Streptococcus pneumoniae strain-dependent lung inflammatory responses in a murine model of pneumococcal pneumonia

2003 ◽  
Vol 29 (5) ◽  
pp. 808-816 ◽  
Author(s):  
Jacqueline Mohler ◽  
Esther Azoulay-Dupuis ◽  
Cécile Amory-Rivier ◽  
Jean Xavier Mazoit ◽  
Jean Pierre P. Bédos ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Murine Model ◽  
Pneumococcal Pneumonia ◽  
Inflammatory Responses ◽  
Dependent Lung ◽  
Strain Dependent

scholarly journals Monocyte Chemoattractant Protein 1 Does Not Contribute to Protective Immunity against Pneumococcal Pneumonia

2006 ◽  
Vol 74 (12) ◽  
pp. 7021-7023 ◽  
Author(s):  
Mark C. Dessing ◽  
Alex F. de Vos ◽  
Sandrine Florquin ◽  
Tom van der Poll
Keyword(s):  
Streptococcus Pneumoniae ◽  
Protective Immunity ◽  
Pneumococcal Pneumonia ◽  
Inflammatory Responses ◽  
Strongly Correlated ◽  
Wild Type ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein

ABSTRACT To determine the role of monocyte chemoattractant protein 1 (MCP-1) during pneumococcal pneumonia, MCP-1 knockout and wild-type mice were infected with Streptococcus pneumoniae. Pulmonary MCP-1 levels were strongly correlated to bacterial loads in wild-type mice. However, MCP-1 knockout and wild-type mice were indistinguishable with respect to bacterial growth, inflammatory responses, and lethality.

ANALYSIS OF BURN AND NON-BURN WOUND INFLAMMATORY RESPONSES IN A MURINE MODEL OF INJURY

Shock ◽  
2006 ◽  
Vol 25 (Supplement 1) ◽  
pp. 89
Author(s):  
T Daniel ◽  
WJ Hubbard ◽  
IH Chaudry ◽  
MA Choudhry ◽  
MG Schwacha
Keyword(s):  
Murine Model ◽  
Inflammatory Responses ◽  
Burn Wound

scholarly journals Host and Bacterial Factors Contributing to the Clearance of Colonization by Streptococcus pneumoniae in a Murine Model

2005 ◽  
Vol 73 (11) ◽  
pp. 7718-7726 ◽  
Author(s):  
Annemarie M. C. van Rossum ◽  
Elena S. Lysenko ◽  
Jeffrey N. Weiser
Keyword(s):  
Streptococcus Pneumoniae ◽  
Time Course ◽  
Inflammatory Responses ◽  
Adaptive Immune Response ◽  
Interleukin 12 ◽  
Cell Mediated Immunity ◽  
T Helper 1 ◽  
Independent Manner ◽  
Immunodeficient Mice ◽  
Human Host Factors

ABSTRACT Nasopharyngeal colonization is the first step in the interaction between Streptococcus pneumoniae (the pneumococcus) and its human host. Factors that contribute to clearance of colonization are likely to affect the spread of the pneumococcus and the rate of pneumococcal disease in the population. To identify host and bacterial factors contributing to this process, we examined the time course of colonization using genetically modified mice and pneumococci. Severe combined immunodeficient mice remained persistently colonized (>6 weeks). Major histocompatibility complex II-deficient mice, but not μMT mice, were unable to clear colonization and showed a diminished T helper 1 response. Thus, CD4+ T cells, rather than the generation of specific antibody, appear to be required for effective Th1-mediated clearance. In addition, the microbial pattern recognition receptor toll-like receptor 2 (TLR2), but not TLR4, was necessary for efficient clearance of colonization. In contrast, no role of complement component 3, inducible nitric oxide synthetase, interleukin 12 (IL-12), or IL-4 could be demonstrated. Expression of the pneumococcal toxin pneumolysin enhanced acute localized inflammatory responses and promoted clearance of colonization in a TLR4-independent manner. We conclude that both innate and CD4+ T-cell-mediated immunity and proinflammatory bacterial factors, rather than a humoral adaptive immune response, are important for clearance of S. pneumoniae from the murine nasopharynx.

scholarly journals Senkyunolide I Protects against Sepsis-Associated Encephalopathy by Attenuating Sleep Deprivation in a Murine Model of Cecal Ligation and Puncture

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jian Xie ◽  
Zhen-zhen Zhao ◽  
Peng Li ◽  
Cheng-long Zhu ◽  
Yu Guo ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Cognitive Dysfunction ◽  
Murine Model ◽  
Inflammatory Responses ◽  
Cecal Ligation ◽  
Signaling Proteins ◽  
Cecal Ligation And Puncture ◽  
Inflammatory Signaling ◽  
Tnf Α ◽  
Senkyunolide I

Sepsis may lead to sleep deprivation, which will promote the development of neuroinflammation and mediate the progression of sepsis-associated encephalopathy (SAE). Senkyunolide I, an active component derived from an herb medicine, has been shown to provide a sedative effect to improve sleep. However, its role in sepsis is unclear. The present study was performed to investigate whether Senkyunolide I protected against SAE in a murine model of cecal ligation and puncture (CLP). Here, we showed that Senkyunolide I treatment improved the 7-day survival rate and reduced the excessive release of cytokines including TNF-α, IL-6, and IL-1β. A fear conditioning test was performed, and the results showed that Senkyunolide I attenuated CLP-induced cognitive dysfunction. Senkyunolide I treatment also decreased the phosphorylation levels of inflammatory signaling proteins, including p-ERK, p-JNK, p-P38, and p-P65, and the level of inflammatory cytokines, including TNF-α, IL-6, and IL-1β, in the hippocampus homogenate. Sleep deprivation was attenuated by Senkyunolide I administration, as demonstrated by the modification of the BDNF and c-FOS expression. When sleep deprivation was induced manually, the protective effect of Senkyunolide I against inflammatory responses and cognitive dysfunction was reversed. Our data demonstrated that Senkyunolide I could protect against sepsis-associated encephalopathy in a murine model of sepsis via relieving sleep deprivation.

scholarly journals Severity and properties of cardiac damage caused by Streptococcus pneumoniae are strain dependent

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0204032 ◽  
Author(s):  
Anukul T. Shenoy ◽  
Sarah M. Beno ◽  
Terry Brissac ◽  
Jeremiah W. Bell ◽  
Lea Novak ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Cardiac Damage ◽  
Strain Dependent

Distribution and annual changes in the proportion of Streptococcus pneumoniae serotypes in Japanese adults with pneumococcal pneumonia from 2011 to 2017

2019 ◽  
Vol 25 (11) ◽  
pp. 925-929 ◽  
Author(s):  
Shingo Noguchi ◽  
Kazuhiro Yatera ◽  
Kentaro Akata ◽  
Bin Chang ◽  
Hiroaki Ikegami ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Pneumococcal Pneumonia ◽  
Japanese Adults ◽  
Annual Changes

scholarly journals Experimental Evolution In Vivo To Identify Selective Pressures during Pneumococcal Colonization

mSystems ◽  
2020 ◽  
Vol 5 (3) ◽  
Author(s):  
Vaughn S. Cooper ◽  
Erin Honsa ◽  
Hannah Rowe ◽  
Christopher Deitrick ◽  
Amy R. Iverson ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Murine Model ◽  
Experimental Evolution ◽  
Nasal Colonization ◽  
Content Type ◽  
Selective Pressures ◽  
Specific Tissue ◽  
Tissue Tropisms ◽  
Insight Into

ABSTRACT Experimental evolution is a powerful technique to understand how populations evolve from selective pressures imparted by the surrounding environment. With the advancement of whole-population genomic sequencing, it is possible to identify and track multiple contending genotypes associated with adaptations to specific selective pressures. This approach has been used repeatedly with model species in vitro, but only rarely in vivo. Herein we report results of replicate experimentally evolved populations of Streptococcus pneumoniae propagated by repeated murine nasal colonization with the aim of identifying gene products under strong selection as well as the population genetic dynamics of infection cycles. Frameshift mutations in one gene, dltB, responsible for incorporation of d-alanine into teichoic acids on the bacterial surface, evolved repeatedly and swept to high frequency. Targeted deletions of dltB produced a fitness advantage during initial nasal colonization coupled with a corresponding fitness disadvantage in the lungs during pulmonary infection. The underlying mechanism behind the fitness trade-off between these two niches was found to be enhanced adherence to respiratory cells balanced by increased sensitivity to host-derived antimicrobial peptides, a finding recapitulated in the murine model. Additional mutations that are predicted to affect trace metal transport, central metabolism, and regulation of biofilm production and competence were also selected. These data indicate that experimental evolution can be applied to murine models of pathogenesis to gain insight into organism-specific tissue tropisms. IMPORTANCE Evolution is a powerful force that can be experimentally harnessed to gain insight into how populations evolve in response to selective pressures. Herein we tested the applicability of experimental evolutionary approaches to gain insight into how the major human pathogen Streptococcus pneumoniae responds to repeated colonization events using a murine model. These studies revealed the population dynamics of repeated colonization events and demonstrated that in vivo experimental evolution resulted in highly reproducible trajectories that reflect the environmental niche encountered during nasal colonization. Mutations impacting the surface charge of the bacteria were repeatedly selected during colonization and provided a fitness benefit in this niche that was counterbalanced by a corresponding fitness defect during lung infection. These data indicate that experimental evolution can be applied to models of pathogenesis to gain insight into organism-specific tissue tropisms.

scholarly journals Delayed Administration of Recombinant Plasma Gelsolin Improves Survival in a Murine Model of Penicillin-Susceptible and Penicillin-Resistant Pneumococcal Pneumonia

2019 ◽  
Vol 220 (9) ◽  
pp. 1498-1502 ◽  
Author(s):  
Zhiping Yang ◽  
Alice Bedugnis ◽  
Susan Levinson ◽  
Mark Dinubile ◽  
Thomas Stossel ◽  
...  
Keyword(s):  
Weight Loss ◽  
Antimicrobial Resistance ◽  
Mouse Model ◽  
Murine Model ◽  
Pneumococcal Pneumonia ◽  
Preclinical Models ◽  
Antibiotic Resistant ◽  
Plasma Gelsolin ◽  
Beneficial Effects ◽  
Serious Infections

Abstract Therapy to enhance host immune defenses may improve outcomes in serious infections, especially for antibiotic-resistant pathogens. Recombinant human plasma gelsolin (rhu-pGSN), a normally circulating protein, has beneficial effects in diverse preclinical models of inflammation and injury. We evaluated delayed therapy (24–48 hours after challenge) with rhu-pGSN in a mouse model of pneumococcal pneumonia. rhu-pGSN without antibiotics increased survival and reduced morbidity and weight loss after infection with either penicillin-susceptible or penicillin-resistant pneumococci (serotypes 3 and 14, respectively). rhu-pGSN improves outcomes in a highly lethal pneumococcal pneumonia model when given after a clinically relevant delay, even in the setting of antimicrobial resistance.

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