• Tuberculosis and Respiratory Diseases
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• v.65 no.4
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• pp.261-268
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• 2008

The role of atypical bacterial infection in the pathogenesis of asthma is a subject of continuing debate. There is an increasing body of literature concerning the association between the atypical bacteria such as Mycoplasma pneumoniae (M. pneumoniae) and asthma pathogenesis. Moreover, many studies investigating such a link have been uncontrolled and have provided conflicting evidence, in part due to the difficulty in accurately diagnosing infection with these atypical pathogens. This manuscript will review the relationship between M. pneumoniae infection and asthma pathogenesis.

• Clinical and Experimental Pediatrics
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• v.53 no.1
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• pp.1-6
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• 2010

Transient tachypnea of the newborn (TTN), respiratory distress syndrome (RDS), and persistent pulmonary hypertension of the newborn (PPHN) are the three most common disorders that cause respiratory distress after birth. An understanding of the pathophysiology of these disorders and the development of effective therapeutic strategies is required to control these conditions. Here, we review recent papers on the pathogenesis and treatment of neonatal respiratory disease.

• Tuberculosis and Respiratory Diseases
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• v.42 no.4
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• pp.431-446
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• 1995

• Tuberculosis and Respiratory Diseases
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• v.79 no.4
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• pp.207-213
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• 2016

Chronic obstructive pulmonary disease (COPD) encompasses several clinical syndromes, most notably emphysema and chronic bronchitis. Most of the current treatments fail to attenuate severity and progression of the disease, thereby requiring better mechanistic understandings of pathogenesis to develop disease-modifying therapeutics. A number of theories on COPD pathogenesis have been promulgated wherein an increase in protease burden from chronic inflammation, exaggerated production of reactive oxygen species and the resulting oxidant injury, or superfluous cell death responses caused by enhanced cellular injury/damage were proposed as the culprit. These hypotheses are not mutually exclusive and together likely represent the multifaceted biological processes involved in COPD pathogenesis. Recent studies demonstrate that mitochondria are involved in innate immune signaling that plays important roles in cigarette smoke-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. These responses are reviewed herein and synthesized into a view of COPD pathogenesis whereby mitochondria play a central role.

• Sleep Medicine and Psychophysiology
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• v.12 no.2
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• pp.105-110
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• 2005

The pathogenesis and mechanism of obstructive sleep apnea (OSA) has been under investigation for over 25 years, but its etiology and mechanism remains elusive. Skeletal (maxillary and/or mandibular hypoplasia or retrodisplacement, inferior displacement of hyoid) and soft tissue (increased volume of soft tissue, adenotonsillar hypertrophy, macroglossia, thickened lateral pharyngeal walls) factors, pharyngeal compliance (increased), pharyngeal muscle factors (impaired strength and endurance of pharyngeal dilators and fixators), sensory factors (impaired mechanoreceptor sensitivity, impaired pharyngeal dilator reflexes), respiratory control system factors (unstable respiratory control) and so on facilitate collapse upper airway. Therefore, OSA may be a heterogeneous disorder, rather than a single disease entity and various pathogenic factors contribute to the OSA varies person to person. As a result, patients may respond to different therapeutic approaches based on the predominant abnormality leading to the sleep-disordered breathing.

• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.525-539
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• 2001

• Tuberculosis and Respiratory Diseases
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• v.45 no.3
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• pp.483-490
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• 1998

• Tuberculosis and Respiratory Diseases
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• v.54 no.2
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• pp.167-177
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• 2003

• IMMUNE NETWORK
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• v.13 no.5
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• pp.163-167
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• 2013

The dynamics of the virus-host interface in the response to respiratory virus infection is not well-understood; however, it is at this juncture that host immunity to infection evolves. Respiratory viruses have been shown to modulate the host response to gain a replication advantage through a variety of mechanisms. Viruses are parasites and must co-opt host genes for replication, and must interface with host cellular machinery to achieve an optimal balance between viral and cellular gene expression. Host cells have numerous strategies to resist infection, replication and virus spread, and only recently are we beginning to understand the network and pathways affected. The following is a short review article covering some of the studies associated with the Tripp laboratory that have addressed how respiratory syncytial virus (RSV) operates at the virus-host interface to affects immune outcome and disease pathogenesis.

• Tuberculosis and Respiratory Diseases
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• v.41 no.4
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• pp.311-318
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• 1994