology

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Streptococcus pyogenes, the Group A Streptococcus (GAS), is the most common cause of bacterial pharyngitis in children and adults. Innate and adaptive host immune responses are fundamental for defense against streptococcal pharyngitis and are central to the clinical manifestation of disease. Host immune responses also contribute to the severe poststreptococcal immune diseases that constitute the major disease burden for this organism. However, until recently, little was known about the host responses elicited during infection. Cellular mediators of innate immunity used during host defense against GAS include epithelial cells, neutrophils, macrophages, and dendritic cells (DCs), which are reported to secrete a number of soluble inflammatory mediators, such as antimicrobial peptides (AMPs); eicosanoids, including PGE and leukotriene B4 (LTB ); chemokines; and proinflammatory cytokines. Th1 and Th17 responses play significant roles in adaptive immunity in both murine models of GAS pharyngitis and in human tonsil tissue. A number of inflammatory complications are associated with GAS pharyngitis, which can lead to chronic disease in patients. These include scarlet fever, tonsillar hypertrophy, and sleep apnea, as well as postinfectious sequelae, such as acute rheumatic fever (ARF), poststreptococcal glomerulonephritis, and guttate psoriasis (GP). This review aims to present the current state of knowledge on innate and adaptive immune responses elicited during GAS pharyngitis, mechanisms by which GAS evades these responses, the emerging role of the pharyngeal microbiota, and how the interplay among these factors can influence the outcome of infection and inflammation-related complications.

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Section: Innate Immune Response To Gas Pharyngitismentioning

confidence: 99%

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Soderholm

Barnett

Sweet

et al. 2017

Journal of Leukocyte Biology

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“…Group A streptococcus is the most frequently identified bacterium in children with acute pharyngotonsillitis (APT), although group B, C, F, and G have also been associated with APT. In Leao SC study higher APT incidence was observed in the female gender and tonsillar exudates was observed with group A and C predominant [1]. To assess the utility of clinical features for diagnosis of APT with GAS in pediatrics with throat cultures showed that clinical presentation should not be used to confirm APT because its performance as a diagnostic test is low.…”

Section: Open Access Mini Reviewmentioning

confidence: 99%

Group A Streptococcal Pharyngotonsillitis

Wan

Cholashki³

2018

BJSTR

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“…The impact of these findings has implications in understanding the role of IL-6 during GAS pharyngitis. IL-6 is a marker of acute pharyngitis (198) and plays an important role, in combination with TGF-β, in promoting Th17 differentiation in murine nasopharyngeal models of pharyngitis (72).…”

Section: Discussionmentioning

confidence: 99%

“…BMDMs are reported to secrete IL-6, TNF-α and IFN-β in response to GAS (104), and PBMCs secrete IL-1β, IL-6, TNF-α and IFN-α (118). Blood samples from patients with acute GAS pharyngitis showed high levels of the pro-inflammatory cytokines TNF-α and IL-6, and reduced levels of the T helper 2 (Th2) signature cytokines IL-4 and IL-10, suggesting that immune responses are skewed away from a Th2 phenotype (198). In a murine nasopharyngeal GAS infection model, analysis of nasal turbinates revealed an early Th17-skewed response, with enhanced secretion of TNF-α, IL-6 and IL-17A (103).…”

Section: Pro-inflammatory Cytokinesmentioning

confidence: 99%

“…Epithelial cells strongly secrete IL-6 and TNF-α in response to GAS infection (105,112), with one study speculating that significant pro-inflammatory responses by epithelial cells would lead to tissue destruction in vivo, allowing GAS to disseminate deeper into host tissues (112). Blood samples from patients with acute GAS pharyngitis also showed high levels of IL-6 and TNF-α (198), further indicating that these cytokines are important in the pathology of this disease. Despite GAS employing a vast array of virulence factors to dampen host responses during infection, the ability of GAS to target the production of IL-6 and TNF-α during infection is relatively unknown.…”

Section: Group a Streptococcus M1t1 Expression Of Slo Blocks The Hostmentioning

confidence: 99%

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The Group A Streptococcus M1T1 clone post-transcriptionally modifies innate immune signalling to promote infection

Soderholm¹

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Streptococcus pyogenes, the Group A Streptococcus (GAS), is the most common cause of bacterial pharyngitis in children and adults. Host innate and adaptive immune responses mediate defence against streptococcal pharyngitis and are also central to the clinical manifestation of the disease. The ability of GAS to invade the host and establish infection likely involves subversion of host immune defences, however the signalling pathways and immune responses elicited during streptococcal pharyngitis, particularly by epithelial cells, are currently not well understood. This thesis focuses on characterising the inflammatory responses of primary human tonsil epithelial (TEpi) cells during intracellular infection with two distinct GAS strains; the laboratory-adapted M6 strain JRS4 and the M1T1 clinical isolate 5448. M1T1 is a globally-disseminated GAS clone that is the most commonly isolated serotype (approximately 20% of all isolates) in high income countries (1). This thesis aims to investigate innate immune responses triggered and/or subverted by these different GAS strains in order to uncover why the M1T1 strain is such a successful pathogen. The pharyngeal and tonsil epithelia are important components of innate immune defence against GAS infection. They primarily act as a physical barrier, but also secrete antimicrobial peptides and cytokines/chemokines that have direct antimicrobial effects and/or signal to immune cells. Previous studies have investigated epithelial immune responses to GAS infection by utilising a number of different cell types, largely immortalised and nonpharyngeal-derived cell lines such as HEp-2 and HaCaT cells, which may not respond in the same manner as pharyngeal cells to GAS infection. Nonetheless, several studies that have used tonsil explant tissue or pharyngeal-derived cell lines appear to be congruent with studies that have used nonpharyngeal cell lines to examine a number of immune mediators secreted in response to GAS infection. Next generation Illumina RNA sequencing was employed to characterise the inflammatory gene expression profile of JRS4-and 5448-infected TEpi cells during early intracellular infection, as reported in Chapter 4. I found that, whilst infection with either GAS strain induced the mRNA expression of a similar array of host inflammatory genes, the transcriptional response to 5448infection was of a much higher magnitude compared to JRS4-infection. Sequential window acquisition of all theoretical fragment ion mass spectra (SWATH-MS) was also employed to characterise changes in the host proteome during early GAS infection, and proteins that significantly changed in abundance during 5448-infection consisted mainly of those involved in metabolic and trafficking pathways, as well as transcriptional regulation.

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Evaluation of cytokines produced by β-hemolytic streptococcus in acute pharyngotonsillitis

Abstract: The Groups A and C showed higher cytokine levels than the Groups B and control, suggesting similar immunological patterns.

Cited by 5 publications

References 18 publications

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Group A Streptococcal Pharyngotonsillitis

The Group A Streptococcus M1T1 clone post-transcriptionally modifies innate immune signalling to promote infection

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Evaluation of cytokines produced by β-hemolytic streptococcus in acute pharyngotonsillitis

Abstract: The Groups A and C showed higher cytokine levels than the Groups B and control, suggesting similar immunological patterns.

Cited by 5 publications

References 18 publications

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Group A streptococcal pharyngitis: Immune responses involved in bacterial clearance and GAS-associated immunopathologies

Group A Streptococcal Pharyngotonsillitis

The Group A Streptococcus M1​​​​​​​T1 clone post-transcriptionally modifies innate immune signalling to promote infection

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The Group A Streptococcus M1T1 clone post-transcriptionally modifies innate immune signalling to promote infection