الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Asthma is an inflammatory disease of the airways, with a worldwide-unexplained
increasing incidence. Marked inflammation of the bronchial mucosa is a common feature
of asthma and leads to structural changes of the lung tissue. Multiple risk factors are
discussed to contribute to the development of asthma in patients with underlying atopy.
C. pneumoniae has been discussed as a possible cofactor causing asthma. An association of
C. pneumoniaeinfection with asthma was first described in the early 1990s
(155)
and
epidemiological and clinical data support the suggestion that C. pneumoniae infection may
partly explain the increased incidence of asthma.
In 1986 Grayston and coworkers described C. pneumoniae strain isolated from eight
students at the University of Washington, Seattle, who had acute respiratory tract
infections
(61)
.
C. pneumoniaeis an intracellular gram-negative parasite mainly infecting epithelial
cells and macrophages. In contrast to most bacteria, C. pneumoniaemust invade cells for
replication. Therefore, Chlamydia uses several proteins that share high homologies with
host proteins
(67)
. Both intracellular growth and the use of host like proteins prevent
recognition of C. pneumoniaeinfections by the host immune system. However, growing
C. pneumoniaeneed not necessarily destroy the host cell, allowing infected cells to survive
and further proliferate. By this pathway, C. pneumoniaecan be distributed to daughter cells
of the originally infected cell, persisting as a slow-spreading latent infection
(67)
.
C. pneumoniaeis a common respiratory pathogen that may cause acute illness in
both the upper and lower respiratory tracts
(186)
. It has been estimated that most people have
2 or 3 C. pneumoniaeinfections during their lifetime
(60)
. This condition has been reported
as a possible etiologic agent in asthma since Hahn et al
(155)
showed an association between
C. pneumoniaeserology and asthma in 1991.
C. pneumoniae infection can initiate
(150)
and exacerbate
(187)
asthma and persistent
infection. This may contribute to chronic asthma symptoms in some patients
(150)
. These
associations were determined by seroepidemiologic observations, case series, isolation or
direct detection of the organism in specimens
(176)
.
The diagnosis of acute C. pneumoniae infection is usually based on serologic criteria
that include the presence of IgM antibodies and/or rise in IgG antibodies
(153)
. The absence
of an increase in IgM suggests reinfection rather than primary infection. Reinfection or
reactivation of C. pneumoniaeinfection is followed by elevated IgG antibody levels that
persist for months or years, whereas IgA levels decay much more rapidly. For this reason,
IgA antibody is considered a more reliable marker for chronic C. pneumoniaeinfection
(154)
.
Our study aimed to investigate the role of C. pneumoniaeinfection in the
pathophysiology of bronchial asthma.
The current study included 35 clinically diagnosed asthmatic patients as defined by
the American Thoracic Society
(152)
attended the Clinical Physiology Unit of Medical
Research Institute (MRI). They were asymptomatic atthe time of the study and their
asthma clinically stable before the study. Inhaled corticosteroids, ketotifen, and disodium cromoglycate stopped 2 weeks before the study; other anti-asthma drugs stopped 8 hours
before the study. All patients should be free from any other pulmonary tract infection.
The current study included 15 normal subjects as a control group; none of them had
ever suffered from asthma, allergic disease or any bronchial or respiratory tract infection
within four to five months before the beginning of the study.
All patients and normal subjects should be non-smokers.
A- Physiological parameters:
1. Pulmonary flow rates were assessed in asthmatic patients as well as in control
subjects. The pulmonary flow rates were measured using computerized dry
spirometer (Jaeger from Germany) with automatic dosimeter for methacholine
inhalation challenge. They included: forced vital capacity (FVC), forced expiratory
volume in one second (FEV
1), FEV
1
/FVC %, and forced expiratory flow rate
between 25% and 75% (FEF25-75%
).
2. Methacholine inhalational challenge was performed only for the asthmatic patients
to assess BHR. The provocational dose of methacholine causing 20% DROP in FEV
1
(PD20-FE Vı
) was obtained.
B- Serological parameters:
• All serum samples from asthmatic patients, and control subjects evaluated for
C. pneumoniae specific IgG, IgA, and IgM antibodies by respectivecommercially
available ELISA kits (R-Biopharm AG, Germany).
After data were collected, it was revised, coded and fed to statistical software SPSS version
16.
The results revealed the following:
• A significant difference in FEV1/FVC%, and FEF25-75%
% pred was detected between
asthmatic patients and control subjects (P = 0.000,and 0.000). Although, no significant
difference was detected between asthmatic patients and control subjects in
FVC % pred, and FEV1
% pred.
• A significant difference in IgM was detected between asthmatic patients and control
subjects (P = 0.035). Although, no significant difference was detected between
asthmatic patients and control subjects in IgA, andIgG.
• The PD20-FEVı
mean value for the asthmatic patients was 0.038 ± 0.049 mg/ml.
• A significant negative intermediate correlations between IgM, and
FVC % pred (r = -0.487, P = 0.003), between IgM, and FEV
1
% pred (r = -0.395,
P = 0.019), between IgG, and FVC % pred (r = -0.366, P = 0.031), and between IgG,
and FEV
1
% pred (r = -0.433, P = 0.009) was detected among asthmatics.
• No significant correlation between IgA and any of pulmonary function tests (FVC%
pred, FEV
1% pred, FEV1/FVC% and the FEF25-75%
% pred) was detected among
asthmatics.
No significant correlation between PD 20-FEVı
and Sample index of IgA, IgM, and IgG
was detected among asthmatics.
It is concluded that C. pneumoniaeinfection whether recent infection which detected
by prevalence of IgM or reinfection which detected by prevalence of IgG was associated
with more decline in FEV1
% predicted, and FVC% predicted in asthmatic patients
illustrating that recent or reactivation of C. pneumoniaeinfection can exaggerate asthma in
previously asthmatic patients but not initiate asthma in healthy subjects.