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The interplay between immune response and bacterial infection in COPD : Focus Upon non-typeable Haemophilus influenzae

Su, Yu Ching LU ; Jalalvand, Farshid LU ; Thegerström, John LU and Riesbeck, Kristian LU orcid (2018) In Frontiers in Immunology 9(NOV).
Abstract

Chronic obstructive pulmonary disease (COPD) is a debilitating respiratory disease and one of the leading causes of morbidity and mortality worldwide. It is characterized by persistent respiratory symptoms and airflow limitation due to abnormalities in the lower airway following consistent exposure to noxious particles or gases. Acute exacerbations of COPD (AECOPD) are characterized by increased cough, purulent sputum production, and dyspnea. The AECOPD is mostly associated with infection caused by common cold viruses or bacteria, or co-infections. Chronic and persistent infection by nontypeable Haemophilus influenzae (NTHi), a Gram-negative coccobacillus, contributes to almost half of the infective exacerbations caused by bacteria.... (More)

Chronic obstructive pulmonary disease (COPD) is a debilitating respiratory disease and one of the leading causes of morbidity and mortality worldwide. It is characterized by persistent respiratory symptoms and airflow limitation due to abnormalities in the lower airway following consistent exposure to noxious particles or gases. Acute exacerbations of COPD (AECOPD) are characterized by increased cough, purulent sputum production, and dyspnea. The AECOPD is mostly associated with infection caused by common cold viruses or bacteria, or co-infections. Chronic and persistent infection by nontypeable Haemophilus influenzae (NTHi), a Gram-negative coccobacillus, contributes to almost half of the infective exacerbations caused by bacteria. This is supported by reports that NTHi is commonly isolated in the sputum from COPD patients during exacerbations. Persistent colonization of NTHi in the lower airway requires a plethora of phenotypic adaptation and virulent mechanisms that are developed over time to cope with changing environmental pressures in the airway such as host immuno-inflammatory response. Chronic inhalation of noxious irritants in COPD causes a changed balance in the lung microbiome, abnormal inflammatory response, and an impaired airway immune system. These conditions significantly provide an opportunistic platform for NTHi colonization and infection resulting in a “vicious circle.” Episodes of large inflammation as the consequences of multiple interactions between airway immune cells and NTHi, accumulatively contribute to COPD exacerbations and may result in worsening of the clinical status. In this review, we discuss in detail the interplay and crosstalk between airway immune residents and NTHi, and their effect in AECOPD for better understanding of NTHi pathogenesis in COPD patients.

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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Airway, COPD, Exacerbation, Immune response, Infection, Inflammation, Non-typeable Haemophilus influenza
in
Frontiers in Immunology
volume
9
issue
NOV
article number
02530
publisher
Frontiers Media S. A.
external identifiers
  • scopus:85056297722
  • pmid:30455693
ISSN
1664-3224
DOI
10.3389/fimmu.2018.02530
project
The respiratory tract pathogen Haemophilus influenzae - pathogenesis, antimicrobial resistance and epidemiology
Host-dependent pathogenicity and phasevarions in human airway pathogens
language
English
LU publication?
yes
id
6e94950e-a240-4abb-8b32-37f4731b55c1
date added to LUP
2018-11-22 10:38:47
date last changed
2024-04-01 15:56:33
@article{6e94950e-a240-4abb-8b32-37f4731b55c1,
  abstract     = {{<p>Chronic obstructive pulmonary disease (COPD) is a debilitating respiratory disease and one of the leading causes of morbidity and mortality worldwide. It is characterized by persistent respiratory symptoms and airflow limitation due to abnormalities in the lower airway following consistent exposure to noxious particles or gases. Acute exacerbations of COPD (AECOPD) are characterized by increased cough, purulent sputum production, and dyspnea. The AECOPD is mostly associated with infection caused by common cold viruses or bacteria, or co-infections. Chronic and persistent infection by nontypeable Haemophilus influenzae (NTHi), a Gram-negative coccobacillus, contributes to almost half of the infective exacerbations caused by bacteria. This is supported by reports that NTHi is commonly isolated in the sputum from COPD patients during exacerbations. Persistent colonization of NTHi in the lower airway requires a plethora of phenotypic adaptation and virulent mechanisms that are developed over time to cope with changing environmental pressures in the airway such as host immuno-inflammatory response. Chronic inhalation of noxious irritants in COPD causes a changed balance in the lung microbiome, abnormal inflammatory response, and an impaired airway immune system. These conditions significantly provide an opportunistic platform for NTHi colonization and infection resulting in a “vicious circle.” Episodes of large inflammation as the consequences of multiple interactions between airway immune cells and NTHi, accumulatively contribute to COPD exacerbations and may result in worsening of the clinical status. In this review, we discuss in detail the interplay and crosstalk between airway immune residents and NTHi, and their effect in AECOPD for better understanding of NTHi pathogenesis in COPD patients.</p>}},
  author       = {{Su, Yu Ching and Jalalvand, Farshid and Thegerström, John and Riesbeck, Kristian}},
  issn         = {{1664-3224}},
  keywords     = {{Airway; COPD; Exacerbation; Immune response; Infection; Inflammation; Non-typeable Haemophilus influenza}},
  language     = {{eng}},
  month        = {{11}},
  number       = {{NOV}},
  publisher    = {{Frontiers Media S. A.}},
  series       = {{Frontiers in Immunology}},
  title        = {{The interplay between immune response and bacterial infection in COPD : Focus Upon non-typeable Haemophilus influenzae}},
  url          = {{http://dx.doi.org/10.3389/fimmu.2018.02530}},
  doi          = {{10.3389/fimmu.2018.02530}},
  volume       = {{9}},
  year         = {{2018}},
}