Role of nontypeable Haemophilus Influenzae in exacerbations and progression of chronic obstructive pulmonary disease

Eldika, Nader; Sethi, Sanjay

doi:10.1097/01.mcp.0000208451.50231.8f

Cited by 55 publications

(41 citation statements)

References 41 publications

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“…The mechanisms underlying the association between NT H. influenzae acquisition and exacerbations are poorly understood (5,18). In a prospective study of COPD patients, Murphy et al (19) noted that selected sputum isolates of apparent NT H. influenzae had an altered phenotype, including slower growth in broth culture and a tendency to form aggregates.…”

Section: Infection With Nontypeable (Nt)mentioning

confidence: 99%

Presence of Copper- and Zinc-Containing Superoxide Dismutase in Commensal Haemophilus haemolyticus Isolates Can Be Used as a Marker To Discriminate Them from Nontypeable H. influenzae Isolates

Fung¹,

O'Dwyer²,

Sinha³

et al. 2006

J Clin Microbiol

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Section: Infection With Nontypeable (Nt)mentioning

confidence: 99%

Presence of Copper- and Zinc-Containing Superoxide Dismutase in Commensal Haemophilus haemolyticus Isolates Can Be Used as a Marker To Discriminate Them from Nontypeable H. influenzae Isolates

Fung¹,

O'Dwyer²,

Sinha³

et al. 2006

J Clin Microbiol

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“…Invasive infections were most commonly associated with the encapsulated type b strain (H. influenzae type b [Hib]); however, the introduction of Hib conjugate polysaccharide vaccines has dramatically reduced the incidence of these infections. Conversely, nontypeable strains (nontypeable H. influenzae [NTHI]) do not express a polysaccharide capsule and are frequently associated with mucosal infections including otitis media, chronic bronchitis, and community-acquired pneumonia (1,11,26). The development of an effective vaccine to prevent NTHI infection has been hampered by the marked intra-and interstrain heterogeneity of surface antigens in this genetically diverse species.…”

mentioning

confidence: 99%

Natural Antibody to Conserved Targets ofHaemophilus influenzaeLimits Colonization of the Murine Nasopharynx

Zola¹,

Лысенко²,

Weiser

2009

Infect Immun

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Nasopharyngeal colonization represents the initial interaction between Haemophilus influenzae and its human host. Factors that influence bacterial carriage likely affect transmission and incidence of infection. Therefore, we investigated host factors involved in limiting H. influenzae colonization in BALB/c mice, as colonization can be established in this genetic background. Unlike what is observed in the C57BL/6 background, initial colonization of BALB/c mice was mainly limited by adaptive immune components. This effect on colonization did not require either CD4-or CD8-positive T cells. Instead, initial colonization by genetically diverse strains was limited by preexisting natural antibody with a lesser contribution of complement activity and the presence of neutrophils. Natural serum immunoglobulin from mice was able to bind to the bacterial surface and exhibited complement-dependent bactericidal activity against these genetically diverse H. influenzae strains. Moreover, natural immunoglobulin G (IgG) recognizing these strains was detected at the nasopharyngeal mucosal surface. This antibody-mediated effect required exposure to the normal mouse microbial flora, since mice raised under germfree (GF) conditions showed increased levels of H. influenzae colonization that were not limited by adaptive immunity. In addition, serum IgG from GF mice exhibited less surface binding to H. influenzae, suggesting that natural antibody, induced through prior exposure to the microbial flora, mediated the observed reduction in initial colonization. The broad effect of natural IgG against genetically diverse isolates suggests the presence of conserved species-wide protective targets of antibody.

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“…The airway epithelium is a primary interface with the outside world and is a target of the toxic particles and gases from tobacco smoke and other environmental agents that are the main cause of COPD. As indicated by changes in gene expression, airway epithelial cells respond dynamically to the inciting stimuli (6) and are the focus of viral (7) and bacterial (8)(9)(10) infections that exacerbate COPD and accelerate deterioration of lung function. The characteristic pathologic changes in the airway epithelium (Figures 1 and 2) are integral to the initiation and progression of COPD.…”

mentioning

confidence: 99%

Airway Epithelial Stem Cells and the Pathophysiology of Chronic Obstructive Pulmonary Disease

Randell

2006

Proceedings of the American Thoracic Society

121

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Characteristic pathologic changes in chronic obstructive pulmonary disease (COPD) include an increased fractional volume of bronchiolar epithelial cells, fibrous thickening of the airway wall, and luminal inflammatory mucus exudates, which are positively correlated with airflow limitation and disease severity. The mechanisms driving general epithelial expansion, mucous secretory cell hyperplasia, and mucus accumulation must relate to the effects of initial toxic exposures on patterns of epithelial stem and progenitor cell proliferation and differentiation, eventually resulting in a self-perpetuating, and difficult to reverse, cycle of injury and repair. In this review, current concepts in stem cell biology and progenitor-progeny relationships related to COPD are discussed, focusing on the factors, pathways, and mechanisms leading to mucous secretory cell hyperplasia and mucus accumulation in the airways. A better understanding of alterations in airway epithelial phenotype in COPD will provide a logical basis for novel therapeutic approaches.Keywords: epithelium; hyperplasia; metaplasia; mucus hypersecretion; stem cellsThe human and societal toll of chronic obstructive pulmonary disease (COPD) is considerable, and there is a clear need for better prevention and early detection/intervention, including more specific and effective therapies for all stages of the disease. COPD is characterized by, and defined as, sustained and largely irreversible airflow limitation on forced exhalation, associated with known risk factors and excluding other specific causes (1, 2). The key pathologic changes underlying the physiologic hallmarks are loss of lung elasticity and small airway tethers due to emphysema, thickening of the small airway wall to reduce caliber, and luminal obstruction with inflammatory mucoid secretions (3-5). The airway epithelium is a primary interface with the outside world and is a target of the toxic particles and gases from tobacco smoke and other environmental agents that are the main cause of COPD. As indicated by changes in gene expression, airway epithelial cells respond dynamically to the inciting stimuli (6) and are the focus of viral (7) and bacterial (8-10) infections that exacerbate COPD and accelerate deterioration of lung function. The characteristic pathologic changes in the airway epithelium (Figures 1 and 2) are integral to the initiation and progression of COPD. Generalized epithelial hyperplasia, mucous secretory cell hyperplasia, squamous metaplasia, and mucus accumulation must result from disruptions in normal cell and tissue dynamics caused by both the initial stimuli and the spiral of infectious complications. Locations of stem cells, patterns of cell migration/differentiation, and the regulatory mecha-

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Role of nontypeable Haemophilus Influenzae in exacerbations and progression of chronic obstructive pulmonary disease

Abstract: Though much has been learnt about nontypeable H. influenzae in chronic obstructive pulmonary disease, new therapeutic and preventive approaches require an even greater understanding of this host-pathogen interaction.

Cited by 55 publications

References 41 publications

Presence of Copper- and Zinc-Containing Superoxide Dismutase in Commensal Haemophilus haemolyticus Isolates Can Be Used as a Marker To Discriminate Them from Nontypeable H. influenzae Isolates

Presence of Copper- and Zinc-Containing Superoxide Dismutase in Commensal Haemophilus haemolyticus Isolates Can Be Used as a Marker To Discriminate Them from Nontypeable H. influenzae Isolates

Natural Antibody to Conserved Targets ofHaemophilus influenzaeLimits Colonization of the Murine Nasopharynx

Airway Epithelial Stem Cells and the Pathophysiology of Chronic Obstructive Pulmonary Disease

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