scholarly journals sEH promotes macrophage phagocytosis and lung clearance of Streptococcus pneumoniae

2021 ◽  
Author(s):  
Hong Li ◽  
J. Alyce Bradbury ◽  
Matthew L. Edin ◽  
Joan P. Graves ◽  
Artiom Gruzdev ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Lung Clearance ◽  
Macrophage Phagocytosis

scholarly journals Cigarette Smoke Exposure Impairs Pulmonary Bacterial Clearance and Alveolar Macrophage Complement-Mediated Phagocytosis of Streptococcus pneumoniae

2009 ◽  
Vol 78 (3) ◽  
pp. 1214-1220 ◽  
Author(s):  
John C. Phipps ◽  
David M. Aronoff ◽  
Jeffrey L. Curtis ◽  
Deepti Goel ◽  
Edmund O'Brien ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Alveolar Macrophage ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Whole Body ◽  
Cigarette Smoke Exposure ◽  
Necrosis Factor Alpha ◽  
Macrophage Phagocytosis

ABSTRACT Cigarette smoke exposure increases the risk of pulmonary and invasive infections caused by Streptococcus pneumoniae, the most commonly isolated organism from patients with community-acquired pneumonia. Despite this association, the mechanisms by which cigarette smoke exposure diminishes host defense against S. pneumoniae infections are poorly understood. In this study, we compared the responses of BALB/c mice following an intratracheal challenge with S. pneumoniae after 5 weeks of exposure to room air or cigarette smoke in a whole-body exposure chamber in vivo and the effects of cigarette smoke on alveolar macrophage phagocytosis of S. pneumoniae in vitro. Bacterial burdens in cigarette smoke-exposed mice were increased at 24 and 48 h postinfection, and this was accompanied by a more pronounced clinical appearance of illness, hypothermia, and increased lung homogenate cytokines interleukin-1β (IL-1β), IL-6, IL-10, and tumor necrosis factor alpha (TNF-α). We also found greater numbers of neutrophils in bronchoalveolar lavage fluid recovered from cigarette smoke-exposed mice following a challenge with heat-killed S. pneumoniae. Interestingly, overnight culture of alveolar macrophages with 1% cigarette smoke extract, a level that did not affect alveolar macrophage viability, reduced complement-mediated phagocytosis of S. pneumoniae, while the ingestion of unopsonized bacteria or IgG-coated microspheres was not affected. This murine model provides robust additional support to the hypothesis that cigarette smoke exposure increases the risk of pneumococcal pneumonia and defines a novel cellular mechanism to help explain this immunosuppressive effect.

scholarly journals A molecular link between cell wall biosynthesis, translation fidelity, and stringent response in Streptococcus pneumoniae

2021 ◽  
Vol 118 (14) ◽  
pp. e2018089118
Author(s):  
Surya D. Aggarwal ◽  
Adrian J. Lloyd ◽  
Saigopalakrishna S. Yerneni ◽  
Ana Rita Narciso ◽  
Jennifer Shepherd ◽  
...  
Keyword(s):  
Cell Wall ◽  
Streptococcus Pneumoniae ◽  
Stress Responses ◽  
Stringent Response ◽  
Optimal Growth ◽  
Causal Link ◽  
Cell Wall Biosynthesis ◽  
Dependent Manner ◽  
Translation Control ◽  
Macrophage Phagocytosis

Survival in the human host requires bacteria to respond to unfavorable conditions. In the important Gram-positive pathogen Streptococcus pneumoniae, cell wall biosynthesis proteins MurM and MurN are tRNA-dependent amino acyl transferases which lead to the production of branched muropeptides. We demonstrate that wild-type cells experience optimal growth under mildly acidic stressed conditions, but ΔmurMN strain displays growth arrest and extensive lysis. Furthermore, these stress conditions compromise the efficiency with which alanyl-tRNAAla synthetase can avoid noncognate mischarging of tRNAAla with serine, which is toxic to cells. The observed growth defects are rescued by inhibition of the stringent response pathway or by overexpression of the editing domain of alanyl-tRNAAla synthetase that enables detoxification of tRNA misacylation. Furthermore, MurM can incorporate seryl groups from mischarged Seryl-tRNAAlaUGC into cell wall precursors with exquisite specificity. We conclude that MurM contributes to the fidelity of translation control and modulates the stress response by decreasing the pool of mischarged tRNAs. Finally, we show that enhanced lysis of ΔmurMN pneumococci is caused by LytA, and the murMN operon influences macrophage phagocytosis in a LytA-dependent manner. Thus, MurMN attenuates stress responses with consequences for host–pathogen interactions. Our data suggest a causal link between misaminoacylated tRNA accumulation and activation of the stringent response. In order to prevent potential corruption of translation, consumption of seryl-tRNAAla by MurM may represent a first line of defense. When this mechanism is overwhelmed or absent (ΔmurMN), the stringent response shuts down translation to avoid toxic generation of mistranslated/misfolded proteins.

scholarly journals Long-term impairment of Streptococcus pneumoniae lung clearance is observed after initial infection with influenza A virus but not human metapneumovirus in mice

2011 ◽  
Vol 92 (7) ◽  
pp. 1662-1665 ◽  
Author(s):  
Herbert P. Ludewick ◽  
Laetitia Aerts ◽  
Marie-Eve Hamelin ◽  
Guy Boivin
Keyword(s):  
Streptococcus Pneumoniae ◽  
Influenza A Virus ◽  
Influenza A ◽  
Respiratory Tract Infections ◽  
Human Metapneumovirus ◽  
Influenza Viruses ◽  
Lung Clearance ◽  
Bacterial Replication ◽  
Tract Infections

Human metapneumovirus (hMPV) is a paramyxovirus responsible for respiratory tract infections in humans. Our objective was to investigate whether hMPV could predispose to long-term bacterial susceptibility, such as previously observed with influenza viruses. BALB/c mice were infected with hMPV or influenza A and, 14 days following viral infection, challenged with Streptococcus pneumoniae. Only mice previously infected with influenza A demonstrated an 8 % weight loss of their body weight 72 h following S. pneumoniae infection, which correlated with an enhanced lung bacterial replication of >7 log10 compared with pneumococcus infection alone. This enhanced bacterial replication was not related to altered macrophage or neutrophil recruitment or deficient production of critical cytokines. However, bacterial challenge induced the production of gamma interferon in bronchoalveolar lavages of influenza-infected mice, but not in those of hMPV-infected animals. In conclusion, hMPV does not cause long-term impairment of pneumococcus lung clearance, in contrast to influenza A virus.

Impacto de los serotipos 22F y 33F en la epidemiología y patogénesis de Streptococcus pneumoniae causantes de enfermedad neumocócica invasiva en España

Vacunas ◽  
2019 ◽  
Vol 20 ◽  
pp. 36
Author(s):  
J. Sempere ◽  
F. González-Camacho ◽  
M.D. Vicioso ◽  
I. del Río Menéndez ◽  
J. Yuste ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae

Der terminale Komplementkomplex ist für die Ausbildung einer suffizienten Immunantwort gegen Streptococcus pneumoniae im ZNS notwendig

2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
B Obermaier ◽  
B Angele ◽  
T Hughes ◽  
H.W Pfister ◽  
P.B Morgan ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae
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