Cigarette Smoke-Induced Lung Disease Predisposes to More Severe Infection with Nontypeable Haemophilus influenzae: Protective Effects of Andrographolide

2016 ◽  
Vol 79 (5) ◽  
pp. 1308-1315 ◽  
Author(s):  
W. S. Daniel Tan ◽  
Hong Yong Peh ◽  
Wupeng Liao ◽  
Chu Hui Pang ◽  
Tze Khee Chan ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Lung Disease ◽  
Cigarette Smoke ◽  
Severe Infection ◽  
Protective Effects ◽  
Nontypeable Haemophilus Influenzae

scholarly journals Combined exposure to cigarette smoke and nontypeable Haemophilus influenzae drives development of a COPD phenotype in mice

2014 ◽  
Vol 15 (1) ◽  
pp. 11 ◽  
Author(s):  
Shyamala Ganesan ◽  
Adam T Comstock ◽  
Brenton Kinker ◽  
Peter Mancuso ◽  
James M Beck ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Cigarette Smoke ◽  
Combined Exposure ◽  
Nontypeable Haemophilus Influenzae

scholarly journals Mechanisms of clearance of nontypeable Haemophilus influenzae from cigarette smoke-exposed mouse lungs

2010 ◽  
Vol 36 (5) ◽  
pp. 1131-1142 ◽  
Author(s):  
G. J. Gaschler ◽  
C. C. J. Zavitz ◽  
C. M. T. Bauer ◽  
M. R. Stampfli
Keyword(s):  
Haemophilus Influenzae ◽  
Cigarette Smoke ◽  
Nontypeable Haemophilus Influenzae ◽  
Mouse Lungs

scholarly journals Cigarette Smoke Primes the Pulmonary Environment to IL-1α/CXCR-2–Dependent Nontypeable Haemophilus influenzae–Exacerbated Neutrophilia in Mice

2014 ◽  
Vol 193 (6) ◽  
pp. 3134-3145 ◽  
Author(s):  
Jake K. Nikota ◽  
Pamela Shen ◽  
Mathieu C. Morissette ◽  
Kimberly Fernandes ◽  
Abraham Roos ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Cigarette Smoke ◽  
Nontypeable Haemophilus Influenzae

scholarly journals Antibacterial Defense of Human Airway Epithelial Cells from Chronic Obstructive Pulmonary Disease Patients Induced by Acute Exposure to Nontypeable Haemophilus influenzae: Modulation by Cigarette Smoke

2017 ◽  
Vol 9 (4) ◽  
pp. 359-374 ◽  
Author(s):  
Gimano D. Amatngalim ◽  
Jasmijn A. Schrumpf ◽  
Almira Henic ◽  
Esther Dronkers ◽  
Renate M. Verhoosel ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Antibacterial Activity ◽  
Epithelial Cells ◽  
Haemophilus Influenzae ◽  
Cigarette Smoke ◽  
Airway Epithelial Cells ◽  
Chronic Obstructive ◽  
Airway Epithelial ◽  
Nontypeable Haemophilus Influenzae ◽  
Obstructive Pulmonary Disease

Antimicrobial proteins and peptides (AMPs) are a central component of the antibacterial activity of airway epithelial cells. It has been proposed that a decrease in antibacterial lung defense contributes to an increased susceptibility to microbial infection in smokers and patients with chronic obstructive pulmonary disease (COPD). However, whether reduced AMP expression in the epithelium contributes to this lower defense is largely unknown. We investigated the bacterial killing activity and expression of AMPs by air-liquid interface-cultured primary bronchial epithelial cells from COPD patients and non-COPD (ex-)smokers that were stimulated with nontypeable Haemophilus influenzae (NTHi). In addition, the effect of cigarette smoke on AMP expression and the activation of signaling pathways was determined. COPD cell cultures displayed reduced antibacterial activity, whereas smoke exposure suppressed the NTHi-induced expression of AMPs and further increased IL-8 expression in COPD and non-COPD cultures. Moreover, smoke exposure impaired NTHi-induced activation of NF-κB, but not MAP-kinase signaling. Our findings demonstrate that the antibacterial activity of cultured airway epithelial cells induced by acute bacterial exposure was reduced in COPD and suppressed by cigarette smoke, whereas inflammatory responses persisted. These findings help to explain the imbalance between protective antibacterial and destructive inflammatory innate immune responses in COPD.

scholarly journals Antisera Against Certain Conserved Surface-Exposed Peptides of Nontypeable Haemophilus influenzae Are Protective

PLoS ONE ◽  
2015 ◽  
Vol 10 (9) ◽  
pp. e0136867 ◽  
Author(s):  
Paul W. Whitby ◽  
Thomas W. Seale ◽  
Daniel J. Morton ◽  
Terrence L. Stull
Keyword(s):  
Haemophilus Influenzae ◽  
Nontypeable Haemophilus Influenzae

Spontaneous Bacterial Peritonitis Caused by Nontypeable Haemophilus influenzae in a Previously Healthy Child

2013 ◽  
Vol 32 (6) ◽  
pp. 704
Author(s):  
Anastasia Dimopoulou ◽  
Dimitra Dimopoulou ◽  
Efstratios Christianakis ◽  
Dimitrios Bourikas ◽  
Ioannis Alexandrou ◽  
...  
Keyword(s):  
Haemophilus Influenzae ◽  
Healthy Child ◽  
Spontaneous Bacterial Peritonitis ◽  
Nontypeable Haemophilus Influenzae ◽  
Bacterial Peritonitis

scholarly journals Biofilm Growth Increases Phosphorylcholine Content and Decreases Potency of Nontypeable Haemophilus influenzae Endotoxins

2006 ◽  
Vol 74 (3) ◽  
pp. 1828-1836 ◽  
Author(s):  
Shayla West-Barnette ◽  
Andrea Rockel ◽  
W. Edward Swords
Keyword(s):  
Haemophilus Influenzae ◽  
Inflammatory Responses ◽  
Opportunistic Pathogen ◽  
Host Responses ◽  
Toll Like Receptor ◽  
Nontypeable Haemophilus Influenzae ◽  
Toll Like Receptor 4 ◽  
Biofilm Growth ◽  
Bacterial Endotoxins ◽  
Cell Layers

ABSTRACT Nontypeable Haemophilus influenzae (NTHI) is a common respiratory commensal and opportunistic pathogen. NTHI is normally contained within the airways by host innate defenses that include recognition of bacterial endotoxins by Toll-like receptor 4 (TLR4). NTHI produces lipooligosaccharide (LOS) endotoxins which lack polymeric O side chains and which may contain host glycolipids. We recently showed that NTHI biofilms contain variants with sialylated LOS glycoforms that are essential to biofilm formation. In this study, we show that NTHI forms biofilms on epithelial cell layers. Confocal analysis revealed that sialylated variants were distributed throughout the biofilm, while variants expressing phosphorylcholine (PCho) were found within the biofilm. Consistent with this observation, PCho content of LOS purified from NTHI biofilms was increased compared to LOS from planktonic cultures. Hypothesizing that the observed changes in endotoxin composition could affect bioactivity, we compared inflammatory responses to NTHI LOS purified from biofilm and planktonic cultures. Our results show that endotoxins from biofilms induced weaker host innate responses. While we observed a minimal effect of sialylation on LOS bioactivity, there was a significant decrease in bioactivity associated with PCho substitutions. We thus conclude that biofilm growth increases the proportion of PCho+ variants in an NTHI population, resulting in a net decrease in LOS bioactivity. Thus, in addition to their well-documented resistance phenotypes, our data show that biofilm communities of NTHI bacteria contain variants that evoke less potent host responses.

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