The Pneumococcal Polysaccharide Capsule and Pneumolysin Differentially Affect CXCL8 and IL-6 Release from Cells of the Upper and Lower Respiratory Tract

Küng, Eliane; Coward, William R.; Neill, Daniel R.; Malak, Hesham A.; Mühlemann, Kathrin; Kadioglu, Aras; Hilty, Markus; Hathaway, Lucy J.

doi:10.1371/journal.pone.0092355

Cited by 22 publications

(19 citation statements)

References 32 publications

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“…Antibodies could enhance the ability of neutrophil extracellular traps (NETS) to capture pneumococci [8,9]. Antibodies could counteract the ability of capsule to blunt the release of cytokines such as IL-6 and IL-8 from epithelial cells during the acute phase response [10]. Some non-opsonic, protective, anti-capsular monoclonal antibodies have been shown to decrease IL-8 secretion from leukocytes [11].…”

Section: Multi-modal Protection: Anti-capsular Antibodies Are Not Jusmentioning

confidence: 99%

Opening the OPK Assay Gatekeeper: Harnessing Multi-Modal Protection by Pneumococcal Vaccines

et al. 2019

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Pneumococcal vaccine development is driven by the achievement of high activity in a single gatekeeper assay: the bacterial opsonophagocytic killing (OPK) assay. New evidence challenges the dogma that anti-capsular antibodies have only a single function that predicts success. The emerging concept of multi-modal protection presents an array of questions that are fundamental to adopting a new vaccine design process. If antibodies have hidden non-opsonic functions that are protective, should these be optimized for better vaccines? What would protein antigens add to protective activity? Are cellular immune functions additive to antibodies for success? Do different organs benefit from different modes of protection? Can vaccine activities beyond OPK protect the immunocompromised host? This commentary raises these issues at a time when capsule-only OPK assay-based vaccines are increasingly seen as a limiting strategy.

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Section: Multi-modal Protection: Anti-capsular Antibodies Are Not Jusmentioning

confidence: 99%

Opening the OPK Assay Gatekeeper: Harnessing Multi-Modal Protection by Pneumococcal Vaccines

et al. 2019

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“…Some bacterial pathogens developed mechanisms to control such innate immune inflammatory response to reduce cell infiltration. For example, it has been shown that the presence of CPS of S. pneumoniae down‐regulates the expression of IL‐8/CXCL8 by upper and lower respiratory tract epithelial cells, reducing neutrophil chemotaxis . Although such a role has not been described for S. suis and epithelial cells, significant higher levels of proinflammatory cytokines and chemokines have clearly been observed when endothelial and phagocytic cells have been stimulated with CPS‐negative mutants .…”

Section: How Does Streptococcus Suis Fight Against Early Host Immune mentioning

confidence: 99%

Initial steps of the pathogenesis of the infection caused byStreptococcus suis: fighting against nonspecific defenses

et al. 2016

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Edited by Wilhelm JustInteractions between a bacterial pathogen and its potentially susceptible host are initiated with the colonization step. During respiratory/oral infection, the pathogens must compete with the normal microflora, resist defense mechanisms of the local mucosal immunity, and finally reach, adhere, and breach the mucosal epithelial cell barrier in order to induce invasive disease. This is the case during infection by the swine and zoonotic pathogen Streptococcus suis, which is able to counteract mucosal barriers to induce severe meningitis and sepsis in swine and in humans. The initial steps of the pathogenesis of S. suis infection has been a neglected area of research, overshadowed by studies on the systemic and central nervous phases of the disease. In this Review article, we provide for the first time, an exclusive focus on S. suis colonization and the potential mechanisms involved in S. suis establishment at the mucosa, as well as the mechanisms regulating mucosal barrier breakdown. The role of mucosal immunity is also addressed. Finally, we demystify the extensive list of putative adhesins and virulence factors reported to be involved in the initial steps of pathogenesis by S. suis.

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“…This is because the transition from a primary colonization bacterium to a pathogenic bacterium involves a complex interaction between S. pneu-moniae and the body's immune system. There are various components associated with S. pneumoniae-induced immune response, such as the capsule and other virulence factors (5)(6)(7). In addition, many immune cells such as neutrophils, monocytes/macrophages, and dendritic cells are involved in this process (6,(8)(9)(10), which are responsible for the release of factors including IL-1α, IL-1β, IL-6, IFN-α, IL-8, and ICAM-1 (6,8).…”

Section: Introductionmentioning

confidence: 99%

Investigation of the Impact of Streptococcus pneumoniae on A549 Pneumocytes

Liu

et al. 2019

Jundishapur J Microbiol

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Background: Streptococcus pneumoniae is a leading pathogen worldwide and its pathogenesis remains unclear. Objectives: The study aimed to investigate the secretion of interleukin-8 (IL-8) and soluble intercellular adhesion molecule-1 (ICAM-1) from A549 pneumocytes stimulated by different S. pneumoniae strains and the mechanism of blood-derived S. pneumoniae (bd-SP) in invading the blood system. Methods: Twenty-three clinical strains of S. pneumoniae isolated in 2009 along with ATCC49619 were cultured and suspended in 2018. Then, A549 pneumocytes were resuspended after culture and collection, and inoculated into culture plates. Streptococcus pneumoniae suspensions were then inoculated. Normal saline was blank control. The plates were incubated for four and eight hours. Then, the suspensions were collected and centrifuged. The supernatant was analyzed for IL-8 and ICAM-1 by ELISA. Results:The concentrations of IL-8 were 180.6, 188.5, 223.4 ± 19.9, and 230.3 ± 38.6 pg/mL for blank control, ATCC49619, blood-derived S. pneumoniae (bd-SP) and sputum-derived S. pneumoniae (sd-SP) at four-hour stimulation, respectively, and 249.2, 275.7, 224.0 ± 27.8, and 242.3 ± 33.1 pg/mL at eight-hour stimulation. The concentrations of ICAM-1 were 14.8, 12.1, 19.9 ± 17.2, and 26.1 ± 28.6 ng/mL for blank control, ATCC49619, bd-SP, and sd-SP at 4 hours, respectively, and 32.6, 150.8, 69.4 ± 45.1, and 58.7 ± 30.1 ng/mL at 8 hours. Conclusions:Streptococcus pneumoniae could upregulate the secretion of IL-8 and ICAM-1 from A549 pneumocytes. No significant difference was found between bd-SP and sd-SP which was in contrast to what was found between clinical S. pneumoniae and ATCC49619. Host response may not be a vital factor for different S. pneumoniae infections.

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The Pneumococcal Polysaccharide Capsule and Pneumolysin Differentially Affect CXCL8 and IL-6 Release from Cells of the Upper and Lower Respiratory Tract

Cited by 22 publications

References 32 publications

Opening the OPK Assay Gatekeeper: Harnessing Multi-Modal Protection by Pneumococcal Vaccines

Opening the OPK Assay Gatekeeper: Harnessing Multi-Modal Protection by Pneumococcal Vaccines

Initial steps of the pathogenesis of the infection caused byStreptococcus suis: fighting against nonspecific defenses

Investigation of the Impact of Streptococcus pneumoniae on A549 Pneumocytes

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